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NEURO RELATED ARTICLES

 

NEURO RELATED ARTICLES

 Miscellaneous

 

Are Scents of Nature an Untapped Well-Being Boost?

https://neurosciencenews.com/olfaction-nature-wellbeing-26133/

 

Practice Makes Perfect: Crystallized Memory Formation Explored

https://neurosciencenews.com/crystallized-memory-practice-26135/

 

Climate Change Threatens Brain Health

https://neurosciencenews.com/brain-health-climate-change-26130/

 

Exercise Can Slow Brain Aging Cognitive Decline

 

https://neurosciencenews.com/exercise-aging-cognition-26110/

 

Covid-19

 

COVID-19 May Damage Vision

 

https://neurosciencenews.com/covid-eye-damage-vision-26105/

 

Pre-Pandemic Brain Wiring Predicted Teen Mental Health During COVID

 

https://neurosciencenews.com/salinece-network-covid-resilience-26138/

 

Dopamine Disruption Linked to Autism

 

https://neurosciencenews.com/dopamine-autism-26109/

 

 

Autism and PTSD Are Vulnerably Linked

https://neurosciencenews.com/asd-ptsd-neuroscience-26067/

 

Key Brain Region Implicated in Autism Sensory Issues

https://neurosciencenews.com/acc-hypersensitivity-asd-26073/

 

Fever Effect May Improve Autism Symptoms

https://neurosciencenews.com/fever-autism-behavior-26102/

 

Gut Microbes Influence Autism-Related Behaviors

https://neurosciencenews.com/microbiome-asd-behavior-26082/

 

Parasomnia: What Happens in the Brain During Sleepwalking?

https://neurosciencenews.com/parasomnia-brain-activity-26090/

 

Exercise Warps Time Perception

https://neurosciencenews.com/exercise-time-perception-26093/

 

 

 

Knowledge

 

Do We Really Learn From Failure?

 

https://neurosciencenews.com/failure-learning-psychology-26084/

 

 

Lack of Sleep in Childhood Linked to Increased Psychosis Risk

https://neurosciencenews.com/psychosis-child-sleep-26069/

 

Dreams Dull the Distress of Emotional Memories Mom’s Stress Hormone Shapes Child’s IQ

 

https://neurosciencenews.com/dreaming-emotional-memory-26099/

 

Sleep Apnea During REM Linked to Memory Decline

https://neurosciencenews.com/rem-sleep-apnea-memory-26109/

 

Scientific Different of Male  Female

 

AI Uncovers Hidden Differences in Male and Female Brain Structures

https://neurosciencenews.com/ai-brain-sex-differences-26101/

 

 

Unlocking Sleep’s Role in Emotional Health

https://neurosciencenews.com/sleep-emotional-health-26046/

 

Sex-Specific Brain Responses to Alcohol Craving

https://neurosciencenews.com/alcohol-brain-sex-differences-26043/

Virtual Reality Shows Promise in Treating Depression

https://neurosciencenews.com/depression-virtual-reality-26044/

 

https://neurosciencenews.com/human-brain-stimulation-neurotech25912/

Training Enhances Word Recognition for Efficient Reading

https://neurosciencenews.com/word-recognition-reading-learning-25947/

 

How Drugs Hijack the Brain’s Reward System

https://neurosciencenews.com/reward-system-drugs-mtorc1-25948/

 

Brain Cells That Enhance Memory Focus and Storage Identified

https://neurosciencenews.com/pac-neurons-memory-25938/

Autism’s Brain Structure Secrets Revealed

https://neurosciencenews.com/autism-brain-structure-25943/

 

How We Optimize Decisions for Mutual Benefit

https://neurosciencenews.com/mutual-benefit-decisions-neuroscience-25932/

 

 

Monoclonal Antibody Slows Rapid Motor Decline in Parkinson’s

https://neurosciencenews.com/monoclonal-antibody-parkinsons-25931/

 

HIV Drugs May Reduce Alzheimer’s Risk

https://neurosciencenews.com/alzheimers-hiv-drug-25936/

 

 

The Mysteries of Dreams and Their Impact on Our Lives

https://neurosciencenews.com/dreaming-sleep-impact-25928/

 

How Sex and Gender Shape Our Cognition

 

Hippocampus Generates Deep Sleep Waves

https://neurosciencenews.com/hippocampus-sleep-waves-memory-25897/

 

Gene Mutation Increases Autism Risk
https://neurosciencenews.com/autism-genetics-kmt2c-25889/


Insomnia Begins in Childhood and Persists Through Life

https://neurosciencenews.com/insomnia-neurodevelopment-25882/

Cannabis in Pregnancy Linked to Autism and ADHD Risk

https://neurosciencenews.com

Inflammation Biomarkers in Blood of Long-COVID Patients

https://neurosciencenews.com/inflammation-blood-long-covid-25880/

 

Early Career Work Schedules Tied to Midlife Health Risks

https://neurosciencenews.com/work-hours-aging-health-25872/

 

How the Brain Regulates Emotion

https://neurosciencenews.com/emotion-regulation-mapping-25870/

 

Genetics of Alcohol Use Explored

https://neurosciencenews.com/genetics-aud-25866/

 

Loneliness, Food Cravings, and the Brain

https://neurosciencenews.com/loneliness-food-cravings-25859/

 

Environmental Toxins Shorten Happy Lifespans

https://neurosciencenews.com/happiness-toxins-psychology-25845/

 

Aging Health: Blended Antioxidants Boost Memory and Cognition

https://neurosciencenews.com/aging-antioxidants-cognition-25846/

 

Compound May Curb Alcohol Dependence

 

https://neurosciencenews.com/aud-compound-neuropharmacology-25840/

 

Keto Diet May Improve Mental Health Symptoms

https://neurosciencenews.com/keto-diet-mental-health-25843/

 

Babies Predict Actions Based on Language Community

https://neurosciencenews.com/language-baby-action-25836/

Emotion vs. Reason: Rethinking Decision-Making

https://neurosciencenews.com/emotion-reason-decision-making-25803/

 

 

When Do Babies Begin to Be Conscious?

 

https://neurosciencenews.com/consciousness-neurodevelopment-25799/

 

Devil in the Details: The Visual World of Prosopometamorphopsia

 

https://neurosciencenews.com/prosopometamorphopsia-visual-neuroscience-25796/

 

Astrocytes Remember: A New Layer of Immune Memory Uncovered

 

https://neurosciencenews.com/astrocytes-immune-memory-25788/

 

Middle Age is A Critical Window for Predicting Brain Health

https://neurosciencenews.com/middle-age-brain-health-25778/

 

Happiness Takes Practice

https://neurosciencenews.com/happiness-practice-25736/

Brain Abnormalities in Children with Developmental Language Disorder

https://neurosciencenews.com/brain-abnormalities-idevelopmental-language-disorder-25764/

 

Brain Circuit Balances Speech and Breath

https://neurosciencenews.com/speech-breathing-brain-25721/

How Brain Networks Sustain Attention

https://neurosciencenews.com/attention-network-brain-25915/

 

 

Autism Genes Link to Sound Sensitivity

https://neurosciencenews.com/autism-genetics-sound-sensitivity-25682/

 

Autism Social Difficulties Linked to Specific Gene

https://neurosciencenews.com/autism-social-genetics-25685/

 

Language Processing Problems: A Prelude to Alzheimer’s

https://neurosciencenews.com/language-processing-alzheimers-25683/

 

Decoding Emotions: Beyond Senses in the Human Brain

https://neurosciencenews.com/sensory-input-emotion-25728/

 

Bilingualism: Native Language Eases Brain’s Effort

https://neurosciencenews.com/bilingual-native-language-brain-25731/

 

AI Maps Brain Tissues to Disease Symptoms

https://neurosciencenews.com/language-ai-brain-disease-25756/

 

Touch and See: Unlocking Early Self-Recognition in Toddlers

https://neurosciencenews.com/toddler-self-recognition-25755/

 

Gene Mutation Increases Autism Risk

Summary: Researchers made significant strides in understanding autism spectrum disorder’s genetic underpinnings. By studying mice with a frameshift mutation in the KMT2C gene, they observed behavioral and cognitive impairments resembling ASD symptoms.

Through extensive molecular analyses, they discovered an unexpected increase in the expression of genes linked to ASD risk due to KMT2C haploinsufficiency, implicating indirect effects on gene expression. Remarkably, treatment with the drug vafidemstat showed promise in correcting these abnormalities, suggesting a potential therapeutic approach for ASD and similar conditions.

Key Facts:

1.       Researchers found that a frameshift mutation in the KMT2C gene, leading to haploinsufficiency, models ASD-like symptoms in mice, including reduced sociality and cognitive impairments.

2.       Contrary to expectations, KMT2C haploinsufficiency resulted in increased expression of ASD-associated genes, indicating an indirect mechanism of transcriptomic dysregulation.

3.       Vafidemstat treatment ameliorated social deficits and normalized gene expression in mutant mice, pointing to a promising therapeutic pathway for ASD.

Source: Juntendo University

Autism spectrum disorder (ASD) encompasses neurodevelopmental conditions where patients display repetitive behavior and impaired sociality. Genetic factors have been shown to influence the development of ASD.

Additionally, recent studies have shown that the genes involved in chromatin modification and gene transcription are involved in the pathogenesis of ASD.

Among the many genes implicated in this process, the gene KMT2C (lysine methyltransferase 2c), which codes for a catalytic unit of H3K4 (histone H3 lysine 4) methyltransferase complex, has been identified to be associated with the development of autism and other neurodevelopmental disorders.

They observed that the altered genes associated with ASD risk were predominant in undifferentiated radial glial cells. Credit: Neuroscience News

Previous studies have shown that haploinsufficiency (a condition where, of the two copies of the gene, only one remains functional) of KMT2C is a risk factor for ASD and other neurodevelopmental disorders. However, the molecular mechanism through which the loss-of-function mutation in KMT2C leads to these conditions remains unclear.

To address this knowledge gap, researchers from Juntendo University, RIKEN, and the University of Tokyo in Japan aimed to provide answers to these questions in a benchmark study published in the journal Molecular Psychiatry on 26 March 2024. The research team included Professor Tadafumi Kato from the Department of Psychiatry and Behavioral Science at Juntendo University Graduate School of Medicine, Dr. Takumi Nakamura and Dr. Atsushi Takata from the RIKEN Center for Brain Science, and Professor Takashi Tsuboi from Graduate School of Arts and Sciences, The University of Tokyo.

To get to the bottom of KMT2C’s role in ASD pathogenesis, the team developed and analyzed genetically engineered strain mice (Kmt2c+/fs) having a frameshift mutation that models the KMT2C haploinsufficiency.

They then performed various behavioral analyses, in which they observed that the mutant mice exhibited lower sociality, inflexibility, auditory hypersensitivity, and cognitive impairments, which are all ASD-related symptoms.

Next, they performed transcriptomic and epigenetic profiling to understand the basis of the molecular changes observed in the mutant mice. What they discovered was remarkable: the genes associated with increased ASD risk showed higher expression in these mutant mice.

Dr. Takata exclaims, “This was somewhat unexpected. KMT2C mediates H3K4 methylation, which is thought to activate gene expression, and thereby KMT2C haploinsufficiency was expected to cause reduced expression of target genes.”

To gain mechanistic insights into their finding, the researchers carried out chromatin immunoprecipitation, a technique to determine the location on the DNA where the protein interacts with it.

They found an overlap between KMT2C and the differentially expressed genes exhibiting reduced expression, suggesting that KMT2C haploinsufficiency leads to ASD-related transcriptomic changes through an indirect effect on gene expression.

Further, to identify the cell types that contribute more to the pathological changes seen in the mutant mice, the researchers performed single-cell RNA sequencing of newborn mice brains. They observed that the altered genes associated with ASD risk were predominant in undifferentiated radial glial cells.

However, a gross change in the cell composition was not observed, implying that the transcriptomic dysregulation does not severely impact cell fate.

Finally, the researchers tested the effects of vafidemstat, a brain penetrant inhibitor of LSD1 (lysine-specific histone demethylase 1A), that could ameliorate histone methylation abnormalities.

They found that vafidemstat improved the social deficits in the mutant mice and had an exceptional rescuing effect by changing the expression levels of the differentially expressed genes to their normal expression level. This finding showed that vafidemstat is a valid drug for mutant mice and can potentially help restore the normal transcriptomic state.

What sets this discovery apart is that it challenges the commonly held belief that ASD disability may not be cured and demonstrates the efficacy of vafidemstat in improving ASD-like phenotypes.

The results open doors to future research to strengthen the foundation for the pharmacologic treatment of ASD and other neurodevelopmental disorders. Prof. Kato concludes, “Our research shows that drugs similar to vafidemstat may be generalizable to multiple categories of psychiatric disorders.”

About this genetics and autism research news

Author: Yoshitaka Nakashima
Source: 
Juntendo University
Contact: Yoshitaka Nakashima – Juntendo University
Image: The image is credited to Neuroscience News

Original Research: Open access.
Transcriptomic dysregulation and autistic-like behaviors in Kmt2c haploinsufficient mice rescued by an LSD1 inhibitor” by Tadafumi Kato et al. Molecular Psychiatry


Abstract

Transcriptomic dysregulation and autistic-like behaviors in Kmt2c haploinsufficient mice rescued by an LSD1 inhibitor

Recent studies have consistently demonstrated that the regulation of chromatin and gene transcription plays a pivotal role in the pathogenesis of neurodevelopmental disorders.

Among many genes involved in these pathways, KMT2C, encoding one of the six known histone H3 lysine 4 (H3K4) methyltransferases in humans and rodents, was identified as a gene whose heterozygous loss-of-function variants are causally associated with autism spectrum disorder (ASD) and the Kleefstra syndrome phenotypic spectrum.

However, little is known about how KMT2C haploinsufficiency causes neurodevelopmental deficits and how these conditions can be treated.

To address this, we developed and analyzed genetically engineered mice with a heterozygous frameshift mutation of Kmt2c (Kmt2c+/fs mice) as a disease model with high etiological validity. In a series of behavioral analyses, the mutant mice exhibit autistic-like behaviors such as impairments in sociality, flexibility, and working memory, demonstrating their face validity as an ASD model.

To investigate the molecular basis of the observed abnormalities, we performed a transcriptomic analysis of their bulk adult brains and found that ASD risk genes were specifically enriched in the upregulated differentially expressed genes (DEGs), whereas KMT2C peaks detected by ChIP-seq were significantly co-localized with the downregulated genes, suggesting an important role of putative indirect effects of Kmt2c haploinsufficiency.

We further performed single-cell RNA sequencing of newborn mouse brains to obtain cell type-resolved insights at an earlier stage.

By integrating findings from ASD exome sequencing, genome-wide association, and postmortem brain studies to characterize DEGs in each cell cluster, we found strong ASD-associated transcriptomic changes in radial glia and immature neurons with no obvious bias toward upregulated or downregulated DEGs. On the other hand, there was no significant gross change in the cellular composition.

Lastly, we explored potential therapeutic agents and demonstrate that vafidemstat, a lysine-specific histone demethylase 1 (LSD1) inhibitor that was effective in other models of neuropsychiatric/neurodevelopmental disorders, ameliorates impairments in sociality but not working memory in adult Kmt2c+/fs mice.

Intriguingly, the administration of vafidemstat was shown to alter the vast majority of DEGs in the direction to normalize the transcriptomic abnormalities in the mutant mice (94.3 and 82.5% of the significant upregulated and downregulated DEGs, respectively, P < 2.2 × 10−16, binomial test), which could be the molecular mechanism underlying the behavioral rescuing.

In summary, our study expands the repertoire of ASD models with high etiological and face validity, elucidates the cell-type resolved molecular alterations due to Kmt2c haploinsufficiency, and demonstrates the efficacy of an LSD1 inhibitor that might be generalizable to multiple categories of psychiatric disorders along with a better understanding of its presumed mechanisms of action.

https://neurosciencenews.com/autism-genetics-kmt2c-25889/

 

How Sex and Gender Shape Our Cognition

 

Summary: Researchers released a new study examining how sex and gender influence cognitive abilities. The study analyzed eight cognitive tasks and found that while spatial cognition correlates more with biological factors such as sex at birth and hormones, verbal cognition is more influenced by sociocultural factors like gender identity.

 

This research underscores the complexity of cognitive differences and stresses the importance of considering both sex-based and gender-based factors in psychological and neuroscientific research. The team’s approach encourages the inclusion of diverse populations to better understand and accurately depict the nuances of cognitive abilities.

 

Key Facts:

 

Spatial cognition is more closely associated with biological factors like sex and hormones, whereas verbal cognition is influenced by sociocultural factors such as gender identity.

The study suggests that sex at birth is not always the primary factor in explaining cognitive differences between genders.

The research advocates for more nuanced methodologies that incorporate both sex and gender measures to capture a comprehensive view of cognitive differences.

Source: University of Montreal

 

Many studies have found sex differences in cognitive abilities. In general, women outperform men on verbal and fine motor tasks, while men outperform women on spatial orientation and mental rotation tasks.

 

However, few studies have considered the influence of sociocultural factors such as gender identity, gender expression (stereotypical male and female behaviors) and sexual orientation in explaining these differences.

 

Now a new study by scientists at Université de Montréal does just that, by examining performance on eight cognitive tasks in relation to both sex-based and gender-based factors.

 

The ongoing research is being done by Mina Guérin, a Ph.D. student in neuropsychology, and Fanny Saulnier, an MSc student in psychiatric sciences, under the supervision of psychiatry professor Robert-Paul Juster.

 

Their results were published in January in the journal Biology of Sex Differences.

 

Gender diversity matters

The findings confirm that sex differences in spatial cognition are indeed better explained by biological factors, i.e., sex assigned at birth and sex hormones. But they also show that sex differences in verbal cognition are better explained by sociocultural factors, i.e., gender identity.

 

In short, spatial cognition seems more related to sex, while verbal cognition seems more related to gender. Sex assigned at birth is not always the most important variable in explaining sex differences in cognition.

 

“Our findings highlight the importance of considering gender diversity when seeking to understand sex differences and gender diversity in cognition,” said Juster.

 

The research team believes their findings will encourage researchers to use more sophisticated methodologies that use both sex and gender measures.

 

“By including people from diverse backgrounds, we can incorporate more sex- and gender-related variables into the analysis and ultimately get a more accurate picture of cognitive differences,” said Guérin. https://neurosciencenews.com/

 

 

Healing Touch: Mental Health Improved with Touch Intervention

https://neurosciencenews.com/

 

Summary: Touch interventions significantly benefit both physical and mental health, with particular advantages for individuals facing health challenges. The study, aggregating hundreds of individual studies, demonstrates that the nature of the touch, the person providing it, or the duration matters less than the frequency, suggesting even brief interactions like hugs can be profoundly impactful.

 

Furthermore, while touch from objects or robots can improve physical well-being, human touch appears essential for alleviating mental health conditions, underscoring the emotional component of touch. The research also highlights the enhanced benefits of parental touch for newborns, emphasizing its potential to support infant health in critical care situations.

 

Key Facts:

 

Touch interventions effectively reduce pain, anxiety, depression, and stress, with greater benefits observed in those with existing health conditions.

Frequency of touch has a more significant impact on well-being than the duration or source of the touch, highlighting the effectiveness of even small gestures of connection.

While non-human touch can aid physical health, human touch is crucial for mental well-being, indicating the importance of an emotional bond in touch interventions.

Source: KNAW

 

You might recognize the comforting feeling when someone offers you a hug at the end of a stressful day or strokes your shoulder when you’re feeling down. But the question remains: can touch really help you feel better, and does it matter who it’s from or how they touch you?

 

To explore these questions, researchers from the Social Brain Lab at the Netherlands Institute for Neuroscience and the University Hospital Essen conducted a large-scale analysis of studies exploring touch interventions.

The benefits of touch on mental and physical health

 

Does touch truly improve someone’s wellbeing? It is an easy question to ask but more complicated to answer. Individual studies often only focus on specific instances and may contradict each other.

 

Combining all these studies together for a large-scale analysis offers a clearer answer: yes, touch substantially improves both physical and mental wellbeing, for example via reduction of pain, anxiety, depression, and stress in adults. But in fact, those with physical or mental health problems (and therefore most in need of support) benefit even more from touch than healthy adults.

 

“This is especially relevant considering how often touch interventions are overlooked” Packheiser, first author, adds.

 

“A key question of our study is to leverage the hundreds of individual studies out there to identify what type of touch works best,” adds professor Keysers, director of the Social Brain Lab.

 

“What if you don’t have a friend or partner close by to hug you? Would touch from a stranger or even a machine also help? And how often?. The study clearly shows that touch can indeed be optimized, but the most important factors are not necessarily those we suspect.”

 

Interestingly, the person touching you, how they touch you, and the duration of their touch doesn’t make a difference in terms of impact. A long-lasting massage by a therapist could therefore be just as effective as a quick hug offered by a friend.

 

That is, until the frequency of the intervention is considered. The more often a touch intervention is offered, the greater the impact. A quick hug could therefore be even more impactful than a massage if it is offered more frequently.

 

Human or non-human touch?

 

The next question was whether touch intervention needs to be human at all. As it turns out, object or robot interventions can be equally effective at improving physical wellbeing.

 

“There are lots of people in need of wellbeing improvements, perhaps because they’re lonely but also because they may be inflicted by clinical conditions. These results indicate that a touch-robot, or even a simple weighted blanket has the potential to help those people”, last author Frédéric Michon explains.

 

However, the benefits of robot and object interventions are less effective for mental wellbeing. Mental health disorders like anxiety or depression might therefore require human touch after all, “perhaps suggestive of the importance for an emotional component associated with the touch”, Michon point out.

 

While the researchers were equally curious about human-to-animal contact, studies exploring this question are still lacking.

 

“It would be useful to see whether an animal’s or pet’s touch could improve wellbeing, and inversely if they also benefit from it, but unfortunately there simply aren’t enough studies, or properly controlled ones, for us to draw any general conclusions on these topics”, Michon clarifies.

 

Touch interventions across ages

 

When the team looked into the impact of touch on newborns, they found out that newborns also benefited significantly from touch. However, the person conducting the touch intervention was more important: the benefits of touch are higher when done by a parent instead of a healthcare worker.

 

“This finding could be impactful”, Packheiser adds.

 

“Death rates due to premature births are high in some countries and the knowledge that a baby benefits more from the touch of their own parent offers another easily implementable form of support for the baby’s health”.

 

Due to a lack of studies, it proved difficult to draw conclusions about children and teenagers.

 

“Large scale studies like this help us draw more general conclusions but they also help us identify where research is lacking”, Michon explains.

 

“We hope that our findings can steer future research to explore lesser-known questions. This includes animal touch, but also touch across ages, and in specific clinical settings like autistic patients, another category that has not been explored extensively”.

 

DECEMBER 12, 2023

4 MIN READ

Why Do We Dream? Maybe to Ensure We Can Literally ‘See’ the World upon Awakening

A theory holds that dreams are a way for the visual cortex of the brain to “defend its turf” against being “taken over” to process inputs from other senses

Dreams have fascinated people for millennia, yet we struggle to understand their purpose. Some theories suggest dreams help us deal with emotions, solve problems or manage hidden desires. Others postulate that they clean up brain waste, make memories stronger or deduce the meaning of random brain activity. A more recent theory suggests nighttime dreams protect visual areas of the brain from being co-opted during sleep by other sensory functions, such as hearing or touch.

David Eagleman, a neuroscientist at Stanford University, has proposed the idea that dreaming is necessary to safeguard the visual cortex—the part of the brain responsible for processing vision. Eagleman’s theory takes into account that the human brain is highly adaptive, with certain areas able to take on new tasks, an ability called neuroplasticity. He argues that neurons compete for survival. The brain, Eagleman explains, distributes its resources by “implementing a do-or-die competition” for brain territory in which sensory areas “gain or lose neural territory when inputs slow, stop or shift.” Experiences over a lifetime reshape the map of the brain. “Just like neighboring nations, neurons stake out their territory and chronically defend them,” he says.

Eagleman points to children who have had half their brain removed because of severe health problems and then regain normal function. The remaining brain reorganizes itself and takes over the roles of the missing sections. Similarly, people who lose sight or hearing show heightened sensitivity in the remaining senses because the region of the brain normally used by the lost sense is taken over by other senses.

Reorganization can happen fast. Studies published in 2007 and 2008 by Lotfi Merabet of Harvard Medical School and his colleagues showed just how quickly this takeover can happen. The 2008 study, in which subjects were blindfolded, revealed that the seizing of an idle area by other senses begins in as little as 90 minutes. And other studies found that this can occur within 45 minutes.

When we sleep, we can smell, hear and feel, but visual information is absent—except during REM sleep. About 90 minutes after drifting off to sleep, you enter REM. It begins when neurons in your brain stem, the stalklike section at the bottom of the organ, signal the beginning of two important tasks. Activity of these neurons, for one, paralyze major muscles, preventing the sleeper from acting out what is happening in the dream. Also, these brain cells send messages directly to the visual cortex, which initiates the dreaming process.

Why does REM follow that timetable? It conforms to when the visual cortex needs to start defending its territory, Eagleman argues. Scans of dreaming people show most of the brain activity associated with REM is within the visual cortex. Dreams are the brain’s way of fighting takeover from other senses, according to Eagleman, and REM activation prompts internally generated activity in the visual cortex as a means to safeguard its territory. As long as the neurons in the visual cortex are actively performing their customary job—in this case, generating visual imagery—they will not be commandeered by nearby neurons that process other sensory information.

Eagleman argues that the more plastic the brain, the more REM sleep is necessary to mount a defense. For babies to develop properly, they must sleep a lot, spending almost 50 percent of their time in REM sleep. But as people age, their brain becomes less flexible. (Think of how easily children learn languages, compared with adults.) At the same time, adults spend less time in REM sleep.

The correlation between adaptability and REM seems to hold across species. According to Eagleman, “Mother Nature drops human brains into the world half-baked and lets experience take over and shape them.” He argues the less hardwired a species’ brain is at birth, the more ability it has to adapt and learn from experience. But this has its disadvantages. For example, fawns and calves are able to walk within hours of birth because the behavior is hardwired. Human babies, with their more adaptable brains, require significantly more REM sleep than animals born with more hardwired brains.

Some researchers—in particular, dream researchers—disagree with Eagleman’s hypothesis. One example that raises doubts is the fact that the blind mole rat does not see and still experiences REM sleep. Yet some evolutionary adaptations are vestigial remnants of traits that were useful in the past but have become less significant as animals have evolved. So perhaps there was no pressure for blind mole rats to lose REM activity as they evolved without vision.

Antonio Zadra, a dream researcher at the University of Montreal, claims Eagleman’s theory “has little to do with actual dreaming and explains almost nothing about dreams per se, as opposed to REM sleep.” He asserts the theory “is, for me and many others who actually work in the field, silly and overly reductionistic and simplistic.”

Deirdre Leigh Barrett, a psychologist at Harvard University, former president of the International Association for the Study of Dreams and author of The Committee of Sleep, however, is more willing to consider Eagleman’s hypothesis. “It’s very convincing that there's a correlation between smarter animals and more elaborate brains,” she says. As far as dreams defending brain real estate, “I have a little more trouble with the visual argument, but it’s interesting.”

Eagleman says that his theory can accommodate other explanations for dreams and that REM sleep may serve many purposes besides protecting the visual cortex. Think of dreaming like a computer screen saver that is set to go off every 90 minutes—except that instead of protecting against frozen images, dreams prevent the visual cortex from being usurped by other functions. These visual hallucinations in the night may let us see during the day.

https://www.scientificamerican.com/article/why-do-we-dream-maybe-to-ensure-we-can-literally-see-the-world-upon-awakening/

 

 

 

 

Sleep Brainwaves Flush Brain of Waste

FeaturedNeurologyNeuroscience

Summary: A new study unveiled a crucial role of sleep: brainwaves facilitating the cleansing of the brain by flushing out waste. This discovery not only underscores the brain’s non-dormant state during sleep but also highlights a sophisticated system where neurons’ synchronized activity powers the flow of cerebrospinal fluid, effectively removing metabolic waste and potentially neurodegenerative disease-causing toxins.

This insight opens up possibilities for enhancing brain cleaning processes to combat neurological diseases and improve sleep efficiency, hinting at a future where optimized sleep could lead to better health outcomes.

Key Facts:

1.     Brainwaves Propel Cleansing Fluids: During sleep, neurons coordinate to produce rhythmic waves that drive the movement of fluid through the brain, washing away waste.

2.     Potential for Disease Prevention: Understanding and enhancing this cleansing process could delay or prevent diseases like Alzheimer’s and Parkinson’s by ensuring the effective removal of brain waste.

3.     Implications for Sleep Quality: This research suggests that improving the brain’s waste removal efficiency could allow for healthier brains even with less sleep, offering new avenues for treating sleep disorders and enhancing overall well-being.

Source: Washington University

There lies a paradox in sleep. Its apparent tranquility juxtaposes with the brain’s bustling activity. The night is still, but the brain is far from dormant. During sleep, brain cells produce bursts of electrical pulses that cumulate into rhythmic waves – a sign of heightened brain cell function.

But why is the brain active when we are resting?

Slow brain waves are associated with restful, refreshing sleep. And now, scientists at Washington University School of Medicine in St. Louis have found that brain waves help flush waste out of the brain during sleep. Individual nerve cells coordinate to produce rhythmic waves that propel fluid through dense brain tissue, washing the tissue in the process.

“These neurons are miniature pumps. Synchronized neural activity powers fluid flow and removal of debris from the brain,” explained first author Li-Feng Jiang-Xie, PhD, a postdoctoral research associate in the Department of Pathology & Immunology.

 

“If we can build on this process, there is the possibility of delaying or even preventing neurological diseases, including Alzheimer’s and Parkinson’s disease, in which excess waste – such as metabolic waste and junk proteins – accumulate in the brain and lead to neurodegeneration.”

 

The findings are published Feb. 28 in Nature.

 

Brain cells orchestrate thoughts, feelings and body movements, and form dynamic networks essential for memory formation and problem-solving. But to perform such energy-demanding tasks, brain cells require fuel. Their consumption of nutrients from the diet creates metabolic waste in the process.

“It is critical that the brain disposes of metabolic waste that can build up and contribute to neurodegenerative diseases,” said Jonathan Kipnis, PhD, the Alan A. and Edith L. Wolff Distinguished Professor of Pathology & Immunology and a BJC Investigator. Kipnis is the senior author on the paper.

“We knew that sleep is a time when the brain initiates a cleaning process to flush out waste and toxins it accumulates during wakefulness. But we didn’t know how that happens. These findings might be able to point us toward strategies and potential therapies to speed up the removal of damaging waste and to remove it before it can lead to dire consequences.”

But cleaning the dense brain is no simple task. Cerebrospinal fluid surrounding the brain enters and weaves through intricate cellular webs, collecting toxic waste as it travels. Upon exiting the brain, contaminated fluid must pass through a barrier before spilling into the lymphatic vessels in the dura mater – the outer tissue layer enveloping the brain underneath the skull. But what powers the movement of fluid into, through and out of the brain?

Studying the brains of sleeping mice, the researchers found that neurons drive cleaning efforts by firing electrical signals in a coordinated fashion to generate rhythmic waves in the brain, Jiang-Xie explained. They determined that such waves propel the fluid movement.

The research team silenced specific brain regions so that neurons in those regions didn’t create rhythmic waves. Without these waves, fresh cerebrospinal fluid could not flow through the silenced brain regions and trapped waste couldn’t leave the brain tissue.

One of the reasons that we sleep is to cleanse the brain,” Kipnis said.

“And if we can enhance this cleansing process, perhaps it’s possible to sleep less and remain healthy. Not everyone has the benefit of eight hours of sleep each night, and loss of sleep has an impact on health.

“Other studies have shown that mice that are genetically wired to sleep less have healthy brains. Could it be because they clean waste from their brains more efficiently? Could we help people living with insomnia by enhancing their brain’s cleaning abilities so they can get by on less sleep?”

Brain wave patterns change throughout sleep cycles. Of note, taller brain waves with larger amplitude move fluid with more force. The researchers are now interested in understanding why neurons fire waves with varying rhythmicity during sleep and which regions of the brain are most vulnerable to waste accumulation.

“We think the brain-cleaning process is similar to washing dishes,” neurobiologist Jiang-Xie explained.

“You start, for example, with a large, slow, rhythmic wiping motion to clean soluble wastes splattered across the plate. Then you decrease the range of the motion and increase the speed of these movements to remove particularly sticky food waste on the plate.

“Despite the varying amplitude and rhythm of your hand movements, the overarching objective remains consistent: to remove different types of waste from dishes. Maybe the brain adjusts its cleaning method depending on the type and amount of waste.”

https://neurosciencenews.com/sleep-brainwaves-flush-waste-25678/

Your brain needs a really good lawyer

Sigal Samuel is a senior reporter for Vox’s Future Perfect and co-host of the Future Perfect podcast. She writes primarily about the future of consciousness, tracking advances in artificial intelligence and neuroscience and their staggering ethical implications. She also writes about how to make the world better for all of us now, from improving mental health to alleviating poverty to protecting nature.

Before joining Vox, Sigal was the religion editor at the Atlantic. Her work has also been published in outlets like BuzzFeed, the Daily Beast, the Rumpus, and Electric Literature. She has appeared on NPR, BBC, and CBC. Sigal is also the author of two award-winning books. Osnat and Her Dove, a children’s book, tells the true story of the world’s first female rabbi. The Mystics of Mile End, a novel, tells the story of a dysfunctional family dealing with mysticism, madness, and mathematics in Montreal. Sigal earned her MFA in creative writing from the University of British Columbia and her BA in philosophy from McGill University. Learn more about Sigal here.


Ethics Statement

Future Perfect coverage may include stories about organizations that writers have made personal donations to. This does not in any way affect the editorial independence of our coverage, and this information will be disclosed clearly when relevant.

Future Perfect is supported in part by grants from 
foundations and individual donors. Future Perfect prizes its editorial independence, and all editorial decisions are made separately from fundraising and commercial considerations. See Vox’s ethics and guidelines for more.

Your brain needs new rights

Rafael Yuste, a Columbia University neuroscientist, started to get freaked out by his own neurotech research a dozen years ago. At his lab, employing a method called optogenetics, he found that he could manipulate the visual perception of mice by using a laser to activate specific neurons in the visual cortex of the brain. When he made certain images artificially appear in their brains, the mice behaved as though the images were real. Yuste discovered he could run them like puppets.

He’d created the mouse version of the movie Inception. And mice are mammals, with brains similar to our own. How long, he wondered, until someone tries to do this to humans?

In 2017, Yuste gathered around 30 experts to meet at Columbia’s Morningside campus, where they spent days discussing the ethics of neurotech. As Yuste’s mouse experiments showed, it’s not just mental privacy that’s at stake; there’s also the risk of someone using neurotechnology to manipulate our minds. While some brain-computer interfaces only aim to “read” what’s happening in your brain, others also aim to “write” to the brain — that is, to directly change what your neurons are up to.

The group of experts, now known as the Morningside Group, published Nature paper later that year making four policy recommendations, which Yuste later expanded to five. Think of them as new human rights for the age of neurotechnology:

1. Mental privacy: You should have the right to seclude your brain data so that it’s not stored or sold without your consent.

2. Personal identity: You should have the right to be protected from alterations to your sense of self that you did not authorize.

3. Free will: You should retain ultimate control over your decision-making, without unknown manipulation from neurotechnologies.

4. Fair access to mental augmentation: When it comes to mental enhancement, everyone should enjoy equality of access, so that neurotechnology doesn’t only benefit the rich.

5. Protection from bias: Neurotechnology algorithms should be designed in ways that do not perpetuate bias against particular groups.

But Yuste wasn’t content to just write academic papers about how we need new rights. He wanted to get the rights enshrined in law.

“I’m a person of action,” Yuste told me. “It’s not enough to just talk about a problem. You have to do something about it.”

Gut Bacteria May Play Role in Vision Loss

https://neurosciencenews.com/gut-bacteria-vision-loss-25660/

Speech Speed May Indicate Aging Brain Health

https://neurosciencenews.com/speech-speed-brain-health-aging-25661/

Researchers Overrate Their Ethical Practices

https://neurosciencenews.com/research-ethics-25667/

Unlocking the Brain’s Fear Circuitry: A Pathway to Survival Responses

https://neurosciencenews.com/fear-response-neuroscience-25656/

https://www.iqrasense.com/death-and-after-life/the-journey-of-a-muslim-believer-after-death-islamic-beliefs-according-to-hadith.html 

Mapping the Brain’s ‘Dysfunctome’

https://neurosciencenews.com/dysfunctiome-brain-mapping-25651/

Relaxing Words Steer Sleep Quality

https://neurosciencenews.com/auditory-stimuli-sleep-25652/

Ultrasound Brain Stimulation: A Significant Leap in Neurotherapy

https://neurosciencenews.com/ultrasound-brain-stimulation-neurotherapy-25653/

Sleep, Circadian Rhythm, and Mental Health

Featured Neuroscience Psychology ·February 19, 2024

Summary: A new study highlights the critical link between sleep, circadian rhythms, and psychiatric disorders, suggesting that disturbances in sleep and internal body clocks can trigger or exacerbate mental health issues. The research underscores the prevalence of sleep-circadian disturbances across all psychiatric disorders, pointing to the need for holistic treatments that address these factors.

The review emphasizes the potential of new therapeutic approaches, such as light therapy and cognitive behavioral therapy for insomnia (CBT-I), to improve mental health outcomes. This work, incorporating insights from an international team, marks a step forward in understanding and treating psychiatric conditions by focusing on sleep and circadian science.

Key Facts:

Prevalence of Sleep-Circadian Disturbances: Sleep and circadian rhythm disturbances are commonly found across psychiatric disorders, with significant impacts on conditions like insomnia, bipolar disorder, and early psychosis.

Potential Mechanisms: The review explores mechanisms such as genetic predispositions, exposure to light, and changes in neuroplasticity that contribute to the link between sleep-circadian disturbances and psychiatric disorders.

Therapeutic Approaches: Highlighting the effectiveness of treatments like light therapy and CBT-I, the review suggests targeting sleep and circadian factors could lead to innovative treatments for psychiatric conditions.

Source: i) University of Southampton  ii) https://neurosciencenews.com/sleep-circadian-rhythm-mental-health-25633/

 

Problems with our sleep and internal body clock can trigger or worsen a range of psychiatric disorders, according to a new review of recent research evidence.

 

The review, published today [19 February] in Proceedings of the National Academy of Sciences (PNAS), suggests gaining a better understanding of the relationship between sleep, circadian rhythms and mental health could unlock new holistic treatments to alleviate mental health problems.

“Sleep-circadian disturbances are the rule, rather than the exception, across every category of psychiatric disorders,” says Dr Sarah L. Chellappa from the University of Southampton, senior author of the review. “Sleep disturbances, such as insomnia, are well understood in the development and maintenance of psychiatric disorders, but our understanding of circadian disturbances lags behind.

“It is important to understand how these factors interact so we can develop and apply sleep-circadian interventions that benefit the sleep and mental health symptoms of patients.”

An international team of researchers from the University of Southampton, Kings College London, Stanford University and other institutions explored recent evidence on sleep and circadian factors, focusing on adolescents and young adults with psychiatric disorders. This is a time when people are most at risk of developing mental health disorders and when disruption to sleep and circadian rhythms are likely to occur.

Insomnia is more common in people with mental health disorders than in the general population – during remission, acute episodes and especially in early psychosis, where difficulty falling and staying asleep affects over half of individuals.

Around a quarter to a third of people with mood disorders have both insomnia and hypersomnia, where patients find it hard to sleep at night, but are sleepier in the daytime. Similar proportions of people with psychosis experience this combination of sleep disorders.

Meanwhile, the few studies looking at circadian rhythm sleep-wake disorders (CRSWD) suggest that 32 per cent of patients with bipolar disorder go to sleep and wake later than usual (a condition called Delayed Sleep-Wake Phase Disorder). Body clock processes (such as endogenous cortisol rhythms) have been reported to run seven hours ahead during manic episodes and four to five hours behind during the depressive phase. Timing is normalised upon successful treatment.

What are the mechanisms?

The researchers examined the possible mechanisms behind sleep-circadian disturbances in psychiatric disorders. During adolescence, physiological changes in how we sleep combine with behavioural changes, such as staying up later, getting less sleep on school nights and sleeping in on weekends.

Dr Nicholas Meyer, from King’s College London, who co-led the review said: “This variability in the duration and timing of sleep can lead to a misalignment between our body clock and our sleep-wake rhythms can increase the risk of sleep disturbances and adverse mental health outcomes.”

Researchers also looked at the role of genes, exposure to light, neuroplasticity and other possible factors. Those with a genetic predisposition towards a reduced change in activity levels between rest and wake phases are more likely to experience depression, mood instability, and neuroticism. Population-level surveys show self-reported time outdoors was associated with a lower probability of mood disorder. Sleep is thought to play a key role in how the brain forms new neural connections and processes emotional memories.

New treatments

Dr Renske Lok, from Stanford University, who co-led the review said: “Targeting sleep and circadian risk factors presents the opportunity to develop new preventative measures and therapies. Some of these are population-level considerations, such as the timing of school and work days, or changes in the built environment to optimise light exposure. Others are personalised interventions tailored to individual circadian parameters.”

Cognitive Behavioural Therapy for Insomnia (CBT-I) has been shown to reduce anxiety and depressive symptoms, as well as trauma symptoms in people experiencing PTSD.

In unipolar and bipolar depression, light therapy (delivered on rising in the morning) was effective compared with a placebo. Using it in combination with medication was also more effective than using medication alone. Other findings suggest light is effective in treating perinatal depression.

The timing of medication, meals and exercise could also impact circadian phases. Taking melatonin in the evening can help people with Delayed Sleep-Wake Phase Disorder to shift their body clock forward towards a more conventional sleep pattern and may have beneficial effects in comorbid psychiatric disorders. Nightshift work can adversely affect mental health but eating in the daytime rather than during the night could help, with research showing daytime eating prevents mood impairment.

The review also points to innovative multicomponent interventions, such as Transdiagnostic Intervention for Sleep and Circadian dysfunction (Trans-C). This combines modules that address different aspects of sleep and circadian rhythms into a sleep health framework that applies to a range of mental health disorders.

Dr Chellappa said: “Collectively, research into mental health is poised to take advantage of extraordinary advances in sleep and circadian science and translate these into improved understanding and treatment of psychiatric disorders.”

Funding: The research was funded by the Alexander Von Humboldt Foundation.

https://neurosciencenews.com/sleep-circadian-rhythm-mental-health-25633/

https://neurosciencenews.com/long-covid-brain-fog-25645/

AI Unlocks Secrets of Human Imagination and Memory Formation

FeaturedNeuroscience

Summary: A new study employs generative AI to shed light on how the human brain processes memories for learning, imagination, and planning. The study used a computational model resembling the hippocampus and neocortex’s neural networks to simulate memory encoding and retrieval.

This model demonstrated how the neocortex forms efficient conceptual representations from experiences, allowing for both the recreation of past events and the generation of new ones. The research highlights the brain’s ability to reconstruct memories with unique details, offering insights into memory’s role in survival and prediction.

Key Facts:

1.      The AI model simulates the interaction between the hippocampus and neocortex in memory processing.

2.      The neocortex forms “conceptual” representations, enabling the brain to recreate past experiences and imagine new scenarios.

3.      The study provides insights into memory’s role in survival, predicting future events, and understanding memory distortions.

Source: UCL

Recent advances in generative AI help to explain how memories enable us to learn about the world, re-live old experiences and construct totally new experiences for imagination and planning, according to a new study by UCL researchers.

The study, published in Nature Human Behaviour and funded by Wellcome, uses an AI computational model – known as a generative neural network – to simulate how neural networks in the brain learn from and remember a series of events (each one represented by a simple scene).

The model featured networks representing the hippocampus and neocortex, to investigate how they interact. Both parts of the brain are known to work together during memory, imagination and planning.

Humans need to make predictions to survive (e.g. to avoid danger or to find food), and the AI networks suggest how, when we replay memories while resting, it helps our brains pick up on patterns from past experiences that can be used to make these predictions. Credit: Neuroscience News

Lead author, PhD student Eleanor Spens (UCL Institute of Cognitive Neuroscience), said: “Recent advances in the generative networks used in AI show how information can be extracted from experience so that we can both recollect a specific experience and also flexibly imagine what new experiences might be like.

“We think of remembering as imagining the past based on concepts, combining some stored details with our expectations about what might have happened.”

Humans need to make predictions to survive (e.g. to avoid danger or to find food), and the AI networks suggest how, when we replay memories while resting, it helps our brains pick up on patterns from past experiences that can be used to make these predictions.

Researchers played 10,000 images of simple scenes to the model. The hippocampal network rapidly encoded each scene as it was experienced. It then replayed the scenes over and over again to train the generative neural network in the neocortex.

The neocortical network learned to pass the activity of the thousands of input neurons (neurons that receive visual information) representing each scene through smaller intermediate layers of neurons (the smallest containing only 20 neurons), to recreate the scenes as patterns of activity in its thousands of output neurons (neurons that predict the visual information).

This caused the neocortical network to learn highly efficient “conceptual” representations of the scenes that capture their meaning (e.g. the arrangements of walls and objects) – allowing both the recreation of old scenes and the generation of completely new ones.

Consequently, the hippocampus was able to encode the meaning of new scenes presented to it, rather than having to encode every single detail, enabling it to focus resources on encoding unique features that the neocortex couldn’t reproduce – such as new types of objects.

The model explains how the neocortex slowly acquires conceptual knowledge and how, together with the hippocampus, this allows us to “re-experience” events by reconstructing them in our minds.

The model also explains how new events can be generated during imagination and planning for the future, and why existing memories often contain “gist-like” distortions – in which unique features are generalised and remembered as more like the features in previous events.  

Senior author, Professor Neil Burgess (UCL Institute of Cognitive Neuroscience and UCL Queen Square Institute of Neurology), explained: “The way that memories are re-constructed, rather than being veridical records of the past, shows us how the meaning or gist of an experience is recombined with unique details, and how this can result in biases in how we remember things.”

https://neurosciencenews.com/ai-imagination-memory-25498/

Brain Activity Now Watchable and Listenable

FeaturedNeuroscienceOpen Neuroscience Articles

Summary: Researchers developed an innovated a technique to convert complex neuroimaging data into audiovisual formats. By transforming brain activity and blood flow data from behaviors like running or grooming in mice into synchronized piano and violin sounds, accompanied by video, they offer an intuitive approach to explore the brain’s intricate workings.

This method not only makes it easier to identify patterns in large datasets but also enhances the understanding of the dynamic relationship between neuronal activity and behavior. The toolkit represents a significant step forward in neuroscientific research, enabling scientists to intuitively screen and interpret vast amounts of brain data.

Key Facts:

1.      Audiovisual Data Conversion: The toolkit translates neuroimaging data into a combination of musical notes and video, with different instruments representing various types of brain activity.

2.      Enhanced Pattern Recognition: This approach allows researchers to more easily identify correlations between specific brain activities and behaviors, enriching the analysis of complex neuroimaging datasets.

3.      Applications Across Experiments: Demonstrated across different experimental settings, including 2D and 3D brain imaging techniques, this method provides a versatile tool for neuroscientific exploration.

Source: PLOS

Complex neuroimaging data can be explored through translation into an audiovisual format – a video with accompanying musical soundtrack – to help interpret what happens in the brain when performing certain behaviors.

David Thibodeaux and colleagues at Columbia University, US, present this technique in the open-access journal PLOS ONE on February 21, 2024. Examples of these beautiful “brain movies” are included below. 

Recent technological advances have made it possible for multiple components of activity in the awake brain to be recorded in real time. Scientists can now observe, for instance, what happens in a mouse’s brain when it performs specific behaviors or receives a certain stimulus.

However, such research produces large quantities of data that can be difficult to intuitively explore to gain insights into the biological mechanisms behind brain activity patterns. 

Prior research has shown that some brain imaging data can be translated into audible representations. Building on such approaches, Thibodeaux and colleagues developed a flexible toolkit that enables translation of different types of brain imaging data—and accompanying video recordings of lab animal behavior—into audiovisual representations. 

The researchers then demonstrated the new technique in three different experimental settings, showing how audiovisual representations can be prepared with data from various brain imaging approaches, including 2D wide-field optical mapping (WFOM) and 3D swept confocally aligned planar excitation (SCAPE) microscopy. 

The toolkit was applied to previously-collected WFOM data that detected both neural activity and brain blood flow changes in mice engaging in different behaviors, such as running or grooming.

Neuronal data was represented by piano sounds that struck in time with spikes in brain activity, with the volume of each note indicating magnitude of activity and its pitch indicating the location in the brain where the activity occurred. Meanwhile, blood flow data were represented by violin sounds.

The piano and violin sounds, played in real time, demonstrate the coupled relationship between neuronal activity and blood flow. Viewed alongside a video of the mouse, a viewer can discern which patterns of brain activity corresponded to different behaviors.  

The authors note that their toolkit is not a substitute for quantitative analysis of neuroimaging data. Nonetheless, it could help scientists screen large datasets for patterns that might otherwise have gone unnoticed and are worth further analysis. 

The authors add: “Listening to and seeing representations of [brain activity] data is an immersive experience that can tap into this capacity of ours to recognize and interpret patterns (consider the online security feature that asks you to “select traffic lights in this image” – a challenge beyond most computers, but trivial for our brains)…[It] is almost impossible to watch and focus on both the time-varying [brain activity] data and the behavior video at the same time, our eyes will need to flick back and forth to see things that happen together.

“You generally need to continually replay clips over and over to be able to figure out what happened at a particular moment. Having an auditory representation of the data makes it much simpler to see (and hear) when things happen at the exact same time.”

https://neurosciencenews.com/brain-activity-audiovisual-25640/

Mapping Love and Sex in the Brain

Summary: Researchers developed the first comprehensive brain map showing activity in prairie voles during mating and bonding, uncovering 68 brain regions involved in forming enduring monogamous relationships. This study challenges previous assumptions that male and female brains operate differently during these processes, revealing nearly identical patterns of brain activity in both sexes.

Surprisingly, the most significant predictor of bonding-related brain activity was found to be male ejaculation, suggesting a profound emotional state that facilitates pair bonding. This groundbreaking research not only offers insights into the neurobiological basis of monogamy but also hints at potential parallels in human relationship formation and maintenance.

Key Facts:

1.      Comprehensive Brain Activity Mapping: The study identified 68 distinct brain regions involved in the stages of mating, bonding, and the development of stable relationships in prairie voles.

2.      Gender Similarities in Brain Patterns: Contrary to previous beliefs, the research found nearly identical patterns of brain activity in both male and female voles during bonding processes.

3.      Emotional State Tied to Male Ejaculation: The strongest predictor of bonding-related brain activity was male ejaculation, indicating its significant role in facilitating pair bonding and potentially suggesting orgasm-like responses in both sexes.

Source: UT Austin

How does sex relate to lasting love?

To answer that question, scientists have long studied a small Midwestern rodent called the prairie vole, one of the few mammals known to form long-term, monogamous relationships.

A team of researchers including Steven Phelps at The University of Texas at Austin has created the first brain-wide map of regions that are active in prairie voles during mating and pair bonding.

The researchers found that bonding voles experience a storm of brain activity distributed across 68 distinct brain regions that make up seven brain-wide circuits. The brain activity correlates with three stages of behavior: mating, bonding and the emergence of a stable, enduring bond.

Most of these brain regions the researchers identified were not previously associated with bonding, so the map reveals new places to look in the human brain to understand how we form and maintain close relationships.

Earlier studies concluded that male and female brains often use fundamentally different mechanisms to produce the same behaviors, such as mating and nurturing offspring. But in this study, bonding males and females had nearly identical patterns of brain activity.

“That was a surprise,” said Phelps, a professor of integrative biology at UT Austin and senior author of the new study in the journal eLife.

“Sex hormones like testosterone, estrogen and progesterone are important for sexual, aggressive and parental behaviors, so the prevailing hypothesis was that brain activity during mating and bonding would also be different between the sexes.”

Compared with humans, prairie voles have whirlwind courtships. Within half an hour of being together, a male and female begin to have sex, and they will do so repeatedly, often many times an hour.

Within a day, their amorousness will lead the pair to form a bond that can last a lifetime. Bonded pairs will groom each other, console each other when stressed, defend their shared territory and rear their young together.

The researchers were able to pinpoint with high resolution which brain cells were active in vole brains at various points over the course of the process that leads to and includes bonding.

This is the first time such a method has been applied to prairie voles. By studying more than 200 prairie voles across multiple times during mating and bonding, the researchers produced an unprecedented and foundational data set.

The strongest predictor of activity across the 68 brain regions that the researchers identified surprised them. It was male ejaculation, suggesting the experience elicits a profound emotional state—and not only in the affected males. Females, too, had more bonding-related brain activity with males who reached that milestone.

“The brain and behavior data suggest that both sexes may be having orgasm-like responses, and these ‘orgasms’ coordinate the formation of a bond,” Phelps said. “If true, it would imply that orgasms can serve as a means to promote connection, as has long been suggested in humans.”

Phelps cautioned that it’s impossible to know whether a female prairie vole is having an orgasm simply by watching its sexual behavior, though previous research has found that some female animals such as monkeys have these physiological responses.

In addition to Phelps, the study’s co-authors are Morgan Gustison, a former postdoctoral researcher at UT Austin now at the University of Western Ontario, Rodrigo Muñoz-Castañeda at Weill Cornell Medicine, and Pavel Osten at Cold Spring Harbor Laboratory.

Funding: The National Institutes of Health funded the research.

 

https://neurosciencenews.com/intimacy-brain-mapping-25649/

 

Smiling Alters Emotional Perceptions

FeaturedNeurosciencePsychology

Summary: Researchers discovered that a brief, electrically induced smile can make neutral faces seem happier, a revelation that holds promise for understanding emotional perception and potentially treating affective disorders. The study utilized facial electrical stimulation, a technique inspired by Charles Darwin’s work, to produce quick, involuntary smiles in participants.

This novel approach demonstrated that even a fleeting smile could significantly alter emotional perception, marking the first evidence of its kind. With implications for theoretical debates and clinical applications, this research could pave the way for new treatments for conditions like depression, Parkinson’s, and autism by enhancing facial emotion recognition.

Key Facts:

1.      Innovative Experimentation: Utilizing electrical stimulation, the study is the first to show that activating smile muscles makes neutral faces appear more joyful.

2.      Historical Inspiration: The technique modernizes methods developed by Duchenne de Boulogne and featured by Charles Darwin, applying controlled electrical currents to induce smiles with precision.

3.      Potential Clinical Applications: The findings open new avenues for exploring treatments for mood disorders and conditions affecting emotional expression, like Parkinson’s and autism, through improved understanding of facial feedback in emotion perception.

Source: University of Essex

Smiling for just a split second makes people more likely to see happiness in expressionless faces, new University of Essex research has revealed. 

The study led by Dr Sebastian Korb, from the Department of Psychology, shows that even a brief weak grin makes faces appear more joyful. 

The pioneering experiment used electrical stimulation to spark smiles and was inspired by photographs made famous by Charles Darwin. 

A painless current manipulated muscles momentarily into action – creating a short uncontrollable smile. 

This is the first time facial electrical stimulation has been shown to affect emotional perception. 

Dr Korb hopes the research can explore potential treatments for depression or disorders that affect expression, like Parkinson’s and autism.  

He said: “The finding that a controlled, brief and weak activation of facial muscles can literally create the illusion of happiness in an otherwise neutral or even slightly sad looking face, is ground-breaking. 

“It is relevant for theoretical debates about the role of facial feedback in emotion perception and has potential for future clinical applications.” 

Dr Korb used a modernised version of a technique first developed in the 19th century by the French physician Duchenne de Boulogne. 

Darwin published drawings of Duchenne’s work in The Expression of the Emotions in Man and Animals – his third major work on evolution. 

However, the voltage was dialled down for the new experiments to ensure the safety of participants and better control the smiles. 

By using computers, the team were able to control the onset of smiles with millisecond precision. 

In total 47 people took part in the Essex study which was published in Social Cognitive and Affective Neuroscience. 

They were shown digital avatars and asked to assess whether they looked happy or sad. In half the trials, smiling muscles were activated at the onset of the face. 

It emerged that producing a weak smile for 500 milliseconds was enough to induce the perception of happiness. 

Dr Korb says the results help us understand facial feedback and he hopes to expand the study. 

He said: “We are currently conducting more al research to further explore the phenomenon in healthy participants.  

“In the future, however, we hope to apply this technique to explore facial emotion recognition, for people with conditions like Parkinson’s, who are known to have reduced spontaneous facial mimicry and impaired facial emotion recognition.  

“Moreover, we have published guidelines to allow other researchers to safely start using electrical facial muscle stimulation.” 

https://neurosciencenews.com/smiling-emotional-perception-25643/

 

Genes and Nutrition Shape Baby Brain Growth

FeaturedGeneticsNeuroscience·February 20, 2024

Summary: Researchers uncovered how both maternal and fetal genes, alongside nutritional factors, influence the development of a baby’s cerebral cortex. Their research, leveraging the UK Biobank’s extensive data, found a direct association between higher birth weight, influenced by specific genetic variants, and increased cortical surface area.

 

The study highlights the significant roles of fetal insulin-related genes and maternal genes aiding toxin elimination in brain growth. Intriguingly, exposure to nutritional stresses like wartime famine showed a generational impact, emphasizing the critical interplay between genetics and environmental factors in prenatal and early life brain development.

 

Key Facts:

 

Genetic and Nutritional Influences: Genetic variants in both the mother and baby that contribute to birth weight are closely linked to the growth of the cerebral cortex, with maternal and fetal genes playing distinct roles.

Impact of Food Availability: The study demonstrates that the availability of food can modulate the influence of these genetic variants on brain development, with maternal detoxification genes being more crucial during times of famine.

Generational Effects: Exposure to extreme conditions such as the Dutch winter famine of 1944-45 highlighted the enduring impact of maternal genes on offspring’s cortical development, suggesting a transgenerational transmission of adaptive traits.

Source: University of Montreal

 

A new population-based study led by CHU Sainte-Justine researcher and Université de Montréal medical professor Tomas Paus reveals the roles of maternal and fetal genes in the growth of a baby’s cerebral cortex.

 

Published last week in Nature Communications, the study shows that genetic variants associated with higher birth weight are also associated with greater growth of the cerebral cortex.

 

However, food abundance or scarcity seems to influence the extent of the role played by the genes of the mother and the unborn baby.

With postdoctoral fellow Daniel Vosberg, Paus analyzed birth weight, birthweight genes and brain magnetic resonance imaging (MRI) data from several thousand adults in the UK Biobank, a biomedical database in the United Kingdom.

 

These analyses confirmed that higher birth weight is associated with larger cortex size (measured by surface area). In addition, the genetic variants present in the mother and baby that are associated with birthweight are also associated with cortical surface. In the baby, genes associated with insulin action are decisive, while in the mother, genetic variants favoring toxin elimination at the cellular level play a major role.

 

The two groups of genetic variants are not always equally important in determining cortex size.

 

“By comparing data by birth year and using statistical modeling and cellular interaction analysis, we’ve demonstrated the role of exposure to food restriction during gestation or infancy,” said Paus.

 

Exposed to wartime famine

In those who were exposed to wartime famine during the “Dutch winter” of 1944–45, maternal detoxification genes had the greatest impact on cortical growth.

 

This trait seems to be transmitted from one generation to the next, since the association is also found in the children of people who were thus exposed. In others, cortical growth is mainly associated with genes associated with fetal insulin action.

 

The analyses suggest that the genes that counteract the negative effects of food restriction, particularly in terms of cellular stress and immune activation, are critical.

 

“In times of famine, when cells are multiplying, the risk of errors is much greater,” said Paus. “That could explain why, in this context, the genes responsible for DNA repair are decisive for the baby’s brain growth.”

 

With a better understanding of the relationship between low birth weight and brain growth, and the importance of malnourishment as a mediating factor, the researchers will next evaluate the best way to promote cortical growth after birth in small babies.

 

In collaboration with CHU Sainte-Justine pediatrician and UdeM clinical associate professor Thuy Mai Luu, “we’ll soon be launching a pilot project to determine the best way to support optimal brain development in low-birth-weight babies,” said Paus.

https://neurosciencenews.com/genes-nutrition-neurodevelopment-25635/

Decision Making: The Brain’s Blueprint for Future Insights

FeaturedNeuroscience·February 20, 2024

Summary: Researchers made a breakthrough in understanding how the brain makes decisions about future information, pinpointing the lateral habenula as a key player in this process. Their study demonstrates that humans and animals evaluate the worth of cognitive rewards, such as information about the future, using mental rules that the brain applies to both tangible rewards and the intangible satisfaction of curiosity.

 

This research not only sheds light on the fundamental mechanisms of decision-making but also offers potential pathways for treating mental health disorders characterized by impaired decision-making, such as OCD, anxiety, and depression, by targeting specific neural circuits involved in processing uncertainty and cognitive rewards.

 

Key Facts:

 

Lateral Habenula’s Role: The study identifies the lateral habenula, an ancient brain structure, as crucial in regulating decision-making about physical and cognitive rewards.

Mental Rules for Decision-Making: Researchers discovered that the brain uses a set of mental rules to decide the value of information about the future, revealing how much individuals are willing to pay to resolve uncertainty.

Implications for Mental Health: The findings have significant implications for understanding and treating mental illnesses that affect decision-making, pointing towards more personalized medicine approaches by pinpointing specific malfunctions in uncertainty processing.

Source: WUSTL

 

Researchers at Washington University School of Medicine in St. Louis have new insight on what goes on inside people’s heads as they make decisions to obtain information about the future.

 

The scientists identified a set of mental rules that governs decision-making about physical rewards—for example, food or money—and cognitive rewards—like the joy felt when accessing sought information.

 

They also identified the part of the brain that regulates this type of decision-making. The process occurs in the lateral habenula, an ancient brain structure shared by species as distantly related as people and fish.

The study is published in Nature Neuroscience.

 

The findings not only offer insight into the body’s most mysterious organ but have the potential to help people struggling with tough choices, whether due to the inherent complexity of certain decisions—such as whether to take a genetic test that might return unwelcome information—or due to mental illnesses that affect the ability to make decisions, such as obsessive-compulsive disorder (OCD), anxiety and depression.

 

“Identifying the circuits involved with assigning value to cognitive rewards, like information about the future, is really important, because that kind of valuation is often what breaks down in mental disorders,” said senior author Ilya Monosov, a professor of neuroscience at Washington University.

 

“If we can understand exactly what part of the decision-making process is malfunctioning in an individual, we may be able to target that aspect of the process precisely and treat some mental illnesses more effectively.”

 

Making a choice between two options often requires weighing the values of and making trade-offs between multiple factors. Some of these factors are concrete and practical. But there are also intangible factors that can provide powerful motivation to choose one option over another, such as the desire to satisfy curiosity and gain information.

 

Some information has practical value, of course, such as advance warning of an incoming hurricane. But experiments have shown that people and animals value obtaining information even when they cannot parlay it into something useful.

 

“Take, for example, a student who turns in a final exam and then wants to know the results immediately,” said co-first author Yang-Yang Feng, an MD/Ph.D. student who designed and led the the study’s experiments with human participants.

 

“Finding out your score today versus finding out in a week won’t change the results or gain you any kind of advantage. But some people want to know so badly that they will pay to find out early. That’s called non-instrumental information seeking, trying to obtain information for its own sake.”

 

Historically, the drive to obtain practical rewards, such as money or food, and the drive to obtain information have been studied as separate phenomena. This division is artificial and oversimplifies the choices people make in the real world, the researchers said.

 

Feng and co-first author Ethan Bromberg-Martin, a senior scientist in Monosov’s lab, designed experiments that required participants to make trade-offs between rewards and non-instrumental information, to come to a final decision.

 

Study participants were given a choice between two options, each of which gave them a chance at obtaining a few cents. The amount of money they could win and the likelihood of winning it varied. Some of the options came with the promise to learn the outcome early, before actual money arrived. In separate experiments, monkeys were offered analogous choices, with juice as the reward instead of money.

 

“By analyzing the trade-offs individuals made, we were able to work out some of the rules that individuals use to decide how much they’re willing to pay for information,” Bromberg-Martin said. “These rules generalized between humans and animals, suggesting that this abstract value may be conserved through evolution.”

 

One of the key principles they uncovered is that individuals seek information largely to resolve uncertainty. The more uncertainty, the more they are willing to pay for information about it. Intuitively, this makes sense.

 

You would probably be willing to pay more to find out the outcome of a $100 bet than a $1 bet, especially if you could get the information sooner rather than later. These and other principles form a logical framework that the brain relies on to make choices.

 

But sometimes the system malfunctions.

 

“Some people with OCD exhibit what’s known as checking behaviors, where they go back and check the same thing over and over,” Monosov said. “This is aberrant information-seeking behavior, and it is basically due to a misprocessing of uncertainty.”

 

As part of this study, the team discovered that decision-making algorithms are implemented through a neurological circuit that culminates in the lateral habenula, a tiny structure located deep in the brain. The lateral habenula is a major regulator of dopamine and has been linked to mental illnesses including depression, anxiety and OCD.

 

The team is working on using tasks requiring participants to make choices, similar to those in this study, to classify people with OCD into subtypes that correspond to how their brains process uncertainty. Doing so would be a step toward more targeted therapies.

“A person may be fine in some regards, but their uncertainty processing is off in one specific way,” Monosov said.

“Rather than saying that someone has a broad mental disorder such as OCD, we could say that their uncertainty processing is broken in this specific way, and here’s how we can modulate it. It’s a step toward more personalized medicine for mental illnesses.”

https://neurosciencenews.com/decision-making-brain-insight-25637/

 

Ripples of Recall: Brain Waves Play Key Role in Memory

Summary: Researchers have advanced our understanding of the neuronal basis of spatial memory. Their research reveals that during spatial memory tasks, different types of nerve cells activate in unison, coordinated by brain waves known as “ripples.”

 

This discovery highlights the intricate process of how our brains link locations to objects, a fundamental aspect of associative memory that can deteriorate in conditions like Alzheimer’s disease. The findings not only deepen our comprehension of human memory but also pave the way for potential new treatments for memory impairments.

 

Key Facts:

 

Diverse Neuronal Activation: The study found that specific nerve cells respond to objects and locations during memory retrieval, working together to form associative memories.

Role of Brain Waves: Hippocampal ripples were observed to play a crucial role in coordinating these nerve cells, suggesting their importance in memory formation and retrieval.

Potential for Future Therapies: Understanding the neuronal basis of spatial and associative memory could lead to new therapeutic approaches for treating memory disorders such as Alzheimer’s.

Source: University of Bonn

Spatial navigation and spatial memory play a central role in our lives. Without these abilities, we would hardly be able to find our way around our surroundings and would find it difficult to remember past events. However, the neuronal basis of spatial memory is far from being fully understood.

A research group led by Prof. Lukas Kunz, who has recently joined the University Hospital Bonn (UKB), has gained new insights into this gap in knowledge. Together with scientists from New York and Freiburg, he discovered that different types of nerve cells become active together during spatial memory and are coordinated by brain waves (“ripples”).

The results have now been published in the journal Nature Neuroscience.

Associative memory allows that different pieces of information are linked together. “In the context of spatial memory, associative memory enables us to remember the locations of certain objects in the spatial environment,” explains Prof. Kunz, research group leader for Cognitive and Translational Neuroscience at the Department of Epileptology at the UKB. He is also a member of the Transdisciplinary Research Area (TRA) “Life & Health” at the University of Bonn.

“For example, we can remember where in the house we put our keys”. At older age or in certain diseases such as Alzheimer’s, however, this ability is limited.

“It is therefore important to investigate the neuronal basis of different forms of human memory,” says Prof. Kunz. In the long term, this could help develop new therapies for memory impairments.

Nerve cells play an important role in associative memory

Nerve cells are active while information is retrieved from memory. To further investigate this phenomenon, the researchers recorded the activity of individual nerve cells in epilepsy patients performing a memory task.

“In a virtual world, the participants were asked to remember the locations of different objects,” explains Prof. Kunz.

The recordings showed that different types of nerve cells became active during this memory task. Some nerve cells responded to certain objects, while other nerve cells activated in response to certain locations. The scientists observed that interactions between the different types of nerve cells became stronger over time when participants remembered the right object in the right place.

Brain waves coordinate the nerve cells

In addition to place and object neurons, the researchers observed hippocampal brain waves (“ripples”) that also occurred during the memory task, presumably playing a crucial role in the formation and retrieval of associative memories.

“Ripples could be important for the connection of different types of nerve cells and the formation of complex memories. It will be exciting to further investigate this idea in future studies,” explains Prof. Kunz.

It will also be interesting to study how memory performance is modulated when ripples are suppressed or triggered, providing insights into the causal relevance of ripples.

Prof. Kunz intends to continue the findings that he gained with his colleagues at Columbia University’s School of Engineering and Applied Science in New York and the University of Freiburg at the University Hospital Bonn.

“The department of epileptology at the UKB is well-known for its excellent brain research. The department has the unique opportunity to record the activity of individual nerve cells in the human brain in the video EEG monitoring unit, which is the heart of every epilepsy center.

“This provides exciting insights into the functioning of the human brain, which is only possible at a few research centers worldwide,” describes Prof. Kunz.

In his interdisciplinary research, he builds on the close exchange with other researchers and medical doctors, which is essential for the development of new research ideas.

https://neurosciencenews.com/memory-brain-waves-25630/

 

 

 

Why We Learn Better From People We Like

Summary: Our brains favor learning from individuals we like over those we dislike, a phenomenon crucial for memory integration.

Through experiments involving everyday objects, the study demonstrated that our ability to connect information and form new inferences is significantly affected by our personal feelings towards the information provider. This selective memory integration can shape our perceptions and beliefs, even in neutral contexts, suggesting an innate bias in how we assimilate information.

The findings highlight the fundamental role of personal preferences in learning and the potential for reinforcing polarization in society.

Key Facts:

1.      Our brains preferentially learn from and integrate information presented by people we like, affecting how we connect new experiences.

2.      This bias in memory integration can influence our beliefs and perceptions, potentially leading to selective memory and reinforced polarization.

3.      The research provides a fundamental insight into how personal preferences impact learning processes, extending beyond social media filter bubbles to basic brain functions.

Source: Lund University

Our brains are “programmed” to learn more from people we like – and less from those we dislike. This has been shown by researchers in cognitive neuroscience in a series of experiments.

Memory serves a vital function, enabling us to learn from new experiences and update existing knowledge. We learn both from individual experiences and from connecting them to draw new conclusions about the world.

This way, we can make inferences about things that we don’t necessarily have direct experience of. This is called memory integration and makes learning quick and flexible.

Inês Bramão, associate professor of psychology at Lund University, provides an example of memory integration: Say you’re walking in a park. You see a man with a dog. A few hours later, you see the dog in the city with a woman. Your brain quickly makes the connection that the man and woman are a couple even though you have never seen them together. 

“Making such inferences is adaptive and helpful. But of course, there’s a risk that our brain draws incorrect conclusions or remembers selectively”, says Inês Bramão.

Important who provides the information 

To examine what affects our ability to learn and make inferences, Inês Bramão, along with colleagues Marius Boeltzig and Mikael Johansson, set up experiments where participants were tasked with remembering and connecting different objects. It could be a bowl, ball, spoon, scissors, or other everyday objects. It turned out that memory integration, i.e., the ability to remember and connect information across learning events, was influenced by who presented it.

If it was a person the participant liked, connecting the information was easier compared to when the information came from someone the participant disliked. The participants provided individual definitions of ‘like’ and ‘dislike’ based on aspects such as political views, major, eating habits, favorite sports, hobbies, and music.

Can be translated to politics 

The findings can be applied in real life, according to the researchers. Inês Bramão takes a hypothetical example from politics: 

“A political party argues for raising taxes to benefit healthcare. Later, you visit a healthcare center and notice improvements have been made. If you sympathize with the party that wanted to improve healthcare through higher taxes, you’re likely to attribute the improvements to the tax increase, even though the improvements might have had a completely different cause”.

About fundamental mechanisms 

There’s already vast research describing that people learn information differently depending on the source and how that characterizes polarization and knowledge resistance. 

“What our research shows is how these significant phenomena can partly be traced back to fundamental principles that govern how our memory works”, says Mikael Johansson, professor of psychology at Lund University. “

We are more inclined to form new connections and update knowledge from information presented by groups we favor. Such preferred groups typically provide information that aligns with our pre-existing beliefs and ideas, potentially reinforcing polarized viewpoints”.

Innate way of handling information 

Understanding the roots of polarization, resistance to new knowledge, and related phenomena from basic brain functions offers a deeper insight into these complex behaviors, the researchers argue. So, it’s not just about filter bubbles on social media but also about an innate way of assimilating information. 

“Particularly striking is that we integrate information differently depending on who is saying something, even when the information is completely neutral. In real life, where information often triggers stronger reactions, these effects could be even more prominent”, says Mikael Johansson.

About this learning and memory research news

Author: Lotte Billing
Source: 
Lund University
Contact: Lotte Billing – Lund University
Image: The image is credited to Neuroscience News

Original Research: Open access.
Ingroup sources enhance associative inference” by Ines Bramao et al. Communications Psychology


Abstract

Ingroup sources enhance associative inference

Episodic memory encompasses flexible processes that enable us to create and update knowledge by making novel inferences across overlapping but distinct events. Here we examined whether an ingroup source enhances the capacity to draw such inferences.

In three studies with US-American samples (NStudy1 = 53, NStudy2 = 68, NStudy3 = 68), we investigated the ability to make indirect associations, inferable from overlapping events, presented by ingroup or outgroup sources.

Participants were better at making inferences based on events presented by ingroup compared to outgroup sources (Studies 1 and 3). When the sources did not form a team, the effect was not replicated (Study 2). Furthermore, we show that this ingroup advantage may be linked to differing source monitoring resources allocated to ingroup and outgroup sources.

Altogether, our findings demonstrate that inferential processes are facilitated for ingroup information, potentially contributing to spreading biased information from ingroup sources into expanding knowledge networks, ultimately maintaining and strengthening polarized beliefs.

 

The Impact of Borderline Personality Disorder on Jealousy and Relationship Retention

FeaturedNeurosciencePsychology

Summary: Individuals with borderline personality (BPD) features are more prone to suspicious jealousy, which significantly influences their romantic relationships. This suspiciousness leads to a range of mate retention behaviors, from affection and support to criticism and abuse.

The study highlights the complex role of BPD traits in shaping how individuals navigate romantic engagements, emphasizing the critical influence of emotional regulation on relationship dynamics. It underlines the need for a deeper understanding of BPD features’ impact on interpersonal relationships, offering insights into both the positive and negative strategies employed for mate retention.

Key Facts:

1.      Individuals with BPD traits exhibit higher levels of suspicious jealousy, affecting their approach to mate retention.

2.      This jealousy leads to both positive (benefit-provisioning) and negative (cost-inflicting) behaviors in relationships.

3.      The study’s findings are based on self-reported data and online samples, pointing to the intricate link between BPD features and relationship dynamics.

Source: Neuroscience News

Virgil Zeigler-Hill and Jennifer Vonk’s recent publication in Sexes unveils the intricate dynamics of how borderline personality features influence romantic relationships, with a keen focus on the mechanisms of suspicious jealousy.

This study brings to light that individuals with pronounced features associated with Borderline Personality Disorder (BPD) navigate romantic engagements through a broad spectrum of behaviors aimed at keeping their partners close.

From exhibiting affection and support to engaging in more detrimental actions such as criticism, neglect, or abuse, the behaviors are deeply intertwined with feelings of suspicious jealousy.

BPD is characterized by significant instability in interpersonal relationships, self-image, and emotions, alongside marked impulsivity. The disorder typically manifests in early adulthood across various contexts.

Individuals may experience intense episodes of anger, depression, and anxiety, which can last from a few hours to days. Zeigler-Hill and Vonk extend these findings to include individuals who exhibit borderline personality features but might not meet the full criteria for BPD diagnosis.

These individuals still show tendencies towards emotional dysregulation, fear of abandonment, frequent mood swings, and difficulty controlling anger, which in turn affects their romantic relationships.

In their study, the authors categorize mate retention strategies into two main types: benefit-provisioning and cost-inflicting behaviors.

Benefit-provisioning behaviors aim to positively affect the partner’s well-being through expressions of affection and support. On the other hand, cost-inflicting behaviors have a negative impact, including criticism, neglect, dishonesty, or abuse.

The study’s findings underscore that suspicious jealousy, characterized by doubts about a partner’s fidelity without solid evidence, often arising from personal insecurities or fears, is a significant driver of both types of behaviors in individuals with borderline personality features.

The researchers report that participants with higher levels of borderline personality features demonstrated a greater propensity for suspicious jealousy. This form of jealousy, in turn, increased their likelihood of engaging in both benefit-provisioning behaviors, such as showing affection and support, and cost-inflicting behaviors.

Notably, the study highlights that while benefit-provisioning behaviors can strengthen the bond between partners by fostering trust and intimacy, cost-inflicting behaviors, particularly those involving criticism, neglect, and abuse, can undermine trust, reduce relationship satisfaction, and potentially lead to the relationship’s demise.

Statistically, the study points out a significant correlation between borderline personality features and the increased use of mate retention strategies, both positive and negative. Specifically, individuals with higher borderline personality features were more likely to engage in cost-inflicting behaviors as a means of mate retention, showcasing the complex interplay between emotional dysregulation, fear of abandonment, and relationship dynamics.

This research provides a nuanced understanding of how borderline personality features can shape the landscape of romantic relationships, highlighting the dual nature of suspicious jealousy in promoting behaviors aimed at mate retention.

While the study offers profound insights, it also acknowledges its reliance on self-reported data and online samples, suggesting a need for further investigation through observational studies to validate and expand upon these findings.

By shedding light on the complex relationship between borderline personality features, suspicious jealousy, and mate retention behaviors, Zeigler-Hill and Vonk’s study opens new avenues for understanding and addressing the challenges faced by individuals with these personality features in romantic relationships.

About this mental health, BPD, and relationships research news

Author: Neuroscience News Communications
Source: 
Neuroscience News
Contact: Neuroscience News Communications – Neuroscience News
Image: The image is credited to Neuroscience News

Original Research: Open access.
Borderline Personality Features and Mate Retention Behaviors: The Mediating Roles of Suspicious and Reactive Jealousy” by Virgil Zeigler-Hill et al. Sexes


Abstract

Borderline Personality Features and Mate Retention Behaviors: The Mediating Roles of Suspicious and Reactive Jealousy

We investigated the roles that suspicious jealousy and reactive jealousy might play in the associations between borderline personality features (BPF) and mate retention behaviors.

Study 1 (N = 406) found that BPF had positive indirect associations with benefit-provisioning behaviors and cost-inflicting behaviors through suspicious jealousy but not through reactive jealousy.

Study 2 (N = 334 (a dyadic sample of 167 romantic couples)) revealed actor effects such that BPF had positive indirect associations with benefit-provisioning behaviors and cost-inflicting behaviors through suspicious jealousy for both men and women.

In addition, the positive association between BPF and benefit-provisioning behaviors was mediated by reactive jealousy in women but not in men.

The only partner effect that emerged from these analyses showed that BPF in women were negatively associated with the benefit-provisioning behaviors reported by their male partners.

Discussion focuses on the implications of these results for the function that jealousy might serve in the strategies used by individuals with BPF to maintain their romantic relationships.

Unlocking Cell Death Secrets: Lipids Key to Ferroptosis Control

FeaturedGeneticsNeuroscience

Summary: Researchers have made a groundbreaking discovery, identifying a rare lipid as a crucial factor in ferroptosis, a unique form of cell death. This lipid, characterized by its two polyunsaturated fatty acyl tails, plays a significant role in various conditions, including neurodegenerative diseases and cancer. The findings could revolutionize our approach to treating these diseases by either preventing or inducing ferroptosis.

Key Facts:

1.      Discovery of diPUFA Lipids: A rare lipid with two polyunsaturated fatty acyl tails, known as diPUFA phospholipid, has been found to significantly promote ferroptosis in cells, including those in aging brains and Huntington disease-affected brain tissue.

2.      Potential for Disease Treatment: Understanding the role of diPUFA lipids in ferroptosis opens new avenues for treating neurodegenerative diseases and cancer, by either preventing or inducing cell death.

3.      Interdisciplinary Research: The research was a collaborative effort by Columbia’s Department of Biological Sciences, Department of Chemistry, and the Columbia University Irving Medical Center, highlighting the interdisciplinary approach to uncovering the mechanisms of ferroptosis.

Source: Columbia University

Columbia researchers have found that a rare type of lipid is a key driver of ferroptosis, a form of cell death discovered by Columbia professor Brent Stockwell.

The findings provide new detail on how cells die during ferroptosis and could improve understanding of how to stop ferroptosis in contexts where it is harmfully occurring– in neurodegenerative diseases, for example– or induce it in contexts where it could be useful, such as using it to kill dangerous cancer cells.

The new research found that a rare type of lipid with two polyunsaturated fatty acyl tails, called a diPUFA phospholipid, was present in a range of contexts where ferroptosis was occurring, including in aging brains and Huntington disease-affected brain tissue. The finding indicates that the lipid is efficient at promoting ferroptosis.

The research was conducted by professors in Columbia’s Department of Biological Sciences, Department of Chemistry, and the Columbia University Irving Medical Center.

Stockwell first discovered ferroptosis in 2012, when he found that certain cells were dying because their lipid layers were collapsing– an unusual form of cell death that differs from the most common kind, which begins with the cell forming blisters on its outer surface.

Since that discovery, researchers in Stockwell’s lab and elsewhere have continued to investigate ferroptosis, discovering that it can occur naturally in aging cells, in pathological contexts, and can be induced to treat disease.

Another paper out this month with several co-authors found that a gene named PHLDA2 can sometimes promote ferroptosis by attacking a different lipid, and that this gene can block some tumors from forming.

Together, these papers show that specific lipids promote ferroptosis, so defining the driver lipids in specific cancers is important.

“The discovery that these diPUFA lipids are important drivers of ferroptosis deepens our understanding of this form of cell death, and these lipids’ role in controlling a cell’s homeostasis in general,” Stockwell said.

“Harnessing these lipids may eventually help us identify where ferroptosis has occurred and deliberately manipulate them to either induce cell death or stop it. This can begin to give us both understanding and the power to control cell death.”

https://neurosciencenews.com/ferroptosis-lipids-25622/

Persistent Impact of Smoking on the Immune System

FeaturedNeurologyNeuroscience

Summary: Smoking not only affects immune responses in the short term but also leaves a lasting imprint on the body’s defense mechanisms. Through the Milieu Intérieur cohort of 1,000 healthy volunteers, the study identified smoking, alongside latent cytomegalovirus infection and body mass index, as a key factor influencing immune responses.

This groundbreaking research demonstrates that the effects of smoking on adaptive immunity can persist for 10 to 15 years after cessation, attributed to epigenetic changes in DNA methylation that alter gene expression involved in immune cell metabolism. This insight opens new avenues for understanding how lifestyle choices like smoking can have enduring effects on our health.

Key Facts:

1.      Smoking significantly impacts both innate and adaptive immune responses, with some effects persisting for up to 15 years after quitting.

2.      The study used the Milieu Intérieur cohort to demonstrate how smoking, latent cytomegalovirus infection, and body mass index are major factors affecting immunity.

3.      Long-term effects of smoking on immunity are linked to epigenetic changes, specifically DNA methylation, highlighting the durable influence of smoking on the body’s defense systems.

Source: Institut Pasteur

Like other factors such as age, sex and genetics, smoking has a major impact on immune responses.

This is the finding recently made by a team of scientists at the Institut Pasteur using the Milieu Intérieur cohort of 1,000 healthy volunteers, established to understand variability in immune responses.

In addition to its short-term impact on immunity, smoking also has long-term consequences. For many years after they have quit the habit, smokers are left with effects on some of their bodies’ defense mechanisms acquired while smoking.

Basically, the immune system appears to have something resembling a long-term memory of the effects of smoking. Credit: Neuroscience News

These findings, which for the first time reveal a long-term memory of the effects of smoking on immunity, will be published in the journal Nature on February 14, 2024.

Individuals’ immune systems vary significantly in terms of how effectively they respond to microbial attacks. But how can this variability be explained? What factors cause these differences?

“To answer this key question, we set up the Milieu Intérieur cohort comprising 1,000 healthy individuals aged 20 to 70 in 2011,” comments Darragh Duffy, Head of the Translational Immunology Unit at the Institut Pasteur and last author of the study.

While certain factors such as age, sex and genetics are known to have a significant impact on the immune system, the aim of this new study was to identify which other factors had the most influence.”

The scientists exposed blood samples taken from individuals in the Milieu Intérieur cohort to a wide variety of microbes (viruses, bacteria, etc.) and observed their immune response by measuring levels of secreted cytokines.

Using the large quantities of data gathered for individuals in the cohort, the team then determined which of the 136 investigated variables (body mass index, smoking, number of hours’ sleep, exercise, childhood illnesses, vaccinations, living environment, etc.) had the most influence on the immune responses studied.

Three variables stood out: smoking, latent cytomegalovirus infection and body mass index. “The influence of these three factors on certain immune responses could be equal to that of age, sex or genetics,” points out Darragh Duffy.

As regards smoking, an analysis of the data showed that the inflammatory response, which is immediately triggered by infection with a pathogen, was heightened in smokers, and moreover, the activity of certain cells involved in immune memory was impaired. In other words, this study shows that smoking disrupts not only innate immune mechanisms, but also some adaptive immune mechanisms.

“A comparison of immune responses in smokers and ex-smokers revealed that the inflammatory response returned to normal levels quickly after smoking cessation, while the impact on adaptive immunity persisted for 10 to 15 years,” observes Darragh Duffy.

“This is the first time it has been possible to demonstrate the long-term influence of smoking on immune responses.”

Basically, the immune system appears to have something resembling a long-term memory of the effects of smoking. But how?

“When we realized that the profiles of smokers and ex-smokers were similar, we immediately suspected that epigenetic processes were at play,” says Violaine Saint-André, a bioinformatician in the Institut Pasteur’s Translational Immunology Unit and first author of the study.

“We demonstrated that the long-term effects of smoking on immune responses were linked to differences in DNA methylation – with the potential to modify the expression of genes involved in immune cell metabolism – between smokers, ex-smokers and non-smokers.”

It therefore appears that smoking can induce persistent changes to the immune system through epigenetic mechanisms. 

“This is a major discovery elucidating the impact of smoking on healthy individuals’ immunity and also, by comparison, on the immunity of individuals suffering from various diseases,” concludes Violaine Saint-André.

About this smoking and immune system research news

Author: Rebeyrotte Myriam
Source: 
Institut Pasteur
Contact: Rebeyrotte Myriam – Institut Pasteur
Image: The image is credited to Neuroscience News

Original Research: Open access.
Smoking changes adaptive immunity with persistent effects” by Darragh Duffy et al. Nature


Abstract

Smoking changes adaptive immunity with persistent effects

Individuals differ widely in their immune responses, with age, sex and genetic factors having major roles in this inherent variability. However, the variables that drive such differences in cytokine secretion—a crucial component of the host response to immune challenges—remain poorly defined.

Here we investigated 136 variables and identified smoking, cytomegalovirus latent infection and body mass index as major contributors to variability in cytokine response, with effects of comparable magnitudes with age, sex and genetics.

We find that smoking influences both innate and adaptive immune responses. Notably, its effect on innate responses is quickly lost after smoking cessation and is specifically associated with plasma levels of CEACAM6, whereas its effect on adaptive responses persists long after individuals quit smoking and is associated with epigenetic memory.

This is supported by the association of the past smoking effect on cytokine responses with DNA methylation at specific signal trans-activators and regulators of metabolism.

Our findings identify three novel variables associated with cytokine secretion variability and reveal roles for smoking in the short- and long-term regulation of immune responses. These results have potential clinical implications for the risk of developing infections, cancers or autoimmune diseases. https://neurosciencenews.com/smoking-immune-system-25614/

 

 

Brain Network Steering Left and Right Movements Discovered

FeaturedNeuroscience

Summary: Scientists have identified a new group of neurons that plays a crucial role in controlling left-right movements in walking, bridging a critical gap in our understanding of brainstem and basal ganglia interaction. This discovery provides insights into the brain’s complex navigation system previously linked to the ‘brain’s steering wheel.’

The findings might offer future therapeutic strategies for Parkinson’s disease. By studying mice, the team anticipates similar mechanisms in humans, potentially revolutionizing treatments for movement disorders.

Key Facts:

1.      The study reveals a new group of neurons in the brainstem that receives signals from the basal ganglia to control the direction of movement, offering a deeper understanding of how voluntary movements like walking are coordinated.

2.      Researchers used optogenetics to modify and stimulate these neurons in mice, successfully correcting impaired left or right movements, showcasing the method’s potential for treating motor symptoms in diseases like Parkinson’s.

3.      The basal ganglia’s critical role in voluntary movement has been known, but how it influences left-right movement decisions was unclear until this breakthrough, highlighting the importance of this brain area in motor control.

Source: University of Copenhagen

Have you ever wondered what happens in the brain when we move to the right or left? Most people don’t; they just do it without thinking about it. But this simple movement is actually controlled by a complex process. 

In a new study, researchers have discovered the missing piece in the complex nerve-network needed for left-right turns. The discovery was made by a research team consisting of Assistant Professor Jared Cregg, Professor Ole Kiehn, and their colleagues from the Department of Neuroscience at the University of Copenhagen. 

In 2020, Ole Kiehn, Jared Cregg and their colleagues identified the ‘brain’s steering wheel’ – a network of neurons in the lower part of the brainstem that commands right- and left- movements when walking. At the time, though, it was not clear to them how this right-left circuit is controlled by other parts of the brain, such as the basal ganglia. 

“We have now discovered a new group of neurons in the brainstem which receives information directly from the basal ganglia and control the right-left circuit,” Ole Kiehn explains. 

Eventually, this discovery may be able to help people suffering from Parkinson’s disease. The study has been published in the esteemed scientific journal Nature Neuroscience.  

The basal ganglia are located deep within the brain. For many years now, they have been known to play a key role in controlling voluntary movements. 

Years ago, scientists learned that by stimulating the basal ganglia you can affect right- and left-hand movements in mice. They just did not know how. 

“When walking, you will shorten the step length of the right leg before making a right-hand turn and the left leg before making a left-hand turn. The newly discovered network of neurons is located in a part of the brainstem known as PnO. They are the ones that receive signals from the basal ganglia and adjust the step length as we make a turn, and which thus determine whether we move to the right or left,” Jared Cregg explains. 

The study therefore provides a key to understanding how these absolutely essential movements are produced by the brain. 

In the new study, the researchers studied the brain of mice, as their brainstem closely resembles the human brainstem. Therefore, the researchers expect to find a similar right-left circuit in the human brain.  

https://neurosciencenews.com/basal-ganglia-navigation-25596/

Can AI Be Controlled?

FeaturedNeuroscience

Summary: Dr. Roman V. Yampolskiy, an AI Safety expert, warns of the unprecedented risks associated with artificial intelligence in his forthcoming book, AI: Unexplainable, Unpredictable, Uncontrollable. Through an extensive review, Yampolskiy reveals a lack of evidence proving AI can be safely controlled, pointing out the potential for AI to cause existential catastrophes.

He argues that the inherent unpredictability and advanced autonomy of AI systems pose significant challenges to ensuring their safety and alignment with human values. The book emphasizes the urgent need for increased research and development in AI safety measures to mitigate these risks, advocating for a balanced approach that prioritizes human control and understanding.

Key Facts:

1.      Dr. Yampolskiy’s review found no concrete evidence that AI can be entirely controlled, suggesting that the development of superintelligent AI could lead to outcomes as dire as human extinction.

2.      The complexity and autonomy of AI systems make it difficult to predict their decisions or ensure their actions align with human values, raising concerns over their potential to act in ways that could harm humanity.

3.      Yampolskiy proposes that minimizing AI risks requires transparent, understandable, and modifiable systems, alongside increased efforts in AI safety research.

Source: Taylor and Francis Group

There is no current evidence that AI can be controlled safely, according to an extensive review, and without proof that AI can be controlled, it should not be developed, a researcher warns.

Despite the recognition that the problem of AI control may be one of the most important problems facing humanity, it remains poorly understood, poorly defined, and poorly researched, Dr Roman V. Yampolskiy explains.

In his upcoming book, AI: Unexplainable, Unpredictable, Uncontrollable, AI Safety expert Dr Yampolskiy looks at the ways that AI has the potential to dramatically reshape society, not always to our advantage.

He explains: “We are facing an almost guaranteed event with potential to cause an existential catastrophe. No wonder many consider this to be the most important problem humanity has ever faced. The outcome could be prosperity or extinction, and the fate of the universe hangs in the balance.”

Uncontrollable superintelligence

Dr Yampolskiy has carried out an extensive review of AI scientific literature and states he has found no proof that AI can be safely controlled – and even if there are some partial controls, they would not be enough.

He explains: “Why do so many researchers assume that AI control problem is solvable? To the best of our knowledge, there is no evidence for that, no proof. Before embarking on a quest to build a controlled AI, it is important to show that the problem is solvable.

“This, combined with statistics that show the development of AI superintelligence is an almost guaranteed event, show we should be supporting a significant AI safety effort.”

He argues our ability to produce intelligent software far outstrips our ability to control or even verify it.  After a comprehensive literature review, he suggests advanced intelligent systems can never be fully controllable and so will always present certain level of risk regardless of benefit they provide. He believes it should be the goal of the AI community to minimize such risk while maximizing potential benefit.

What are the obstacles?

AI (and superintelligence), differ from other programs by its ability to learn new behaviors, adjust its performance and act semi-autonomously in novel situations.

One issue with making AI ‘safe’ is that the possible decisions and failures by a superintelligent being as it becomes more capable is infinite, so there are an infinite number of safety issues. Simply predicting the issues not be possible and mitigating against them in security patches may not be enough.

At the same time, Yampolskiy explains, AI cannot explain what it has decided, and/or we cannot understand the explanation given as humans are not smart enough to understand the concepts implemented. If we do not understand AI’s decisions and we only have a ‘black box’, we cannot understand the problem and reduce likelihood of future accidents.

For example, AI systems are already being tasked with making decisions in healthcare, investing, employment, banking and security, to name a few. Such systems should be able to explain how they arrived at their decisions, particularly to show that they are bias free.

Yampolskiy explains: “If we grow accustomed to accepting AI’s answers without an explanation, essentially treating it as an Oracle system, we would not be able to tell if it begins providing wrong or manipulative answers.”

Controlling the uncontrollable

As capability of AI increases, its autonomy also increases but our control over it decreases, Yampolskiy explains, and increased autonomy is synonymous with decreased safety.

For example, for superintelligence to avoid acquiring inaccurate knowledge and remove all bias from its programmers, it could ignore all such knowledge and rediscover/proof everything from scratch, but that would also remove any pro-human bias.

“Less intelligent agents (people) can’t permanently control more intelligent agents (ASIs). This is not because we may fail to find a safe design for superintelligence in the vast space of all possible designs, it is because no such design is possible, it doesn’t exist. Superintelligence is not rebelling, it is uncontrollable to begin with,” he explains.

“Humanity is facing a choice, do we become like babies, taken care of but not in control or do we reject having a helpful guardian but remain in charge and free.”

He suggests that an equilibrium point could be found at which we sacrifice some capability in return for some control, at the cost of providing system with a certain degree of autonomy.

Aligning human values

One control suggestion is to design a machine which precisely follows human orders, but Yampolskiy points out the potential for conflicting orders, misinterpretation or malicious use.

He explains: “Humans in control can result in contradictory or explicitly malevolent orders, while AI in control means that humans are not.”

If AI acted more as an advisor it could bypass issues with misinterpretation of direct orders and potential for malevolent orders, but the author argues for AI to be useful advisor it must have its own superior values.

“Most AI safety researchers are looking for a way to align future superintelligence to values of humanity. Value-aligned AI will be biased by definition, pro-human bias, good or bad is still a bias. The paradox of value-aligned AI is that a person explicitly ordering an AI system to do something may get a “no” while the system tries to do what the person actually wants. Humanity is either protected or respected, but not both,” he explains.

Minimizing risk

To minimize the risk of AI, he says it needs it to be modifiable with ‘undo’ options, limitable, transparent and easy to understand in human language.

He suggests all AI should be categorised as controllable or uncontrollable, and nothing should be taken off the table and limited moratoriums, and even partial bans on certain types of AI technology should be considered.

Instead of being discouraged, he says: “Rather it is a reason, for more people, to dig deeper and to increase effort, and funding for AI Safety and Security research. We may not ever get to 100% safe AI, but we can make AI safer in proportion to our efforts, which is a lot better than doing nothing. We need to use this opportunity wisely.”

https://neurosciencenews.com/

 

Exploring Brain Scan Hesitancy

MRI brain findings

FeaturedNeurologyNeuroscience

Summary: Asian Americans, particularly South and East Asian older adults, exhibit greater hesitancy towards participating in health research involving MRI brain scans compared to their white counterparts. The study surveyed older adults on their perceptions of MRI scans, willingness to learn scan results, and attitudes towards research participation and dementia.

Findings indicate a need for culturally sensitive approaches to encourage participation and improve representation in health studies. Addressing these hesitancies could lead to more inclusive research outcomes and better understanding of health issues affecting diverse populations.

Key Facts:

1.      South Asian and East Asian older adults show less interest than white older adults in learning about MRI scan findings and participating in research not directly beneficial to them.

2.      The study highlights the importance of understanding and addressing the concerns of different Asian American subgroups to enhance research diversity.

3.      Supported by Rutgers Institute for Health and other initiatives, this research underscores the need for culturally tailored recruitment strategies in health studies.

Source: Rutgers University

Asian Americans are less likely than their white peers to participate in health research involving MRIs and addressing this hesitancy could improve research, according to a Rutgers Health-led study.

Findings by the researchers, published in Alzheimer’s & Dementia: Translational Research & Clinical Interventions, a journal of the Alzheimer’s Association, surveyed older adults about their experiences and perceptions of MRI brain imaging scans, their desire to learn results of scans and their attitudes related to dementia and overall research participation.

According to the study, South Asian older adults – those 65 and older – are less likely than older white adults to believe that healthy people should participate in research studies when it may not benefit them.

South Asian and East Asian older adults also have less desire to learn about findings from an MRI brain scan – commonly used in clinical research studies – than older white adults.

“Addressing hesitancy toward participation may improve representation of a group that does not usually take part in research studies,” said Karthik Kota, an assistant professor of medicine and a geriatrician at Rutgers Robert Wood Johnson Medical School and lead author of the study.

Asian Americans represent the fastest-growing racial group in the United States and the fastest-growing group of adults over 65. As age is the biggest risk factor for dementia, this group is at higher risk for dementia. In a prior pilot study, Rutgers Health researchers encountered unexpected hesitancy from these groups related to MRI scans.

In the latest study, 256 respondents answered what type of MRI results they wanted to learn of – including receiving serious findings without treatment options or benign ones common with aging – and questions on research and brain health attitudes.

Researchers found similarly low desire to learn of MRI results in South Asians and East Asians despite the groups showing differing support for research participation and future dementia or stroke worries.

Researchers said the findings reinforce the need to separate different Asian American subgroups when conducting health-related research.

“Understanding concerns older Asian adults have about MRI brain findings could allow for more culturally appropriate return of scan results,” Kota said.

“Progress in this area will not only affect how researchers recruit for studies, but also the expectations that the public may have when interacting with researchers.”

Research was supported by the Resource Center for Alzheimer’s and Dementia Research in Asian and Pacific Americans at the Rutgers Institute for Health, Health Care Policy and Aging Research (IFH), as well as the South Asian Total Health Initiative and the RWJBarnabas Health Chinese Medical Program.

Coauthors of the study include Alice Dawson, Julia Papas, Victor Sotelo and William Hu of the Department of Neurology at Rutgers Robert Wood Johnson Medical School and the Center for Healthy Aging at IFH; and Guibin Su, Mei-Ling Li, Woowon Lee, Jaunis Estervil, Melissa Marquez, Shromona Sarkar and Lisa Lanza of IFH.

https://neurosciencenews.com/brain-scan-hesitancy-25590/

Women Scan For Danger When Walking at Night

Neuroscience

Summary: A new study highlights the stark differences in how men and women perceive safety while walking at night.

Through an innovative use of heat maps generated by participants’ focus on photographs of campus areas, the study found women were significantly more likely to scan for potential safety hazards in their surroundings, unlike men who focused on direct paths or specific objects.

This research, involving nearly 600 participants, underscores the gender-specific experiences of navigating public spaces after dark, calling for inclusive urban planning that addresses these distinct safety perceptions.

Key Facts:

1.      Women participants consistently scanned for potential safety hazards around the periphery of images, indicating a unique concern for safety while walking at night.

2.      Men’s attention was primarily directed towards paths and fixed objects, showing a different approach to navigating public spaces.

3.      The study’s findings suggest the need for urban and campus planning to consider the diverse safety needs and perceptions of all genders to create more inclusive environments.

Source: Brigham Young University

An eye-catching new study shows just how different the experience of walking home at night is for women versus men.

The study, led by Brigham Young University public health professor Robbie Chaney, provides clear visual evidence of the constant environmental scanning women conduct as they walk in the dark, a safety consideration the study shows is unique to their experience.

Chaney and co-authors Alyssa Baer and Ida Tovar showed pictures of campus areas at four Utah universities — Utah Valley University, Westminster, Brigham Young University and University of Utah — to participants and asked them to click on areas in the photos that caught their attention.

Women focused significantly more on potential safety hazards — the periphery of the images — while men looked directly at focal points or their intended destination.

“The resulting heat maps represent perhaps what people are thinking or feeling or doing as they are moving through these spaces,” Chaney said. “Before we started the study, we expected to see some differences, but we didn’t expect to see them so contrasting. It’s really visually striking.”

Nearly 600 individuals took part in the study, published recently in the journal Violence and Gender, with 56% of participants being female and 44% being male. Each participant looked at 16 images and were told to imagine themselves walking through those areas. They used a Qualtrics heat map tool to click on the areas of the image that stood out the most to them.

While men tended to focus on the path or a fixed object (like a light, the walking path or a garbage can), the women’s visual pattern represented a scanning of the perimeter (bushes, dark areas next to a path).

Chaney, along with Baer and Tovar — both BYU undergrads at the time of the study’s inception — say the findings provide some insight into what it is like to walk home as a woman, which could be multiplied through years or a lifetime of experiences.

“This project has been a fantastic conversation starter to bring awareness to lived experiences, particularly of women in this case,” said Baer, who recently finished graduate school at George Washington University and now works in Washington, D.C. “My hope is that in having concrete data we are able to start conversations that lead to meaningful action.”

Authors said the data suggests that because environment is perceived and experienced differently by women and men, decision makers in building campus and community environments should consider the varied experiences, perceptions and safety of both.

“Why can’t we live in a world where women don’t have to think about these things? It’s heartbreaking to hear of things women close to me have dealt with,” Chaney said. “It would be nice to work towards a world where there is no difference between the heat maps in these sets of images. That is the hope of the public health discipline.”

 https://neurosciencenews.com/women-walking-vision-night-25595/

 

 

 

 

https://www.jugantor.com/international/770417/যুক্তরাষ্ট্রের-পর-উগ্র-ইসরাইলিদের-ওপর-নিষেধাজ্ঞার-কথা-ভাবছে-কানাডা

https://www.prothomalo.com/world/m9s7mbs5la

 

 

Fasting May Reduce Inflammation

FeaturedNeurologyNeuroscience

Summary: Researchers uncovered a new mechanism by which fasting reduces inflammation, a key factor in chronic diseases.

Their study reveals that fasting increases blood levels of arachidonic acid, which inhibits the NLRP3 inflammasome, thereby reducing inflammation. This discovery sheds light on the anti-inflammatory effects of fasting and offers insights into the benefits of calorie restriction for conditions like obesity, diabetes, heart disease, and neurodegenerative disorders.

The research also provides clues to how drugs like aspirin might function, further highlighting the intricate relationship between diet, inflammation, and disease prevention.

Key Facts:

1.      Fasting elevates arachidonic acid levels in the blood, leading to reduced activity of the NLRP3 inflammasome and inflammation.

2.      The findings offer a potential explanation for how fasting and calorie restriction can protect against chronic inflammation-related diseases.

3.      This research may also explain the anti-inflammatory effects of non-steroidal anti-inflammatory drugs like aspirin, which increase arachidonic acid levels.

Source: University of Cambridge

Cambridge scientists may have discovered a new way that fasting helps reduce inflammation, a potentially damaging side-effect of the body’s immune system that underlies a number of chronic diseases.

In a paper titled “Arachidonic acid inhibition of the NLRP3 inflammasome is a mechanism to explain the anti-inflammatory effects of fasting,” published in Cell Reports, the team describes how fasting raises levels of a chemical in the blood known as arachidonic acid, which inhibits inflammation.

The researchers say it may also help explain some of the beneficial effects of drugs such as aspirin.

Scientists have known for some time that our diet—particularly a high-calorie Western diet—can increase our risk of diseases including obesity, type 2 diabetes and heart disease, which are linked to chronic inflammation in the body.

Studies have shown that some patients who have a high-fat diet have increased levels of inflammasome activity. Credit: Neuroscience News

Inflammation is our body’s natural response to injury or infection, but this process can be triggered by other mechanisms, including by the so-called “inflammasome,” which acts like an alarm within our body’s cells, triggering inflammation to help protect our body when it senses damage.

But the inflammasome can trigger inflammation in unintentional ways—one of its functions is to destroy unwanted cells, which can result in the release of the cell’s contents into the body, where they trigger inflammation.

Professor Clare Bryant from the Department of Medicine at the University of Cambridge said, “We’re very interested in trying to understand the causes of chronic inflammation in the context of many human diseases, and in particular the role of the inflammasome.

“What’s become apparent over recent years is that one inflammasome in particular—the NLRP3 inflammasome—is very important in a number of major diseases such as obesity and atherosclerosis, but also in diseases like Alzheimer’s and Parkinson’s disease, many of the diseases of older age people, particularly in the Western world.”

Fasting can help reduce inflammation, but the reason why has not been clear. To help answer this question, a team led by Professor Bryant and colleagues at the University of Cambridge and National Institute for Health in the U.S. studied blood samples from a group of 21 volunteers, who ate a 500-kcal meal and then fasted for 24 hours before consuming a second 500-kcal meal.

The team found that restricting calorie intake increased levels of a lipid known as arachidonic acid. Lipids are molecules that play important roles in our bodies, such as storing energy and transmitting information between cells. As soon as individuals ate a meal again, levels of arachidonic acid dropped.

When the researchers studied arachidonic acid’s effect in immune cells cultured in the lab, they found that it turns down the activity of the NLRP3 inflammasome. This surprised the team, as arachidonic acid was previously thought to be linked with increased levels of inflammation, not decreased levels.

Professor Bryant, a Fellow of Queens’ College, Cambridge, added, “This provides a potential explanation for how changing our diet—in particular by fasting—protects us from inflammation, especially the damaging form that underpins many diseases related to a Western high-calorie diet.

“It’s too early to say whether fasting protects against diseases like Alzheimer’s and Parkinson’s disease, as the effects of arachidonic acid are only short-lived, but our work adds to a growing amount of scientific literature that points to the health benefits of calorie restriction. It suggests that regular fasting over a long period could help reduce the chronic inflammation we associate with these conditions. It’s certainly an attractive idea.”

The findings also hint at one mechanism whereby a high-calorie diet might increase the risk of these diseases. Studies have shown that some patients who have a high-fat diet have increased levels of inflammasome activity.

“There could be a yin and yang effect going on here, whereby too much of the wrong thing is increasing your inflammasome activity and too little is decreasing it,” said Professor Bryant. “Arachidonic acid could be one way in which this is happening.”

The researchers say the discovery may also offer clues to an unexpected way in which so-called non-steroidal anti-inflammatory drugs such as aspirin work. Normally, arachidonic acid is rapidly broken down in the body, but aspirin stops this process, which can lead to an increase in levels of arachidonic acid, which in turn reduce inflammasome activity and hence inflammation.

Professor Bryant said, “It’s important to stress that aspirin should not be taken to reduce risk of long terms diseases without medical guidance, as it can have side effects such as stomach bleeds if taken over a long period.”

https://neurosciencenews.com/fasting-inflammation-25546/

 

City Life’s Influence on Unconscious Racial Bias

FeaturedPsychology

Summary: A new study links the structure of urban environments to the development of unconscious racial biases among its residents. By analyzing data from the Implicit Association Test (IAT) and U.S. Census demographics, researchers have created a model showing that cities with larger, more diverse, and less segregated social networks tend to have lower levels of implicit racial bias.

The study highlights the role of city organization in systemic racism, suggesting that urban planning and community engagement could be key to reducing prejudice. It underscores the importance of integrating diverse communities and promoting inclusive public spaces as strategies for fostering equitable urban living and mitigating racial biases.

Key Facts:

1.      The study analyzed implicit racial bias using IAT scores from approximately 2.7 million individuals, correlating these with urban demographics and population data.

2.      Findings indicate that cities with less segregation and greater diversity in social networks show reduced implicit racial biases among residents.

3.      The research suggests structural changes in urban planning could help diminish unconscious racial prejudices, highlighting the impact of city living on social attitudes.

Source: Santa Fe Institute

The city you live in could be making you, your family, and your friends more unconsciously racist. Or, your city might make you less racist. It depends on how populous, diverse, and segregated your city is, according to a new study that brings together the math of cities with the psychology of how individuals develop unconscious racial biases.

The study, published in the latest issue of Nature Communications, presents data and a mathematical model of exposure and adaptation in social networks that can help explain why there is more unconscious, or implicit, racial bias in some cities than others. The authors hope that local communities and governments can use the findings to help create more just and equitable cities. 

“What I think is most interesting is the implication that there’s a piece of systemic racism that has to do with how people learn and the way cities are organized,” says psychologist Andrew Stier, an SFI Complexity Postdoctoral Fellow and lead author of the study.

Cities create dense networks of social interaction between people. Because of the interactions with many different people, we need to be constantly adapting to new situations and learning, explains SFI External Professor Luís Bettencourt(University of Chicago), a co-leader of SFI’s Cities, Scaling and Sustainability project and co-author of the study.

To see how racial biases emerge from how U.S. cities are organized, Stier turned to the enormous database of the Implicit Association Test (IAT). In the popular online test, volunteer participants are given a pairing of White or Black faces with positive or negative words and asked to categorize a single face or word.

If they are faster to categorize things when White/good are paired they have a White-good bias and if they are faster to categorize things when Black/good are paired they have a Black-good bias.

“People may feel they are not prejudiced, but can unconsciously have a preference for one group or another, and this is revealed by these tests,” Stier says. 

The researchers took the average IAT bias scores from approximately 2.7 million individuals in different geographic areas and linked them to racial demographics and population data from the U.S.

Census to build a model that accounts for how individuals learn biases through their social networks. They found that when these networks are larger, more diverse, and less segregated in cities, implicit racial biases decrease. 

The results suggest that there are structural reasons why cities help or deter people from becoming less racially biased. Perhaps the most pronounced reason is the segregation of different racial groups into different neighborhoods. Related to that is the lack of more cosmopolitan public spaces where a diverse range of people can experience positive interactions with one another.

In cities where people can’t encounter and interact with people and institutions used by other groups, racial biases create major barriers to equity.

These barriers are associated with disparities across essentially all aspects of life including medical care, education, employment, policing, mental health outcomes, and physical health, the authors explain.

https://neurosciencenews.com/city-life-psychology-racism-25565/

How Odors Influence Brain’s Decision Making Mechanism

FeaturedNeuroscience

Summary: Researchers have uncovered a novel function of the hippocampus in decision making, showing that specific brain cells, known as ‘time cells,’ are stimulated by odors to facilitate rapid ‘go, no-go’ decisions.

This study demonstrates how mice learned to associate fruity odors with a reward, leading to quicker and more efficient decision making.

By tracking the activation of these cells in response to scents, the team has revealed a direct link between odor, hippocampal function, and associative learning, suggesting that these cells play a crucial role beyond memory recall, directly influencing the brain’s decision-making process.

Key Facts:

1.      The study identifies ‘time cells’ in the hippocampus as key players in the brain’s decision-making process, stimulated by specific odors to trigger rapid decisions.

2.      Mice were able to associate fruity smells with positive outcomes, showing how odor cues can enhance the learning of decision-making behaviors.

3.      This research sheds light on the intricate relationship between sensory perception and cognitive processes, revealing new insights into the hippocampus’s role in associative learning and decision making.

Source: University of Colorado

Researchers at the University of Colorado Anschutz Medical Campus have discovered that odors stimulate specific brain cells that may play a role in rapid `go, no-go’ decision making.

The study was published online Tuesday in the journal Current Biology.

The scientists focused on the hippocampus, an area of the brain crucial to memory and learning. They knew that so-called `time cells’ played a major role in hippocampal function but didn’t know their role in associative learning.

“These are cells that would remind you to make a decision – do this or do that,” said the study’s senior author Diego Restrepo, PhD, a neuroscientist and professor of cell and developmental biology at the University of Colorado School of Medicine.

The researchers observed that when mice were given the choice of responding to a fruity smell by licking on a spout that delivered sweet water, they quickly learned to lick the fruity smell as opposed to the smell of mineral oil.

“They have to associate the odor with the outcome of what they are doing so that’s why they learn decision making,” said Ming Ma, PhD, a first author of the study and a senior instructor in cell and developmental biology at the CU School of Medicine. “When it’s a fruit odor, they lick and get a reward. When it’s mineral oil they stop licking.”

“The more they learned, the more the cells were stimulated leading to more rapid decoding of the odors and allowing the mice to quickly become proficient at choosing the fruity smell,” said Fabio Simoes de Souza, DSc, another first author of the study and an assistant research professor in cell and developmental biology at the CU School of Medicine.

The catalyst for the decision-making is the odor which travels up the nose sending neural signals to the olfactory bulb and to the hippocampus. The two organs are closely connected. The information is swiftly processed and the brain makes a decision based on the input.

“Before this we didn’t know there were decision making cells in the hippocampus,” Restrepo said. “The hippocampus is multitasking.”

The cells are not always turned on, Restrepo speculated, because otherwise the stimuli might become overwhelming.

The study expands current knowledge of what’s involved in decision-making in the brain, specifically those quick go, no-go decisions that mice and humans make all the time.

“The hippocampus turns on decision-predicting time cells which would give you a hint of what to remember,” Restrepo said. “In the past, time cells were thought to only remind you of events and time. Here we see memory encoded in the neurons and then retrieved instantly when making a decision.”

https://neurosciencenews.com/odor-hippocampus-decision-making-25568/

 

Depression Linked to Higher Body Temperatures

FeaturedNeurosciencePsychology

Summary: A new study suggests a novel link between depression and higher body temperatures, analyzing data from over 20,000 participants worldwide. While the causal relationship remains unclear, findings indicate that body temperature increases with the severity of depression symptoms, offering a potential new avenue for treatment.

The research, leveraging wearable technology for temperature measurement, hints at the benefits of heat-based treatments like saunas for depression, potentially by inducing the body to lower temperatures through mechanisms like sweating. This study opens the door to exploring temperature regulation as a therapeutic strategy for depression, highlighting an innovative approach to addressing rising depression rates globally.

Key Facts:

1.      The study observed a correlation between increased depression symptom severity and higher body temperatures in participants from 106 countries.

2.      It explored the potential of heat-based treatments (e.g., saunas) to reduce depression by triggering the body’s natural cooling responses.

3.      This research is one of the largest to examine the association between body temperature and depression symptoms, utilizing wearable sensors and self-reported data.

Source: UCSF

People with depression have higher body temperatures, suggesting there could be a mental health benefit to lowering the temperatures of those with the disorder, a new UC San Francisco-led study found.

The study, published today in Scientific Reports, doesn’t indicate whether depression raises body temperature or a higher temperature causes depression. It’s also unknown whether the higher body temperature observed in people with depression reflects decreased ability to self-cool, increased generation of heat from metabolic processes or a combination of both.

Researchers analyzed data from more than 20,000 international participants who wore a device that measures body temperature, and also self-reported their body temperatures and depression symptoms daily. The seven-month study began in early 2020 and included data from 106 countries.

The results showed that with each increasing level of depression symptom severity, participants had higher body temperatures. The body temperature data also showed a trend toward higher depression scores in people whose temperatures had less fluctuation throughout a 24-hour period, but this finding didn’t reach significance.

The findings shed light on how a novel depression treatment method might work, said Ashley Mason, Ph.D., the study’s lead author and associate professor of psychiatry at UCSF Weill Institute for Neurosciences.

A small body of existing, causal studies has found that using hot tubs or saunas can reduce depression, possibly by triggering the body to self-cool, for example, through sweating.

“Ironically, heating people up actually can lead to rebound body temperature lowering that lasts longer than simply cooling people down directly, as through an ice bath,” said Mason, who is also a clinical psychologist at the UCSF Osher Center for Integrative Health.

“What if we can track the body temperature of people with depression to time heat-based treatments well?”

“To our knowledge, this is the largest study to date to examine the association between body temperature—assessed using both self-report methods and wearable sensors—and depressive symptoms in a geographically broad sample,” added Mason.

“Given the climbing rates of depression in the United States, we’re excited by the possibilities of a new avenue for treatment.”

https://neurosciencenews.com/

Fruit Flies’ Sensory Evolution: A Whiff of Genetic Secrets

FeaturedGeneticsNeuroscience

Summary: Researchers mapped the sensory evolution of fruit flies, revealing how genetic variations enable them to adapt their sense of smell and taste to diverse environments.

The team discovered that while most genes remain stable across generations, a significant number have evolved, leading to unique olfactory experiences among different fly species.

This study not only highlights the role of stabilising selection in maintaining gene expression levels but also uncovers male-biased gene expression in scent detection, pointing towards sex-specific evolutionary paths.

These findings not only deepen our understanding of fruit flies’ sensory adaptations but also shed light on the broader mechanisms of sensory system evolution across species.

Key Facts:

1.      Researchers found a mix of stabilising selection and significant gene expression changes in Drosophila species, shaping their olfactory senses.

2.      The study identified male-biased gene expression in the front legs of D. melanogaster, suggesting a special role in male scent detection.

3.      This research offers insights into the evolutionary dynamics of sensory systems, with implications for understanding sex differences and sensory perception in a wide range of organisms.

Source: Queen Mary University London

A new study in Nature Communications unveils the hidden world of sensory evolution in fruit flies. By delving into the genes and cells behind their delicate noses and tongues, researchers have discovered surprising secrets about how these tiny insects adapt their senses to different environments. 

“Imagine a world where a ripe peach tastes and smells like tangy vinegar to one fly, but like a burst of summer to another,” explains principal author of the study Dr Roman Arguello, a Lecturer in Genetics, Genomics and Fundamental Cell Biology at Queen Mary University of London. “Our study shows that this is not just possible, but it’s actually quite common.” 

The research team analysed the gene expression patterns in five key scent-detecting tissues across six different Drosophila species. This comprehensive approach allowed them to delve deeper than ever before into the molecular underpinnings of smell. 

One surprising discovery was the prevalence of “stabilising selection,” a force that keeps most genes expressed at the same levels across generations. However, within this sea of stability, the researchers found thousands of genes that had undergone significant changes in expression, shaping the unique olfactory landscapes of different fly species. 

“It’s like finding hidden islands of diversity within a vast ocean of uniformity,” says Dr Arguello. “These changes in gene expression tell us about the evolution of new smells, new sensitivities, and even new ways of using scent to navigate the world.” 

The study also reveals intriguing differences between the sexes. In fruit flies, as in many other animals, males and females often experience the world through different olfactory lenses.

The researchers identified a surprising excess of male-biased gene expression in the front legs of D. melanogaster, suggesting that these limbs play a crucial role in male-specific scent detection. 

“These findings open up exciting new avenues for understanding how sex differences evolve and how they impact animal behavior,” says Dr Arguello. 

The study’s implications extend beyond the fascinating world of flies. It provides valuable insights into the general principles of how sensory systems evolve, offering clues to understanding how other animals, including humans, perceive their chemical environments.

https://neurosciencenews.com/genetics-sensory-evolution-25563/

How the Brain Crafts Words Before Speaking

Summary: A new study utilizes advanced Neuropixels probes to unravel the complexities of how the human brain plans and produces speech. The team identified specific neurons in the prefrontal cortex involved in the language production process, including the separate neural pathways for speaking and listening.

Their findings illustrate how the brain represents phonemes and assembles them into syllables, providing insights that could revolutionize treatments for speech and language disorders.

This research not only enhances our understanding of the neural underpinnings of speech but also opens the door to developing technologies for synthetic speech production, offering hope for individuals with neurological disorders affecting communication.

Key Facts:

1.      Neuropixels probes were used to record activities of individual neurons involved in planning and producing speech, revealing the brain’s intricate processes for language production.

2.      The study identified separate groups of neurons dedicated to speaking and listening, and how the brain constructs speech sounds before they are spoken.

3.      This research could lead to the development of synthetic speech prosthetics and treatments for a wide range of neurological disorders affecting speech and language.

Source: Mass General

By using advanced brain recording techniques, a new study led by researchers from Massachusetts General Hospital (MGH) demonstrates how neurons in the human brain work together to allow people to think about what words they want to say and then produce them aloud through speech.

Together, these findings provide a detailed map of how speech sounds such as consonants and vowels are represented in the brain well before they are even spoken and how they are strung together during language production.

The work, which is published in Nature, reveals insights into the brain’s neurons that enable language production, and which could lead to improvements in the understanding and treatment of speech and language disorders.

“Although speaking usually seems easy, our brains perform many complex cognitive steps in the production of natural speech—including coming up with the words we want to say, planning the articulatory movements and producing our intended vocalizations,” says senior author Ziv Williams, MD, an associate professor in Neurosurgery at MGH and Harvard Medical School.

“Our brains perform these feats surprisingly fast—about three words per second in natural speech—with remarkably few errors. Yet how we precisely achieve this feat has remained a mystery.”

When they used a cutting-edge technology called Neuropixels probes to record the activities of single neurons in the prefrontal cortex, a frontal region of the human brain, Williams and his colleagues identified cells that are involved in language production and that may underlie the ability to speak. They also found that there are separate groups of neurons in the brain dedicated to speaking and listening.

“The use of Neuropixels probes in humans was first pioneered at MGH. These probes are remarkable—they are smaller than the width of a human hair, yet they also have hundreds of channels that are capable of simultaneously recording the activity of dozens or even hundreds of individual neurons,” says Williams who had worked to develop these recording techniques with Sydney Cash, MD, PhD, a professor in Neurology at MGH and Harvard Medical School, who also helped lead the study.

“Use of these probes can therefore offer unprecedented new insights into how neurons in humans collectively act and how they work together to produce complex human behaviors such as language.”

The study showed how neurons in the brain represent some of the most basic elements involved in constructing spoken words—from simple speech sounds called phonemes to their assembly into more complex strings such as syllables.

For example, the consonant “da”, which is produced by touching the tongue to the hard palate behind the teeth, is needed to produce the word dog.

By recording individual neurons, the researchers found that certain neurons become active before this phoneme is spoken out loud. Other neurons reflected more complex aspects of word construction such as the specific assembly of phonemes into syllables.

With their technology, the investigators showed that it’s possible to reliably determine the speech sounds that individuals will say before they articulate them.

In other words, scientists can predict what combination of consonants and vowels will be produced before the words are actually spoken. This capability could be leveraged to build artificial prosthetics or brain-machine interfaces capable of producing synthetic speech, which could benefit a range of patients.

“Disruptions in the speech and language networks are observed in a wide variety of neurological disorders—including stroke, traumatic brain injury, tumors, neurodegenerative disorders, neurodevelopmental disorders, and more,” says Arjun Khanna who is a co-author on the study.

“Our hope is that a better understanding of the basic neural circuitry that enables speech and language will pave the way for the development of treatments for these disorders.”

The researchers hope to expand on their work by studying more complex language processes that will allow them to investigate questions related to how people choose the words that they intend to say and how the brain assembles words into sentences that convey an individual’s thoughts and feelings to others.

Additional authors include William Muñoz, Young Joon Kim, Yoav Kfir, Angelique C. Paulk, Mohsen Jamali, Jing Cai, Martina L Mustroph, Irene Caprara, Richard Hardstone, Mackenna Mejdell, Domokos Meszena, Abigail Zuckerman, and Jeffrey Schweitzer..

Funding: This work was supported by the National Institutes of Health.

https://neurosciencenews.com/speech-production-neurons-25549/

 

 

Mapping the Brain: The Largest Neuron Projectome Unveiled

ElectrophysiologyFeaturedNeuroscience

Summary: Researchers unveiled the most extensive single-neuron projectome database to date, featuring over 10,000 mouse hippocampal neurons.

The study provides an unprecedented view of the spatial connectivity patterns at the mesoscopic level, crucial for understanding learning, memory, and emotional processing in the hippocampus. By employing machine learning algorithms for categorizing axonal trajectories and integrating spatial transcriptome data, researchers identified 43 distinct projectome cell types, revealing intricate projection patterns and soma locations’ correspondence to projection targets.

This work, accessible via the Digital Brain CEBSIT portal, lays the structural foundation for advancing our knowledge of hippocampal functions and their molecular underpinnings.

Key Facts:

1.      The study reconstructed whole-brain axonal morphology of over 10,000 mouse hippocampal neurons, creating the world’s most extensive single-neuron projectome database.

2.      Researchers used machine learning to analyze morphological similarities among neurons, identifying 43 distinct projectome cell types.

3.      The integration of projectome cell types with spatial transcriptome data revealed potential molecular and circuit targets for hippocampal functions, all accessible through a dedicated online platform.

Source: Chinese Academy of Science

A study published in Science on Feb. 1 reported a comprehensive database of single-neuron projectomes consisting of over 10,000 mouse hippocampal neurons, thus revealing the spatial connectivity patterns of mouse hippocampal neurons at the mesoscopic level.   

The study was conducted by teams from the Center for Excellence in Brain Science and Intelligence Technology (CEBSIT), the Institute of Neuroscience of the Chinese Academy of Sciences (CAS), the HUST-Suzhou Institute for Brainsmatics, Hainan University, the Kunming Institute of Zoology of CAS, Lingang Laboratory, and the Shanghai Center for Brain Science and Brain-Inspired Technology.  

The hippocampus serves as an essential brain region for learning and memory as well as various brain functions such as spatial cognition and emotional processing. It is one of the most extensively studied brain regions.

Hippocampal neurons project widely to the brain-wide targets; thus, it is critical to investigate the projection patterns of hippocampal neurons at the single-neuron level.   

This study reconstructed the whole-brain axonal morphology of over 10,000 neurons in the mouse hippocampus at a single-cell resolution with the neuronal cell bodies covering all subregions and multiple locations along different hippocampal axes, making this the most extensive single-neuron projectome database in the world.   

This study took an innovative approach to categorize axonal trajectories with machine learning algorithms, thus allowing for a more efficient analysis of the morphological similarities among 341 projection patterns for mouse hippocampal neurons and ultimately identifying 43 distinct projectome cell types. It also incorporated the spatial transcriptome of mouse CA1 areas.  

Based on these analyses, the study was able to elucidate the axonal projection pathways of hippocampal neurons along the anterior-posterior axis and reveal new projection patterns of hippocampal neurons. It also outlined the correspondence between hippocampal neuron soma locations and projection targets, and revealed basic organization principles of bilateral projections.

Furthermore, correlation analysis of projectome cell types and spatial transcriptome data identified spatial correspondence between various genes and projectome subtypes, providing potential molecular and circuit targets for hippocampal functions.  

Taken together, this study provides a structural basis for future studies of hippocampal functions and deciphers the potential correspondences between their soma locations, gene expression, and circuitry functions.  

The database for the hippocampal single-neuron projectomes, along with the database on the hippocampal longitudinal axis and spatial transcriptomes, are now publicly accessible through the Digital Brain CEBSIT portal (https://mouse.digital-brain.cn/hipp).

To facilitate broader usage of the databases, a team from the Computing and Data Center of CEBSIT has developed a website to integrate data visualization, user interface, online analysis, and data downloads.

https://neurosciencenews.com/hippocampus-projectome-25550/

 

Diet and Immunity: Vegan vs. Keto’s Impact on the Body

Summary: A new study reveals distinct immune system responses to vegan and ketogenic diets. Over a two-week period, 20 participants alternated between these diets, allowing researchers to observe changes in innate and adaptive immunity, metabolic pathways, and gut microbiome.

The vegan diet primarily affected innate immunity and red blood cell pathways, while the keto diet influenced adaptive immunity and a wider range of proteins. These findings highlight the rapid and diverse immune responses to dietary changes, opening avenues for diet-based disease prevention and treatment strategies.

Key Facts:

1.      The vegan diet triggered innate immune responses and affected pathways related to red blood cells, while the keto diet influenced adaptive immunity and a broader range of protein levels.

2.      Both diets significantly altered participants’ microbiomes and metabolic processes.

3.      The study’s controlled environment and diverse participant group demonstrate that dietary changes can consistently affect complex bodily systems.

Source: NIH

Researchers at the National Institutes of Health observed rapid and distinct immune system changes in a small study of people who switched to a vegan or a ketogenic (also called keto) diet. Scientists closely monitored various biological responses of people sequentially eating vegan and keto diets for two weeks, in random order.

They found that the vegan diet prompted responses linked to innate immunity—the body’s non-specific first line of defense against pathogens—while the keto diet prompted responses associated with adaptive immunity—pathogen-specific immunity built through exposures in daily life and vaccination.

The work is published in the journal Nature Medicine.

Metabolic changes and shifts in the participants’ microbiomes—communities of bacteria living in the gut—were also observed. More research is needed to determine if these changes are beneficial or detrimental and what effect they could have on nutritional interventions for diseases such as cancer or inflammatory conditions.

Scientific understanding of how different diets impact the human immune system and microbiome is limited. Therapeutic nutritional interventions—which involve changing the diet to improve health—are not well understood, and few studies have directly compared the effects of more than one diet.

The keto diet is a low-carbohydrate diet that is generally high in fat. The vegan diet eliminates animal products and tends to be high in fiber and low in fat.

The study was conducted by researchers from the NIH’s National Institute of Allergy and Infectious Diseases (NIAID) and National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) at the Metabolic Clinical Research Unit in the NIH Clinical Center. The 20 participants were diverse with respect to ethnicity, race, gender, body mass index (BMI), and age.

Each person ate as much as desired of one diet (vegan or keto) for two weeks, followed by as much as desired of the other diet for two weeks. People on the vegan diet, which contained about 10% fat and 75% carbohydrates, chose to consume fewer calories than those on the keto diet, which contained about 76% fat and 10% carbohydrates.

Throughout the study period, blood, urine, and stool were collected for analysis. The effects of the diets were examined using a “multi-omics” approach that analyzed multiple data sets to assess the body’s biochemical, cellular, metabolic, and immune responses, as well as changes to the microbiome. Participants remained on site for the entire month-long study, allowing for careful control of the dietary interventions.

Switching exclusively to the study diets caused notable changes in all participants. The vegan diet significantly impacted pathways linked to the innate immune system, including antiviral responses.

On the other hand, the keto diet led to significant increases in biochemical and cellular processes linked to adaptive immunity, such as pathways associated with T and B cells.

The keto diet affected levels of more proteins in the blood plasma than the vegan diet, as well as proteins from a wider range of tissues, such as the blood, brain and bone marrow. The vegan diet promoted more red blood cell-linked pathways, including those involved in heme metabolism, which could be due to the higher iron content of this diet.

Additionally, both diets produced changes in the microbiomes of the participants, causing shifts in the abundance of gut bacterial species that previously had been linked to the diets.

The keto diet was associated with changes in amino acid metabolism—an increase in human metabolic pathways for the production and degradation of amino acids and a reduction in microbial pathways for these processes—which might reflect the higher amounts of protein consumed by people on this diet.

The distinct metabolic and immune system changes caused by the two diets were observed despite the diversity of the participants, which shows that dietary changes consistently affect widespread and interconnected pathways in the body. More study is needed to examine how these nutritional interventions affect specific components of the immune system.

According to the authors, the results of this study demonstrate that the immune system responds surprisingly rapidly to nutritional interventions. The authors suggest that it may be possible to tailor diets to prevent disease or complement disease treatments, such as by slowing processes associated with cancer or neurodegenerative disorders.

https://neurosciencenews.com/keto-vegan-immunity-25547/

 

প্রতিরাতে যে বিছানায় ঘুমান, শরীর তাতে এলিয়ে দিতেই ঘুম আসে হয়তো বলবেন, ক্লান্তি থেকে এমন হয় চেনা পরিবেশে ঘুম যেন আপনাতে এসে যায়

কিন্তু নতুন একটি জায়গায় গেলেন। হতে পারে কোথাও বেড়াতে গেলেন, হতে পারে হলে কিংবা হোস্টেলে প্রথম উঠেছেন, হতে পারে সেন্টমার্টিনে গেছেন প্রথম রাত্রি যাপন করতে এক হোটেলে। মাঝ রাতে কোনো কারণ ছাড়াই ঘুম ভেঙে গেল, তারপর চেষ্টা করছেন ঘুমাতে। যেন আর ঘুম আসে না রাতে

আরও পড়ুনখোসপাঁচড়া রোগ হলে যা করবেন

যেখানেই যান, নতুন পরিবেশে সহজে ঘুম আসে না। এটি হয়তো আমরা স্বাভাবিক ভাবি। প্রথম রাতটি যেন একটু ঘুম, একটু ঘুমের ব্যাঘাতে কাটে। ঘুমের চেয়ে এপাশ ওপাশ হয় বেশি। ঘুমের চেয়ে ঘুম ভেঙে যায় বেশি

অথচ শরীর ক্লান্ত। পরিবেশ সুন্দর। নরম বিছানা। মনে কোনো দুশ্চিন্তা নেই। তারপরও কেন এমন হয়। কেন অচেনা, অজানা নতুন পরিবেশে আমাদের ঘুম আসে না সহজে!

নতুন পরিবেশে ঘুমের সমস্যাটি সম্পর্কে চিকিৎসকরা অনেক দিন থেকে জানে। চিকিৎসকদের কাছে এটির নাম : First-Night Effect সংক্ষেপে বলে FNE এক দশক আগেই সম্পর্কে চিকিৎসক বিজ্ঞানীরা ধারণা পায়

যে কোনো নতুন পরিবেশে ঘুমের কমতি হওয়াকে বলে এই FNE এটি মূলত প্রথম রাতেই বেশি হয়। তার পরের রাতগুলোতে হয় না অথবা হলে অনেক কম হয় ঘুমের সমস্যা

First Night Effect (FNE)-এর কারণে ঘুমের আর্কিটেকচারের পরিবর্তন হয়। ঘুমের যে দুটি স্টেজ REM এবং Non-REM, তাদের REM স্টেজটির পরিবর্তন হয়। তাতে ঘুমের পরিমাণ কমে যায়, চোখ বন্ধ থাকলেও কোয়ালিটি ঘুম হয় না

অনেকদিন থেকে ভাবা হতো যে নতুন পরিবেশের সঙ্গে খাপ খাইয়ে নিতে সময় নেয় বলে হয়তো এমন হয়। অনেকেই ভাবত যে বিছানা বদল মানে ঘুমের ধকল! ঘুমের উপকরণের সঙ্গে অ্যাডজাস্ট হতে সময় নিচ্ছে বলে এমন হয়

নিয়ে বিজ্ঞানীরা কাজ করতে গিয়ে দেখতে পেল অন্য জিনিস। আমরা যখন ঘুমাই, মস্তিষ্কের সব অংশই ঘুমায়। মানুষের মস্তিষ্ক দুটি ভাগে বিভক্ত। এক একটি ভাগকে হেমিস্ফিয়ার বলে। সহজ করে বললে ডান মস্তিষ্ক এবং বাম মস্তিষ্ক। ঘুমাতে গেলে ডান এবং বাম, দুমস্তিষ্কই একসঙ্গে সমন্বয় করে এবং ঘুমায়

আরও পড়ুনহার্ট সুস্থ রাখতে যেভাবে নিবেন মুখের যত্ন

ঘুমের দুটি স্টেজ আছে সঙ্গে। একটিকে বলে REM বা Rapid Eye Movement-যেখানে চোখ ঘুরে। আরেকটি হলো Non REM-যেখানে চোখ ঘোরে না। ঘুমের শুরুতে Non REM ধাপ শুরু হয়। ধীরে ধীরে REM স্টেজে ঘুম গভীর হয় এবং এই স্টেজেই মানুষ স্বপ্ন দেখে

বিজ্ঞানীরা নতুন জায়গায় ঘুমের এমন ব্যাঘাত হয় কেন, তার কারণ জানার এবং চেষ্টার অনেক আগ থেকেই একটি মজার বিষয় জানত যে-প্রাণীদের অনেকেই রাত্রে ঘুমাতে এক চোখ খোলা রাখে এবং আরেক চোখ বন্ধ করে রাখে। যেমন : ডলফিন, সিল, কিছু মাছ, বিভিন্ন ধরনের মাইগ্রেটরি পাখিদের মাঝে দেখা যায় তাদের অনেকে ঘুমানোর সময় এক চোখে ঘুমায়, আরেক চোখে উড়ে। পরীক্ষা করে দেখল ওই সময়ে প্রাণীগুলোর মস্তিষ্কের এক অংশ জেগে থাকে এবং আরেক অংশ ঘুমিয়ে থাকে। এমনকি পুকুরের হাঁসদের দেখবেন রাতেরবেলা পানিতে সাঁতার কাটছে, আবার অন্ধকারে এক চোখে ঘুমাচ্ছে

মানুষ কোনো নতুন পরিবেশে গেলে মস্তিষ্কে কিছু স্টিমুলেশনের পরিবর্তন হয়। পরিবেশের উদ্দীপনা শুধু পরিবেশ থেকে হয় না। ভালো-মন্দ পরিবেশ যেমনই থাকুক, মস্তিষ্ক স্বয়ংক্রিয়ভাবে কিছু প্রতিক্রিয়া করে। প্রতিক্রিয়াতে আপনার আমার কোনো হাত নেই। না চাইলেও মস্তিষ্ক এমন আচরণ এবং প্রতিক্রিয়া করবে। কারণ হল-হাজার বছরের বিবর্তনে মানুষের মস্তিষ্ক ঠিক এমন করে গড়ে উঠেছে

কিন্তু কী পরিবর্তন হয়, কেন পরিবর্তন হয়, কীভাবে হয় এবং পরিবর্তনের ফলাফল জানলেও প্রথম তিনটির উত্তর বিজ্ঞানীদের কাছে এতদিন ছিল না। বর্তমানে চিকিৎসক কিংবা ঘুম বিজ্ঞানীরা জানে নতুন পরিবেশে কেন আমাদের FNE হয়, কেন এবং কীভাবে আমাদের ঘুমের ব্যাঘাত ঘটে

একটি ঘুম গবেষণা টিম নিয়ে কাজ করতে গিয়ে দেখতে পেল-নতুন পরিবেশে মানুষের মস্তিষ্কের অর্ধেক ঘুমায়, বাকি অর্ধেক জেগে থাকে। ফলে দীর্ঘ জার্নির পরেও হোটেলে প্রথম রাত যেন নির্ঘুম কাটে। পরদিন সকালবেলা দুকাপ কফিতেও যেন ঘুমের ক্লান্তি দূর হয় না

প্রথম রাতে নতুন পরিবেশে মস্তিষ্ক সতর্ক হয়ে ওঠে। মস্তিষ্ক নতুন পরিবেশে অজানা আশঙ্কায় থাকে। বিবর্তনে মানুষের মস্তিষ্ক নতুন পরিবেশে নতুন দৃশ্য, নতুন তাপমাত্রা, নতুন গন্ধ, সব সেন্সরিগুলোর মাধ্যমে সংগৃহীত স্বয়ংক্রিয় উপাত্ত আড়ালে মস্তিষ্ককে সতর্ক করে দেয়। ঘুমের ল্যাবে পরীক্ষা করে বিজ্ঞানীরা দেখেছেন যে, প্রথম রাতে বাম মস্তিষ্ক সতর্ক থাকে এবং ডান মস্তিষ্ক ঘুমায়। কারণ বাম মস্তিষ্কের কাজ বিপদের গন্ধ পাওয়া, আত্মরক্ষার কৌশল নির্ধারণ করা, প্ল্যান করা, সতর্কের সঙ্গে শরীরকে বিপদের হাত থেকে রক্ষা করে

একদল ছাত্রের ওপর গবেষণায় ঘুম বিজ্ঞানীরা দেখল যে, প্রথম রাতে নতুন পরিবেশে তাদের বাম মস্তিষ্কে স্লো ওয়েব তরঙ্গ কম প্রবাহিত হয় এবং ডান মস্তিষ্কে এই প্রবাহ বেশি থাকে। আমরা যখন ঘুমাই, আমাদের গভীর ঘুমের সময় মস্তিষ্কের দুই অংশেই এই স্লো ওয়েব তরঙ্গ বেড়ে যায়। গবেষক দল আরও দেখতে পেল, প্রথম রাত্রিতে বাম মস্তিষ্কের অনেক অংশ যেমন একটিভ থাকে এবং স্লো ওয়েব কম হয়, পরদিন থেকে সেটি চলে যায় এবং দু-মস্তিষ্কের একই অবস্থা থাকে। ছাত্রদের সঙ্গে কথা বলে দু-রাতের ঘুমের পার্থক্য জেনে এবং মস্তিষ্ক স্ক্যানিং করে প্রাপ্ত ফলাফল তুলনা করে বিজ্ঞানীরা বুঝল যে, নতুন পরিবেশে বাম মস্তিষ্ক অজানা অচেনা পরিবেশের অনাকাক্সিক্ষত বিপদের হাত থেকে শরীরকে রক্ষা করতে, সেই সঙ্গে স্বয়ংক্রিয় এবং বিবর্তনমূলক সুবিধা পেতে এমন করে জেগে থাকে, কিন্তু ডান মস্তিষ্ক স্বাভাবিক নিয়মে ঘুমাতে চেষ্টা করে কিংবা ঘুমায়

দুই মস্তিষ্ক প্রথম রাতে নতুন পরিবেশে সমানভাবে ঘুমাতে পারে না অথবা ঘুমায় না। এতে বিবর্তনের দৃষ্টিতে সুবিধা পেলেও শরীরের স্বাভাবিক প্রয়োজন এবং ক্লান্তি থেকে বের হতে পারে না। ফলে প্রথম রাত্রির পরদিন সকাল শারীরিক ক্লান্তি অবসাদ এবং নির্ঘুমতার ছাপ থাকলেও একদিন বা দুদিন পর মস্তিষ্কের আর এমন করার দরকার পড়ে না। তখন পুরো মস্তিষ্কই স্বাভাবিক নিয়মে ঘুম যায় এবং ঘুমের কোয়ালিটিও তখন ভালো হয়

তাহলে এখন থেকে নতুন কোথাও প্রথম রাতে ঘুম না এলে উদ্বিগ্নতার কারণ নেই। ধরে নিতে হবে এটি মস্তিষ্কের একটি বিবর্তনমূলক ধারা এবং গঠন, যা মূলত শরীরের আত্মরক্ষার্থের প্রয়োজনে একটি সতর্কতামূলক ব্যবস্থা

  ডা. অপূর্ব চৌধুরী  

লেখক : চিকিৎসক এবং লেখক, ইংল্যান্ড

https://www.jugantor.com/lifestyle
 

 

Sleep’s Role in Brain Health

FeaturedNeuroscience

Summary: A new study reveals how sleep duration impacts brain health, specifically relating to stroke and dementia risks.

Analyzing brain images of nearly 40,000 middle-aged participants, the study found that both short and long sleep durations are associated with negative changes in brain structure.

These changes include higher presence and volume of white matter hyperintensities (WMH) and reduced fractional anisotropy, indicators of brain aging and dementia risk. The research underscores sleep as a key factor in maintaining brain health and highlights middle age as a critical period for sleep habit adjustments.

Key Facts:

1.      Inadequate sleep, both too little and too much, is linked to increased WMH presence, larger WMH volume, and lower fractional anisotropy.

2.      These brain changes are associated with higher risks of stroke and dementia.

3.      The study emphasizes the importance of optimal sleep (7–9 hours) for brain health in middle-aged individuals.

Source: Yale

Getting either too much or too little sleep is associated with changes in the brain that have been shown to increase the risk of stroke and dementia later in life, a recent study finds.

The research is published in the Journal of the American Heart Association.

“Conditions like stroke or dementia are the end-stage result of a long process that ends tragically,” says Santiago Clocchiatti-Tuozzo, MD, T32 postdoctoral fellow in the Falcone lab at Yale School of Medicine and first author of the study. “We want to learn how to prevent these processes before they happen.”

Long sleep (averaging more than 9 hours per night) was associated with lower fractional anisotropy and with larger WMH volume, but not with risk of WMH presence. Credit: Neuroscience News

In one of the largest neuroimaging studies of its kind to date, the Yale team examined brain images of close to 40,000 healthy, middle-aged participants to evaluate how sleeping habits might impact two measures of brain health: white matter hyperintensities (WMH), which are lesions on the brain indicating brain aging, and fractional anisotropy, which measures the uniformity of water diffusion along nerve axons. More WMH, larger WMH, and lower fractional anisotropy are associated with increased risk of stroke and dementia.

Researchers found that compared with optimal sleep (7–9 hours per night), participants with short sleep had higher risk of WMH presence, larger WMH volume where WMH was present, and lower fractional anisotropy. Long sleep (averaging more than 9 hours per night) was associated with lower fractional anisotropy and with larger WMH volume, but not with risk of WMH presence.

“These findings add to the mounting evidence that sleep is a prime pillar of brain health,” says Clocchiatti-Tuozzo. “It also provides evidence toward helping us understand how sleep and sleep duration can be a modifiable risk factor for brain health later in life.”

Researchers say the study highlights middle age as an important time to adjust our sleeping habits to support brain health.

“Sleep is starting to become a trending topic,” Clocchiatti-Tuozzo says. “We hope this study and others can offer insight into how we can modify sleep in patients to improve brain health in years to come.”

Cyprien Rivier, Daniela Renedo, Victor Torres Lopez, Jacqueline Geer, Brienne Miner, Henry Yaggi, Adam de Havenon, Seyedmedhi Payabvash, Kevin Sheth, Thomas Gill and Guido Falcone were co-authors of the study. https://neurosciencenews.com/

Suboptimal Sleep Duration Is Associated With Poorer Neuroimaging Brain Health Profiles in MiddleAged Individuals Without Stroke or Dementia

Abstract

Background

The American Heart Association's Life's Simple 7, a public health construct capturing key determinants of cardiovascular health, became the Life's Essential 8 after the addition of sleep duration.

Methods and Results

The authors conducted a prospective magnetic resonance neuroimaging study in middleaged individuals without stroke or dementia enrolled in the UK Biobank. Selfreported sleep duration was categorized as short (<7 hours), optimal (7–<9 hours), or long (≥9 hours). Evaluated neuroimaging markers included the presence of white matter hyperintensities (WMHs), volume of WMH, and fractional anisotropy, with the latter evaluated as the average of 48 white matter tracts. Multivariable logistic and linear regression models were used to test for an association between sleep duration and these neuroimaging markers. The authors evaluated 39 771 middleaged individuals. Of these, 28 912 (72.7%) had optimal, 8468 (21.3%) had short, and 2391 (6%) had long sleep duration. Compared with optimal sleep, short sleep was associated with higher risk of WMH presence (odds ratio, 1.11 [95% CI, 1.05–1.18]; P<0.001), larger WMH volume (beta=0.06 [95% CI, 0.04–0.08]; P<0.001), and worse fractional anisotropy profiles (beta=−0.04 [95% CI, −0.06 to −0.02]; P=0.001). Compared with optimal sleep, long sleep duration was associated with larger WMH volume (beta=0.04 [95% CI, 0.01–0.08]; P=0.02) and worse fractional anisotropy profiles (beta=−0.06 [95% CI, −0.1 to −0.02]; P=0.002), but not with WMH presence (P=0.6).

Conclusions

Among middleaged adults without stroke or dementia, suboptimal sleep duration is associated with poorer neuroimaging brain health profiles. Because these neuroimaging markers precede stroke and dementia by several years, these findings are consistent with other findings evaluating early interventions to improve this modifiable risk factor. https://www.ahajournals.org/doi/10.1161/JAHA.123.031514

 

 

Boosting Learning With the Power of Passive Exposure

FeaturedNeuroscience

Summary: Researchers discovered in mice that passive exposure, alongside active training, can significantly enhance the learning process. This study demonstrates how passive exposure to stimuli like sounds or languages helps the brain to form foundational representations, making active learning more efficient.

The findings, which align with prior research in humans, suggest that combining low-effort passive exposure with active training can lead to quicker mastery of new skills, such as learning a musical instrument or a foreign language.

Key Facts:

1.      Mice exposed to sounds passively, in addition to active training, learned to associate sounds with rewards more quickly.

2.      Artificial neural network simulations indicate that passive exposure creates a foundational representation of stimuli in the brain.

3.      The study’s insights align with human research, suggesting a combined approach of passive exposure and active training could enhance complex skill learning.

Source: University of Oregon

Learning a new skill takes deliberate practice over time, but passive exposure to the subject matter at hand can help speed up the process, new University of Oregon research in mice suggests.

The finding, which builds on past research in humans, shows how passive exposure can be a valuable tool for learning. It helps explain how watching movies in a foreign language might supplement grammar drills and vocabulary flashcards, or how listening to recordings of a professional playing piano concertos could help budding musicians improve their own craft.

FeaturedNeuroscience

Summary: Researchers discovered in mice that passive exposure, alongside active training, can significantly enhance the learning process. This study demonstrates how passive exposure to stimuli like sounds or languages helps the brain to form foundational representations, making active learning more efficient.

The findings, which align with prior research in humans, suggest that combining low-effort passive exposure with active training can lead to quicker mastery of new skills, such as learning a musical instrument or a foreign language.

Key Facts:

1.      Mice exposed to sounds passively, in addition to active training, learned to associate sounds with rewards more quickly.

2.      Artificial neural network simulations indicate that passive exposure creates a foundational representation of stimuli in the brain.

3.      The study’s insights align with human research, suggesting a combined approach of passive exposure and active training could enhance complex skill learning.

Source: University of Oregon

Learning a new skill takes deliberate practice over time, but passive exposure to the subject matter at hand can help speed up the process, new University of Oregon research in mice suggests.

The finding, which builds on past research in humans, shows how passive exposure can be a valuable tool for learning. It helps explain how watching movies in a foreign language might supplement grammar drills and vocabulary flashcards, or how listening to recordings of a professional playing piano concertos could help budding musicians improve their own craft.

The study gives additional insight into the possible brain mechanisms behind the effect, helping scientists understand just why passive exposure is so powerful, said James Murray, a UO neuroscientist who led the study alongside fellow UO neuroscientist Santiago Jaramillo, both part of the College of Arts and Sciences.

Because it’s much easier to study what’s happening inside the brain of a rodent than a human, “studying how both active training and passive exposure affect learning in mice opens up exciting possibilities for investigating the neural mechanisms underlying the interplay between them,” Murray added.

The researchers describe their findings in a paper published in the journal eLife.

To study how mice learn, researchers trained the animals to reach for a reward in a particular spot in response to tones that slid up or down in pitch. All of the mice were put through an active training protocol, in which they got feedback on their performance so they knew whether they made the right choice. Some of the mice also got passive exposure, where they heard the sounds while they weren’t engaged in the task.

The mice who were passively exposed to the sounds in addition to being actively trained learned how to select the reward location more quickly, the researchers showed. It didn’t seem to matter whether the passive exposure happened at the beginning of training or was interspersed in small chunks throughout the active training sessions.

Then, to better understand how the learning might be happening in the brain, the researchers trained and tested different artificial neural networks on a simulated version of the learning task. Neural networks, a kind of machine learning algorithm, process information in a way that mimics the way the brain processes information.

Artificial neurons represent real neurons, and learning takes place by modifying the strengths of the connections between those neurons. They’re not a direct replica for the brain, but they can be used to generate hypotheses that can then be tested experimentally.

The modeling suggests that passive exposure to a stimulus lays the groundwork in the brain, creating a hidden representation of that stimulus that captures its most prominent features, like making a pencil outline before diving into a detailed painting. Then, during active learning, the brain links the stimulus to particular behaviors. With passive exposure, the brain is primed to make those connections more quickly.

In the future, the team hopes to record brain activity in mice during a similar learning task, to see if their predictions play out.

While the research was done using a simple task in mice, the findings might also have implications for more complex learning in humans, the researchers suggest. Study co-author Melissa Baese-Berk, a former UO linguist now at the University of Chicago, has previously published studies showing how passive exposure can help adult humans better learn to understand new speech sounds.

“Alongside the previous work on humans from Melissa and her collaborators, our results suggest that, in mice and in humans, a given performance threshold can be achieved with relatively less effort by combining low-effort passive exposure with active training,” Murray said.

“This insight could be helpful for humans learning an instrument or a second language, though more work will be needed to better understand how this applies to more complex tasks and how to optimize training schedules that combine passive exposure with active training.”

https://neurosciencenews.com/passive-exposure-learning-25531/

 

স্ট্রোকে ব্রেনের ভেতরের রক্তনালির মধ্যে এক বা একাধিক রক্তনালি ব্লক হয়ে যায় অথবা ছিঁড়ে যায় ব্রেনের একেকটি অংশ শরীরের একেক অংশকে নিয়ন্ত্রণ করে স্ট্রোকের ফলে ওই রক্তনালি ব্রেনের যে অংশে রক্ত সরবরাহ করে সচল রাখত, সে অংশ তার কার্যক্ষমতা হারায় ফলে শরীরের ওই অংশের কার্যক্রম বন্ধ হয়ে যায় বা কমে যায় বেশিভাগ ক্ষেত্রে ব্রেনের যে কোনো একপাশের রক্তনালি ব্লক হয়ে বা ছিঁড়ে গিয়ে স্ট্রোক হয় সেজন্য স্ট্রোকের লক্ষণও সাধারণত আমাদের শরীরের একপাশে দেখা দেয়

* স্ট্রোকের লক্ষণ

হঠাৎ করে শরীরের এক পাশের হাত-পা অবশ হয়ে যাওয়া, অথবা আলাদাভাবে শুধু একহাত বা পা অবশ হওয়া, কথা জড়িয়ে যাওয়া, মুখ বাঁকা হওয়া, খাবার গিলতে অসুবিধা হওয়া, চোখে ঠিকমতো দেখতে না পারা-ইত্যাদিও স্ট্রোকের লক্ষণ। একজন সুস্থ সবল ব্যক্তির যখন হঠাৎ এসব সমস্যা দেখা দেবে, তখনই ধরে নিতে হবে তিনি স্ট্রোকে আক্রান্ত হয়েছেন। এসব লক্ষণ দেখে নিকটজন স্ট্রোকে আক্রান্ত হয়েছেন সন্দেহ করলেই আমাদের উচিত হবে, রোগীকে তৎক্ষণাৎ নিকটস্থ হাসপাতালে, সম্ভব হলে সব সুযোগ-সুবিধা সম্পন্ন হাসপাতালে নিয়ে যাওয়া। যেখানে অতি দ্রুত ব্রেনের ইমেজিংসহ প্রয়োজনীয় পরীক্ষা-নিরীক্ষা করে স্ট্রোকের আধুনিক চিকিৎসা শুরু করা সম্ভব। এসব রোগীর ক্ষেত্রে স্ট্রোক পরবর্তী প্রতিটি মুহূর্ত মূল্যবান। লক্ষণ শুরু হওয়ার পর যত তাড়াতাড়ি রোগীর চিকিৎসা শুরু করা যায়, ব্রেনের ক্ষতির হার তত কম হয়। স্ট্রোকের কারণে রোগীর শরীরে ঘটে যাওয়া শারীরিক সমস্যার উন্নতির হারও দ্রুত হয়

* চিকিৎসা

বর্তমানে স্ট্রোকের আধুনিক চিকিৎসা হচ্ছে- থ্রম্বোলাইসিস। যেখানে স্ট্রোক হওয়ার সময় থেকে পরবর্তী চার থেকে সাড়ে চার ঘণ্টার মধ্যে সিটি স্ক্যান/এমআরআই-সহ প্রয়োজনীয় পরীক্ষা-নিরীক্ষার পর রোগীর অবস্থা এনালাইসিস করা হয়। রোগী যদি থ্রম্বোলাইসিস চিকিৎসার শর্তাবলী পূরণ করে, তবে সংশ্লিষ্ট রোগীকে স্ট্রোকের এই আধুনিক চিকিৎসা দেওয়া হয়। চিকিৎসায় রেজাল্ট খুবই ভালো। রোগী আরও খারাপ তো হয়- না, বরং এক-দুদিনের মধ্যে প্রায় সম্পূর্ণ সুস্থতা লাভ করে। নিঃসন্দেহে এটি বর্তমান চিকিৎসা বিজ্ঞানের একটি আশীর্বাদ। বাংলাদেশের বেশ কয়েকটি টারশিয়ারি লেভেলের হাসপাতালে স্ট্রোকের সমন্বিত চিকিৎসা চালু আছে। স্ট্রোকের ক্ষেত্রে প্রতিটি মুহূর্ত মূল্যবান। তবে সবার আগে মনে রাখতে হবে Prevention is better than cure. অর্থাৎ আমাদের চেষ্টা থাকবে স্ট্রোক যাতে না হয়

* প্রতিরোধ

যাদের ডায়াবেটিস, হাই ব্লাড প্রেসার, হার্টের অসুখ রক্তে চর্বি বেশি, তাদের স্ট্রোকে আক্রান্ত হওয়ার আশঙ্কা বেশি। সুতরাং যাদের এসব রোগ রয়েছে, স্ট্রোকের হাত থেকে বাঁচতে তাদের উচিত হবে এসব রোগ কঠোরভাবে কন্ট্রোল করা। স্ট্রোকের সঙ্গে সংশ্লিষ্ট এসব রোগের উপযুক্ত কন্ট্রোল ছাড়াও কিছু সচেতনতা এবং সতর্কতাও স্ট্রোকের হাত থেকে আমাদের বাঁচাতে পারে। ধূমপান, শারীরিক নিষ্ক্রিয়তা অর্থাৎ কম কায়িক পরিশ্রম করা, অস্বাস্থ্যকর খাবার অর্থাৎ সুষম খাবার না খাওয়া, অতিরিক্ত ওজন বৃদ্ধি ইত্যাদিও স্ট্রোকের ঝুঁকি বাড়িয়ে দেয়। স্ট্রোক প্রতিরোধে এসব ব্যাপারেও আমাদের সতর্ক থাকতে হবে

* শীতে কি স্ট্রোক বাড়ে

শীতের সঙ্গে স্ট্রোকের সম্পর্ক আছে। অন্যান্য ডাক্তারি কারণ ছাড়াও এর সাধারণ ব্যাখ্যা হলো-শীতে শরীরের তাপমাত্রা কমে আমাদের রক্তনালি সংকুচিত হয়ে প্রেশার বেড়ে যায়। আর প্রেশার বেড়ে যাওয়ার ফলে শীতকালে ব্রেনের রক্তনালি ছিঁড়ে হেমোরেজিক স্ট্রোকের হার বেশি হয়। সেজন্য শীতকালে স্ট্রোকের হাত থেকে বাঁচতে অন্যান্য সতর্কতার সঙ্গে নিয়মিত প্রেশার চেক করাও অত্যাবশ্যক। তাৎক্ষণিক রেজাল্টের ভিত্তিতে হাই প্রেসারের রোগীদের ওষুধও সময়ে সময়ে এডজাস্ট করতে হয়

লেখক: কনসালটেন্ট, নিউরোমেডিসিন, আজগর আলী হাসপাতাল, ঢাকা

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Brain Network for Thirst and Salt Regulation Revealed

FeaturedNeuroscience

Summary: Researchers made a significant breakthrough in understanding how the brain regulates thirst and salt appetite. Their study utilized optogenetic and chemogenetic techniques on mice to explore the parabrachial nucleus (PBN), a key brain region in processing ingestion signals.

They identified two specific neuron populations in the lateral PBN that respond to water and salt intake, revealing how these neurons help modulate consumption behavior and prevent excessive intake. This research provides crucial insights into brain mechanisms controlling fluid balance and related disorders.

Key Facts:

1.      Two distinct neuron populations in the lateral PBN respond to water and salt intake, regulating thirst and salt appetite.

2.      Optogenetic activation of these neurons reduces water and salt consumption, even in deprived conditions.

3.      The findings offer significant insights into neurological control of fluid intake and have implications for understanding disorders caused by excessive water and salt consumption.

Source: Tokyo Institute of Technology

Staying hydrated and consuming appropriate amounts of salt is essential for the survival of terrestrial animals, including humans. The human brain has several regions constituting neural circuits that regulate thirst and salt appetite, in intriguing ways.

Previous studies suggested that water or salt ingestion quickly suppresses thirst and salt appetite before the digestive system absorbs the ingested substances, indicating the presence of sensing and feedback mechanisms in digestive organs that help real-time thirst and salt appetite modulation in response to drinking and feeding. Unfortunately, despite extensive research on this subject, the details of these underlying mechanisms remained elusive.

During the experiments, the researchers offered the mice—either in regular or water- or salt-depleted conditions—water and/or salt water, and monitored neural activities along with the corresponding drinking behaviors. Credit: Neuroscience News

To shed light on this matter, a research team from Japan has recently conducted an in-depth study on the parabrachial nucleus (PBN), the brain’s relay center for ingestion signals coming from digestive organs.

Their latest paper, whose first author is Assistant Professor Takashi Matsuda from Tokyo Institute of Technology, was published in Cell Reports on January 23, 2024.

The researchers conducted a series of in vivo experiments using genetically engineered mice. They introduced optogenetic (and chemogenetic) modifications and in vivo calcium imaging techniques into these mice, enabling them to visualize and control the activation or inhibition of specific neurons in the lateral PBN (LPBN) using light (and chemicals).

During the experiments, the researchers offered the mice—either in regular or water- or salt-depleted conditions—water and/or salt water, and monitored neural activities along with the corresponding drinking behaviors.

In this way, the team identified two distinct subpopulations of cholecystokinin mRNA-positive neurons in the LPBN, which underwent activation during water and salt intake. The neuronal population that responds to water intake projects from the LPBN to the median preoptic nucleus (MnPO), whereas the one that responds to salt intake projects to the ventral bed nucleus of the stria terminalis (vBNST).

Interestingly, if the researchers artificially activated these neuronal populations through optogenetic (genetic control using light) experiments, the mice drank substantially less water and ingested less salt, even if they were previously water- or salt-deprived. Similarly, when the researchers chemically inhibited these neurons, the mice consumed more water and salt than usual.

Therefore, these neuronal populations in the LPBN are involved in feedback mechanisms that reduce thirst and salt appetite upon water or salt ingestion, possibly helping prevent excessive water or salt intake.

These results, alongside their previous neurological studies, also reveal that MnPO and vBNST are the control centers for thirst and salt appetite, integrating promotion and suppression signals from several other brain regions.

“Understanding brain mechanisms controlling water and salt intake behaviors is not only a significant discovery in the fields of neuroscience and physiology, but also contributes valuable insights to understand the mechanisms underlying diseases induced by excessive water and salt intake, such as water intoxication, polydipsia, and salt-sensitive hypertension,” remarks Dr. Matsuda.

Prof. Noda mentions, “Many neural mechanisms governing fluid homeostasis remain undiscovered. We still need to unravel how the signals for inducing and suppressing water and salt intake, accumulated in the MnPO and vBNST, are integrated and function to control intake behaviors.” https://neurosciencenews.com/hydration-salt-neuroscience-25528/

Nasal Lymphatic Network Crucial for Brain CSF Drainage

FeaturedNeuroscience

Summary: Researchers discovered a crucial network of lymphatic vessels at the back of the nose, which significantly contributes to draining cerebrospinal fluid (CSF) from the brain. This study reveals a previously unknown CSF outflow route, offering insights into neurodegenerative conditions.

The research team used transgenic mice with lymphatic markers and advanced imaging to uncover this network, which connects to deep cervical lymph nodes. Their findings indicate potential therapeutic targets for enhancing CSF drainage, especially in age-related neurodegenerative diseases.

Key Facts:

1.      The newly discovered nasopharyngeal lymphatic plexus is a major hub for CSF drainage from the brain.

2.      The study suggests that activating cervical lymphatics could improve CSF outflow, offering a new therapeutic approach for neurodegenerative diseases.

3.      The research team plans to validate these findings in primates, aiming to advance treatments for conditions like Alzheimer’s disease.

Source: Institute for Basic Science

In a groundbreaking study published in Nature, South Korean researchers led by Director KOH Gou Young of the Center for Vascular Research within the Institute for Basic Science (IBS) have uncovered a distinctive network of lymphatic vessels at the back of the nose that plays a critical role in draining cerebrospinal fluid (CSF) from the brain.

The study, sheds light on a previously unknown route for CSF outflow, potentially unlocking new avenues for understanding and treating neurodegenerative conditions.

In our brains, waste products generated as byproducts of metabolic activity are expelled through cerebrospinal fluid (CSF). Accumulation of waste in the brain, if not properly expelled, can damage nerve cells, leading to impaired cognitive function, dementia, and other neurodegenerative brain disorders.

Hence, the regulation of CSF production, circulation, and drainage has long been a focus of scientific attention, especially in relation to age-related conditions like Alzheimer’s disease and other neurodegenerative diseases.

The brain produces around 500 mL of this fluid per day, which is drained from the subarachnoid space. Among the known drainage routes are lymphatic vessels around the cranial nerves and the upper region of the nasal cavity.

Despite well-documented evidence of lymphatics aiding CSF clearance, identifying the exact anatomical connections between the subarachnoid space and extracranial lymphatics has posed a challenge due to their extremely complex structure.

Koh’s team tackled this problem using transgenic mice with lymphatic fluorescent markers, microsurgeries, and advanced imaging techniques. Their efforts revealed a detailed network of lymphatic vessels at the back of the nose that serves as a major hub for CSF outflow to deep cervical lymph nodes in the neck. These lymphatics were found to have distinct features, including unusually shaped valves and short lymphangions.

Lead researcher JIN Hokyung highlighted, “Our study identified the nasopharyngeal lymphatic plexus as a hub for CSF outflow. CSF from specific cranial regions drained through these lymphatics to deep cervical lymph nodes in the neck. This discovery could have significant implications for understanding and treating conditions related to impaired CSF drainage.”

The study also demonstrated that pharmacological activation of the deep cervical lymphatics enhanced CSF drainage in mice.

The researchers were able to successfully modulate cervical lymphatics using phenylephrine (which activates α1-adrenergic receptors, causing smooth-muscle contraction) or sodium nitroprusside (which releases nitric oxide, inducing muscle relaxation and vessel dilation).

Importantly, this feature was preserved during aging, even when the nasopharyngeal lymphatic plexus had shrunk and was functionally impaired.

YOON Jin-Hui, the co-first author of this study, notes, “The deep cervical lymphatics, which remain intact with aging, offer a potential target for therapeutic interventions aimed at improving CSF outflow in individuals with compromised brain health.”

This endeavor was not without its own challenges, however. Deep anesthesia and removal of neck musculature were required to expose the lymphatics in the mice.

These delicate procedures themselves had problems altering the physiological dynamics of CSF drainage because cerebral blood flow and blood pulsing through the vasculature contribute to CSF circulation, which in turn influences CSF outflow.

Also, while the imaging techniques used were informative, researchers believe more advanced methods for imaging live animals (such as synchrotron X-ray imaging) may reveal more features of the dynamics of CSF drainage under physiological conditions.

Director KOH Gou Young of the Center for Vascular Research stated, “We plan to verify all the findings from the mice in primates, including monkeys and humans. We aim to investigate in a reliable animal model whether activating the cervical lymphatic vessels through pharmacological or mechanical means can prevent the exacerbation of Alzheimer’s disease progression by improving CSF clearance.”

https://neurosciencenews.com/nasal-lymphatic-network-csf-drainage-25530/

 

Brain Network for Thirst and Salt Regulation Revealed

 

Handwriting Boosts Brain Connectivity and Learning

Summary: Handwriting, compared to typing, results in more complex brain connectivity patterns, enhancing learning and memory. This study used EEG data from 36 students to compare brain activity while writing by hand and typing.

Handwriting, whether in cursive on a touchscreen or traditional pen and paper, activated extensive brain regions, vital for memory and learning. These findings highlight the importance of balancing traditional handwriting instruction with digital literacy in educational settings.

Key Facts:

1.      Handwriting activates more complex brain connectivity than typing, beneficial for learning and memory.

2.      The study used high-density EEGs to measure brain activity, demonstrating the unique cognitive engagement of handwriting.

3.      The results advocate for maintaining handwriting instruction in schools alongside digital literacy.

Source: Frontiers

As digital devices progressively replace pen and paper, taking notes by hand is becoming increasingly uncommon in schools and universities. Using a keyboard is recommended because it’s often faster than writing by hand. However, the latter has been found to improve spelling accuracy and memory recall.

To find out if the process of forming letters by hand resulted in greater brain connectivity, researchers in Norway now investigated the underlying neural networks involved in both modes of writing.

“We show that when writing by hand, brain connectivity patterns are far more elaborate than when typewriting on a keyboard,” said Prof Audrey van der Meer, a brain researcher at the Norwegian University of Science and Technology and co-author of the study published in Frontiers in Psychology.

“Such widespread brain connectivity is known to be crucial for memory formation and for encoding new information and, therefore, is beneficial for learning.”

The pen is mightier than the (key)board

The researchers collected EEG data from 36 university students who were repeatedly prompted to either write or type a word that appeared on a screen. When writing, they used a digital pen to write in cursive directly on a touchscreen. When typing they used a single finger to press keys on a keyboard.

High-density EEGs, which measure electrical activity in the brain using 256 small sensors sewn in a net and placed over the head, were recorded for five seconds for every prompt.

Connectivity of different brain regions increased when participants wrote by hand, but not when they typed.

“Our findings suggest that visual and movement information obtained through precisely controlled hand movements when using a pen contribute extensively to the brain’s connectivity patterns that promote learning,” van der Meer said.

Movement for memory

Although the participants used digital pens for handwriting, the researchers said that the results are expected to be the same when using a real pen on paper.

“We have shown that the differences in brain activity are related to the careful forming of the letters when writing by hand while making more use of the senses,” van der Meer explained.

Since it is the movement of the fingers carried out when forming letters that promotes brain connectivity, writing in print is also expected to have similar benefits for learning as cursive writing.

On the contrary, the simple movement of hitting a key with the same finger repeatedly is less stimulating for the brain.

“This also explains why children who have learned to write and read on a tablet, can have difficulty differentiating between letters that are mirror images of each other, such as ‘b’ and ‘d’. They literally haven’t felt with their bodies what it feels like to produce those letters,” van der Meer said.

A balancing act

Their findings demonstrate the need to give students the opportunity to use pens, rather than having them type during class, the researchers said. Guidelines to ensure that students receive at least a minimum of handwriting instruction could be an adequate step. For example, cursive writing training has been re-implemented in many US states at the beginning of the year.

At the same time, it is also important to keep up with continuously developing technological advances, they cautioned. This includes awareness of what way of writing offers more advantages under which circumstances.

“There is some evidence that students learn more and remember better when taking handwritten lecture notes, while using a computer with a keyboard may be more practical when writing a long text or essay,” van der Meer concluded.

https://neurosciencenews.com

 

 

 

Stressful Life Events Linked to Poor Biological Health

Summary: Researchers have found a strong link between stressful life events and deteriorating biological health. Analyzing blood concentrations of four key biomarkers in over 4,900 participants, the study reveals how stress disrupts the immune, nervous, and endocrine systems’ communication, increasing the risk of illnesses like cardiovascular disease and depression.

Chronic stressors like financial strain were particularly detrimental, with those experiencing such stress 59% more likely to be in the high-risk group for health issues. This groundbreaking research underscores the profound impact of stress on our biological systems, regardless of genetic predisposition.

Key Facts:

1.      Stressful events, including financial strain, significantly disrupt the healthy interaction of the immune, nervous, and endocrine systems.

2.      Individuals exposed to stress were 61% more likely to be in a high-risk health group, with each additional stressor increasing this likelihood by 19%.

3.      The study establishes that chronic stress can lead to poor biological health, independent of genetic factors.

Source: UCL

People who experience stressful life events or circumstances are more likely to have worse biological health, as indicated by biomarkers involved in the interaction between our immune, nervous and endocrine systems, according to a new study by UCL researchers.

The study, published in the journal Brain, Behavior and Immunity, found that not only major stressful experiences such as bereavement but chronic challenges such as financial strain were detrimental to the healthy interaction of these systems.

The researchers then looked at how earlier exposure to stressful circumstances might affect people’s likelihood of being in the high-risk group. Credit: Neuroscience News

Communication between our immune, nervous, and endocrine systems is necessary to maintain good health. Disruption of these processes is linked to a wide range of mental and physical illnesses, from cardiovascular disease to depression and schizophrenia.

When a threat like stress occurs, signals between the immune, nervous, and endocrine systems are activated and spur physiological and behavioural changes.

In this new study, the researchers analysed blood concentrations of four biomarkers in 4,934 people aged 50 and over who were participants of the English Longitudinal Study of Ageing. Two of these were proteins involved in the innate immune response to inflammation (C-reactive protein and fibrinogen), and two were hormones involved in the physiology of the stress response (cortisol and IGF-1).

The team used a sophisticated statistical technique, latent profile analysis, to identify clusters of biomarker activity. Three groups were identified and labelled as low risk to health, moderate risk, and high risk. The researchers then looked at how earlier exposure to stressful circumstances might affect people’s likelihood of being in the high-risk group.

They found that exposure to stressful circumstances overall, ranging from being an informal carer to experiencing a bereavement or divorce in the last two years, was linked to a 61% increase in likelihood of belonging to the high-risk group four years later.

Separately, the effect was also cumulative, as the likelihood of belonging to the high-risk group increased by 19% for each stressor experienced, for those who experienced more than one stress-inducing circumstance.

People who reported only financial strain – the perception that they may not have enough financial resources to meet their future needs – were 59% more likely, four years later, to belong to the high-risk group.

Lead author, PhD candidate Odessa S. Hamilton (UCL Institute of Epidemiology & Health Care), said: “When the immune and neuroendocrine systems function well together, homeostasis is maintained and health is preserved. But chronic stress can disrupt this biological exchange and lead to disease.

“We found that financial stress was most detrimental to biological health, although more research is needed to establish this for certain. This may be because this form of stress can invade many aspects of our lives, leading to family conflict, social exclusion, and even hunger or homelessness.”

Experiencing stress over a prolonged period of time can disturb the communication between the immune and neuroendocrine systems. That is because our response to stress is similar to our response to sickness, activating some of the same pathways (for instance, both responses trigger the production of immune system signals called pro-inflammatory cytokines).

The researchers also looked at genetic variants previously found to influence our immune-neuroendocrine response and found that the association between stressful life circumstances and belonging to the high-risk group four years later remained true irrespective of genetic predisposition. 

Funding: The research was supported by the National Institute on Aging, the UK’s National Institute for Health and Care Research (NIHR), the Economic and Social Research Council (ESRC), the Biotechnology and Biological Sciences Research Council (BBSRC) and UCL. https://neurosciencenews.com/financial-stress-health-25511/

 

 

Neural Connectivity: A Universal Network Phenomenon

Science is not only compatible with spirituality, it is a profound source of spirituality.(Calr sagan বিজ্ঞান শুধুমাত্র আধ্যাত্মিকতার সাথে সামঞ্জস্যপূর্ণ নয়, এটি আধ্যাত্মিকতার একটি গভীর উৎস।

ElectrophysiologyFeaturedNeuroscience

Summary: A groundbreaking study by physicists and neuroscientists reveals that the connectivity among neurons stems from universal networking principles, not just biological specifics.

Analyzing various model organisms, researchers found a consistent “heavy-tailed” distribution of neural connections, guided by Hebbian dynamics, indicating that neuron connectivity relies on general network organization.

This discovery, transcending biology, potentially applies to non-biological networks like social interactions, offering insights into the fundamental nature of networking.

Key Facts:

1.      The study analyzed neuron connectivity in diverse organisms, including fruit flies, roundworms, and mice, finding a universal “heavy-tailed” pattern.

2.      Researchers developed a model based on Hebbian dynamics, successfully mirroring the observed neural connectivity across different species.

3.      The findings suggest that neuron connections are governed by universal networking principles, potentially applicable to various networks beyond the brain.

Source: University of Chicago

A new study by physicists and neuroscientists from the University of Chicago, Harvard and Yale describes how connectivity among neurons comes about through general principles of networking and self-organization, rather than the biological features of an individual organism.

The research, published on January 17, 2024 in Nature Physics, accurately describes neuronal connectivity in a variety of model organisms and could apply to non-biological networks like social interactions as well.

While the vast number of connections may seem random, networks of brain cells tend to be dominated by a small number of connections that are much stronger than most. Credit: Neuroscience News

“When you’re building simple models to explain biological data, you expect to get a good rough cut that fits some but not all scenarios,” said Stephanie Palmer, PhD, Associate Professor of Physics and Organismal Biology and Anatomy at UChicago and senior author of the paper.

“You don’t expect it to work as well when you dig into the minutiae, but when we did that here, it ended up explaining things in a way that was really satisfying.”

Understanding how neurons connect

Neurons form an intricate web of connections between synapses to communicate and interact with each other. While the vast number of connections may seem random, networks of brain cells tend to be dominated by a small number of connections that are much stronger than most.

This “heavy-tailed” distribution of connections (so-called because of the way it looks when plotted on a graph) forms the backbone of circuitry that allows organisms to think, learn, communicate and move. Despite the importance of these strong connections, scientists were unsure if this heavy-tailed pattern arises because of biological processes specific to different organisms, or due to basic principles of network organization.

To answer these questions, Palmer and Christopher Lynn, PhD, Assistant Professor of Physics at Yale University, and Caroline Holmes, PhD, a postdoctoral researcher at Harvard University, analyzed connectomes, or maps of brain cell connections. The connectome data came from several different classic lab animals, including fruit flies, roundworms, marine worms and the mouse retina.

To understand how neurons form connections to one another, they developed a model based on Hebbian dynamics, a term coined by Canadian psychologist Donald Hebb in 1949 that essentially says, “neurons that fire together, wire together.” This means the more two neurons activate together, the stronger their connection becomes.

Across the board, the researchers found these Hebbian dynamics produce “heavy-tailed” connection strengths just like they saw in the different organisms. The results indicate that this kind of organization arises from general principles of networking, rather than something specific to the biology of fruit flies, mice, or worms.

The model also provided an unexpected explanation for another networking phenomenon called clustering, which describes the tendency of cells to link with other cells via connections they share.

A good example of clustering occurs in social situations. If one person introduces a friend to a third person, those two people are more likely to become friends with them than if they met separately.

“These are mechanisms that everybody agrees are fundamentally going to happen in neuroscience,” Holmes said. “But we see here that if you treat the data carefully and quantitatively, it can give rise to all of these different effects in clustering and distributions, and then you see those things across all of these different organisms.”

Accounting for randomness

As Palmer pointed out, though, biology doesn’t always fit a neat and tidy explanation, and there is still plenty of randomness and noise involved in brain circuits. Neurons sometimes disconnect and rewire with each other — weak connections are pruned, and stronger connections can be formed elsewhere.

This randomness provides a check on the kind of Hebbian organization the researchers found in this data, without which strong connections would grow to dominate the network.

The researchers tweaked their model to account for randomness, which improved its accuracy.

“Without that noise aspect, the model would fail,” Lynn said. “It wouldn’t produce anything that worked, which was surprising to us. It turns out you actually need to balance the Hebbian snowball effect with the randomness to get everything to look like real brains.”

Since these rules arise from general networking principles, the team hopes they can extend this work beyond the brain.

“That’s another cool aspect of this work: the way the science got done,” Palmer said. “The folks on this team have a huge diversity of knowledge, from theoretical physics and big data analysis to biochemical and evolutionary networks. We were focused on the brain here, but now we can talk about other types of networks in future work.”

Funding: The study, “Heavy–tailed neuronal connectivity arises from Hebbian self–organization,” was supported by the National Science Foundation, through the Center for the Physics of Biological Function (PHY–1734030) and a Graduate Research Fellowship (C.M.H.); by the James S. McDonnell Foundation through a Postdoctoral Fellowship Award (C.W.L.); and by the National Institutes of Health BRAIN initiative (R01EB026943).

https://neurosciencenews.com/neural-netowrk-connectivity-25472/

Violent Video Games Do Not Diminish Empathy

FeaturedNeurosciencePsychology

Summary: A recent study challenges the notion that violent video games diminish empathy. Adult subjects, new to such games, participated in an experiment where they played a violent version of Grand Theft Auto V. Their empathic responses were measured before and after the gaming sessions. Surprisingly, the study found no significant impact on empathy or related brain activity.

Key Facts:

1.      The study involved 89 adult males with minimal exposure to violent video games, ensuring unbiased results.

2.      Participants played a violent version of Grand Theft Auto V, but this had no discernible effect on their empathetic responses or brain activity.

3.      The study cautions against conclusive claims about the harmlessness of violent video games, emphasizing the need for careful interpretation and further research.

Source: University of Vienna

Neuroscientists from the University of Vienna and the Karolinska Institute in Stockholm have investigated whether playing violent video games leads to a reduction in human empathy.

To do this, they had adult test subjects play a violent video game repeatedly over the course of an experiment lasting several weeks. Before and after, their empathic responses to the pain of another person were measured. It was found that the violent video game had no discernible effect on empathy and underlying brain activity.

These results have now been published in the renowned journal eLife.

Does that mean that concerns about violence in video games are unfounded? Credit: Neuroscience News

Video games have become an integral part of the everyday life of many children and adults. Many of the most popular video games contain explicit depictions of extreme violence.

Therefore, concerns have been raised that these games may blunt the empathy of their players and could therefore lower the inhibition threshold for real violence. An international research team led by Viennese neuroscientists Claus Lamm and Lukas Lengersdorff has now investigated whether this is actually the case.

The Austrian and Swedish researchers invited a total of 89 adult male subjects to take part in the study. A key selection criterion was that the subjects had had little or no previous contact with violent video games. This ensured that the results were not influenced by different experiences with these games.

In a first experimental study, the baseline level of empathy of the test subjects was assessed. Brain scans were used to record how the test subjects reacted when a second person was administered painful electric shocks. Then, the video game phase of the experiment began, during which the test subjects came to the research laboratory seven times to play a video game for one hour each time.

The participants in the experimental group played a highly violent version of the game Grand Theft Auto V and were given the task of killing as many other game characters as possible. In the control group, all violence had been removed from the game and the participants were given the task of taking photos of other game characters.

Finally, after the video game phase was over, the test subjects were examined a second time to determine whether their empathic responses had changed.

The analysis of the data showed that the video game violence had no discernible effect on the empathic abilities of the test subjects. The reactions of the participants in the experimental group who were confronted with extreme depictions of violence did not differ statistically from those of the participants who only had to take photos.

In addition, there were no significant differences in the activity of brain regions that had been identified in other studies as being associated with empathy – such as the anterior insular and anterior midcingulate cortex. 

Does that mean that concerns about violence in video games are unfounded? The authors advise against jumping to conclusions.

“Precisely because this is such a sensitive topic, we have to be very careful when interpreting these results,” explains lead author Lukas Lengersdorff, who carried out the study as part of his doctoral studies.

“The conclusion should not be that violent video games are now definitively proven to be harmless. Our study lacks the data to make such statements.”

According to the neuroscientist and statistician, the value of the study lies rather in the fact that it allows a sober look at previous results.

“A few hours of video game violence have no significant influence on the empathy of mentally healthy adult test subjects. We can clearly draw this conclusion.

“Our results thus contradict those of previous studies, in which negative effects were reported after just a few minutes of play”. In these previous studies, participants had played the violent video game immediately before data collection.

“Such experimental designs are not able to distinguish the short-term and long-term effects of video games”, explains Lengersdorff.

According to research group leader and co-author Claus Lamm, the study also sets a new standard for future research in this area: “Strong experimental controls and longitudinal research designs that allow causal conclusions to be drawn are needed to make clear statements about the effects of violent video games. We wanted to take a step in this direction with our study”.

Now it is the task of further research to check whether there are no negative consequences even after significantly longer exposure to video game violence – and whether this is also the case for vulnerable subpopulations.

“The most important question is of course: are children and young people also immune to violence in video games? The young brain is highly plastic, so repeated exposure to depictions of violence could have a much greater effect. But of course these questions are difficult to investigate experimentally without running up against the limits of scientific ethics,” says Lamm. https://neurosciencenews.com/empathy-gaming-psychology-25471/

Plant Protein-Based Diet Is Key to Healthier Aging for Women

FeaturedNeuroscience

Summary: A new study reveals that women consuming higher amounts of plant-based protein experience fewer chronic diseases and maintain better health as they age.

Analyzing data from over 48,000 women in the Harvard-based Nurses’ Health Study, the research showed a significant link between plant protein intake and reduced risk of heart disease, cancer, diabetes, and cognitive decline. Protein source matters, with plant proteins being more beneficial for long-term health compared to animal proteins.

Key Facts:

1.      The study analyzed data from 1984 to 2016, involving 48,000 women, initially in good health, aged 38 to 59.

2.      Women with higher intake of plant-based proteins had a 46% higher likelihood of healthy aging, compared to a 6% decrease in those consuming more animal protein.

3.      Plant proteins were strongly linked to better heart health, lower LDL cholesterol, and improved mental health in later years, unlike animal proteins.

Source: Tufts University

Women who consume higher amounts of protein, especially protein from plant-based sources, develop fewer chronic diseases and are more likely to be healthier overall as they age, according to a study led by researchers at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA) at Tufts University and published Jan. 17 in The American Journal of Clinical Nutrition.

Analyzing self-reported data from more than 48,000 women, the researchers saw notably less heart disease, cancer, and diabetes, and cognitive and mental health decline, in those who included more protein in their diets from sources such as fruits, vegetables, bread, beans, legumes, and pasta, compared to those who ate less.

The women were between the ages of 38 and 59 in 1984 and deemed to be in good physical and mental health at the start of the study. Credit: Neuroscience News

“Consuming protein in midlife was linked to promoting good health in older adulthood,” said Andres Ardisson Korat, a scientist at the HNRCA and lead author of the study. “We also found that the source of protein matters. Getting the majority of your protein from plant sources at midlife, plus a small amount of animal protein seems to be conducive to good health and good survival to older ages.”

Findings were derived from the seminal Harvard-based Nurses’ Health Study, which followed female health care professionals from 1984 to 2016. The women were between the ages of 38 and 59 in 1984 and deemed to be in good physical and mental health at the start of the study.

Ardisson Korat and fellow researchers, including senior author Qi Sun of the Harvard T.H. Chan School of Public Health, examined thousands of surveys collected every four years from 1984 to 2016 on how frequently people ate certain foods to pinpoint dietary protein and its effects on healthy aging. They calculated protein intake by multiplying the number of times each food item was consumed by its protein content and then, using the Harvard University Food Composition Database, totaling the amount of protein across all food items.

The researchers then compared the diets of women who didn’t develop 11 chronic diseases or lose a lot of physical function or mental health, with the diets of those who did.

Women who ate more plant-based protein, which in 1984 was defined as protein obtained from bread, vegetables, fruits, pizza, cereal, baked items, mashed potatoes, nuts, beans, peanut butter, and pasta, were 46 percent more likely to be healthy into their later years.

Those who consumed more animal protein such as beef, chicken, milk, fish/seafood, and cheese, however, were 6 percent less likely to stay healthy as they aged.

“Those who consumed greater amounts of animal protein tended to have more chronic disease and didn’t manage to obtain the improved physical function that we normally associate with eating protein,” said Ardisson Korat.

Animal protein was modestly tied with fewer physical limitations in older age, but plant protein had a stronger, more consistent correlation across all observed models, and was more closely linked with sound mental health later in life.

For heart disease in particular, higher plant protein consumption came with lower levels of LDL cholesterol (“bad” cholesterol), blood pressure, and insulin sensitivity, while higher animal protein intake was tied to higher levels, along with increased insulin-like growth factor, which has been detected in multiple cancers.

Dairy protein alone (mainly milk, cheese, pizza, yogurt, and ice cream) was not significantly associated with better health status in older adulthood.

The team acknowledged that the benefits of plant protein might derive from components in plant-based food, rather than the protein—compared to animal foods, plants contain a higher proportion of dietary fiber, micronutrients, and beneficial compounds called polyphenols that are present in plants, rather than exclusively protein.

Ardisson Korat also said data from other groups is needed, as the Nurses’ Health Study surveyed primarily white females working in health care. “The data from the study tended to be very homogeneous in terms of demographic and socioeconomic composition, so it will be valuable to follow up with a study in cohorts that are more diverse. It’s a field that is still evolving,” said Ardisson Korat.

But the team’s findings so far support the recommendation that women eat most of their protein in the form of fruits, vegetables, nuts, and seeds, although they should also consume some fish and animal protein for their iron and vitamin B12 content.

“Dietary protein intake, especially plant protein, in midlife plays an important role in the promotion of healthy aging and in maintaining positive health status at older ages,” Ardisson Korat said.

Funding: Research reported in this article was supported by the U.S. Department of Agriculture’s Agricultural Research Service, and by the National Institutes of Health under award numbers UM1CA186107 (National Cancer Institute), P01CA87969 (National Cancer Institute), R01DK120870 (National Institute of Diabetes and Digestive and Kidney Diseases), U2CDK129670 (National Institute of Diabetes and Digestive and Kidney Diseases), R01DK127601 (National Institute of Diabetes and Digestive and Kidney Diseases), R01HL060712 (National Heart, Lung and Blood Institute), R01HL034594 (National Heart, Lung and Blood Institute), R01HL035464 (National Heart, Lung and Blood Institute), and R01HL088521 (National Heart, Lung and Blood Institute). Andres Ardisson Korat was supported by training grant KL2TR002545 from the National Institutes of Health’s National Center for Advancing Translational Sciences. Complete information on authors, funders, limitations and conflicts of interest is available in the published paper.

The content is solely the responsibility of the authors and does not necessarily represent the official views of the U.S. Department of Agriculture or the National Institutes of Health. https://neurosciencenews.com/plant-protein-deit-aging-women-25473/

 

 

 

 

 

Tracking Brain’s “Wave of Death”: New Insights into Neural End-of-Life

ElectrophysiologyFeaturedNeuroscience

Summary: Researchers have made significant strides in understanding the neurological process of dying.

Their study reveals that during anoxia, or oxygen deprivation, the brain undergoes a series of changes, including a massive release of glutamate and a surge in gamma and beta waves, potentially linked to near-death experiences. This is followed by a ‘wave of death’ – a high-amplitude wave marking the transition towards total cessation of brain activity.

The study, focusing on rats, found that this wave originates in the neocortex’s layer 5 pyramidal neurons and can potentially be reversed under certain conditions, offering new insights into preserving brain function during resuscitation.

Key Facts:

1.      The ‘wave of death’ in the brain, marking the transition to total cessation of brain activity, originates in the neocortex’s layer 5.

2.      This wave can be reversed if resuscitation occurs within a specific time window, indicating the possibility of preserving brain function.

3.      The study provides a deeper understanding of the neural mechanisms as death approaches, challenging the notion of a flat EEG as a definitive marker of ceased brain functions.

Source: Paris Brain Institute

Death is a difficult concept to define from a neurological point of view. It is not a precise moment that marks the switch from life to death, but a process that lasts several minutes and which, in some cases, can be reversible.

In a previous study, researchers from the “Dynamics of Epileptic Networks and Neuronal Excitability” team at Paris Brain Institute showed that after a long period of oxygen deprivation—called anoxia—brain activity undergoes a cascade of successive changes that can now be described precisely.

When the brain stops receiving oxygen, its stores of ATP, the cells’ fuel, are rapidly depleted. This causes a disruption in the electrical balance of neurons and a massive release of glutamate, an essential excitatory neurotransmitter in the nervous system.

After that, the activity of the neurons gradually diminishes until a state of perfect electrical silence— corresponding to a flat electroencephalogram—is reached. Credit: Neuroscience News

“Neural circuits seem to shut down at first… Then we see a surge in brain activity—specifically an increase in gamma and beta waves,” Séverine Mahon, a researcher in neuroscience, explains.

“These waves are usually associated with a conscious experience. In this context, they may be involved in near-death experiences reported by people who have survived cardiorespiratory arrest.”

After that, the activity of the neurons gradually diminishes until a state of perfect electrical silence— corresponding to a flat electroencephalogram—is reached. However, this silence is quickly interrupted by the depolarization of neurons, which takes the form of a high-amplitude wave known as the “wave of death”, which alters the function and structure of the brain.

“This critical event, called anoxic depolarization, induces neuronal death throughout the cortex. Like a swan song, it is the true marker of transition towards the cessation of all brain activity”, Antoine Carton-Leclercq, PhD student and first author of the study, adds.

Until now, researchers did not know where the wave of death is initiated in the cortex or whether it propagates homogeneously across all cortical layers.

“We already knew that it is possible to reverse the effects of anoxic depolarization if we manage to resuscitate the subject within a specific time window,” the researcher adds.

“We still had to understand in which areas of the brain the death wave is likely to do the most damage to preserve brain function as much as possible.”

Following the path of the wave of death

To answer these questions, the researchers used, in rats, measurements of local field potentials and recordings of the electrical activity of individual neurons in different layers of the primary somatosensory cortex—an area that plays a crucial role in body representation and processing of sensory information.

They then compared the electrical activity of these different layers before and during anoxic depolarization.

“We noticed that neuronal activity was relatively homogeneous at the onset of brain anoxia. Then, the wave of death appeared in the pyramidal neurons located in layer 5 of the neocortex and propagated in two directions: upwards, i.e. the surface of the brain, and downwards, i.e. the white matter,” Séverine Mahon explains.

“We have observed this same dynamic under different experimental conditions and believe it could exist in humans.”

These findings also suggest that the deeper layers of the cortex are the most vulnerable to oxygen deprivation—probably because the pyramidal neurons in layer 5 have exceptionally high energy needs. However, when the researchers reoxygenated the rats’ brains, the cells replenished their ATP reserves, leading to the repolarization of neurons and the restoration of synaptic activity.

“This new study advances our understanding of the neural mechanisms underlying changes in brain activity as death approaches. It is now established that, from a physiological point of view, death is a process that takes its time… and that it is currently impossible to dissociate it rigorously from life.

“We also know that a flat EEG does not necessarily mean the definitive cessation of brain functions,” Prof. Stéphane Charpier, head of the research team, concludes.

“We now need to establish the exact conditions under which these functions can be restored and develop neuroprotective drugs to support resuscitation in the event of heart and lung failure.” https://neurosciencenews.com/death-brain-neuroscience-25356/

 

 

 

 

Loud Play, Silent Risk: Video Gaming’s Link to Hearing Loss

Summary: A systematic review indicates a potential risk of irreversible hearing loss and tinnitus among video gamers due to high sound levels. The study, encompassing over 50,000 individuals, found that sound levels in gaming often near or exceed safe limits.

Key findings include sound levels from gaming reaching up to 80-89 decibels in gaming centers and impulse sounds during gameplay hitting as high as 119 decibels, exceeding safe exposure limits. While video games’ popularity continues to rise, with over 3 billion gamers in 2022, this review highlights the need for greater public health efforts to raise awareness about the auditory risks associated with gaming.

Key Facts:

1.      Video gaming sound levels often approach or exceed safe noise exposure limits, potentially leading to hearing loss and tinnitus.

2.      Impulse sounds in games can reach 119 decibels, far exceeding safe limits for children and adults.

3.      The review suggests a need for educational initiatives to promote safe listening practices among gamers.

Source: BMJ

Video gamers worldwide may be risking irreversible hearing loss and/or tinnitus—persistent ringing/buzzing in the ears—finds a systematic review of the available evidence, published in the open access journal BMJ Public Health.

What evidence there is suggests that the sound levels reported in studies of more than 50,000 people often near, or exceed, permissible safe limits, conclude the researchers. 

And given the popularity of these games, greater public health efforts are needed to raise awareness of the potential risks, they urge.

Altogether, these indicated that boys played video games more often than girls, for longer periods of time, and at higher sound intensity levels. Credit: Neuroscience News

While headphones, earbuds, and music venues have been recognised as sources of potentially unsafe sound levels, relatively little attention has been paid to the effects of video games, including e-sports, on hearing loss, say the researchers.

Gamers often play at high-intensity sound levels and for several hours at a time, they add. And one estimate indicates that there were more than 3 billion gamers worldwide in 2022. 

To try and build an evidence base, the researchers trawled research databases looking for relevant studies and white papers, newsletters, reports, and proceedings, collectively referred to as ‘grey literature,’ published at any point in English, Spanish, or Chinese.

Some 14 peer reviewed studies from 9 countries in North America, Europe, South East Asia, Asia and Australasia, and involving a total of 53,833 people, were included in the review.

Eleven were cohort (epidemiological observational) studies, 6 of which looked at the associations between hearing and computer or video games; 4 focused on gaming centres or personal computer rooms, which are popular in Asia; and 1 focused on mobile devices.

Reported sound levels ranged from 43.2 decibels (dB) (mobile devices) up to 80-89 dB (gaming centres) while length of noise exposure varied by mode and frequency of access–from daily to once a month, for at least an hour at a time, averaging 3 hours/week.

Impulse sounds consist of bursts lasting less than 1 second, with peak levels at least 15 dB higher than the background sound. One study reported that impulse sounds reached levels as high as 119 dB during game play; permissible exposure limits are around 100 dB for children and 130–140 dB for adults.

The International Telecommunication Union (ITU), in collaboration with the World Health Organization, describes a time–intensity trade-off, known as an exchange rate, for permissible levels and duration of exposure, explain the researchers. 

For example, a permissible noise exposure level of 80 dB for 40 hours a week with a 3 dB exchange rate means the permissible exposure time halves with every 3 dB increase in noise level: at 83 dB it’s 20 hours; at 86 dB it’s 10 hours; at 92 dB it’s 2.5 hours; and at 98 dB it’s 38 minutes.

For children, the permissible noise exposure level is defined as 75 dB for 40 hours a week. Children can therefore safely listen to an 83 dB sound for around 6.5 hours, 86 dB for around 3.25 hours, 92 dB for 45 minutes, and 98 dB for only 12 minutes a week, explain the researchers.

Six studies reported on video gaming prevalence among young people, which ranged from 20% to 68%. Two South Korean studies reported a prevalence of gaming centre use at around 60%.

Five studies evaluated associations between gaming and self-reported hearing loss, hearing thresholds, or tinnitus. Of these, 2 found that  school pupils’ gaming centre use was linked to increased odds of severe tinnitus and high-frequency sound hearing loss in both ears.

Another large observational study reported that video gaming was associated with increased odds of self-reported hearing loss severity.

One study reported that over 10 million people in the USA may be exposed to ‘loud’ or ‘very loud’ sound levels from video or computer games. 

One study measured sound levels of 5 video games through headphones attached to the gaming console, and found that these averaged 88.5, 87.6, 85.6 and 91.2 dB for 4 separate shooter games, and 85.6 dB for a racing game.

The authors therefore concluded that the daily level of sound exposure from these video games is close to maximum permissible levels of sound exposure.

An additional 16 peer-reviewed articles and 14 grey literature sources mention gaming as a potential source of excessive sound exposure.

One grey literature source sought to discover gamers’ preferred listening levels while wearing headphones.  The author concluded that gaming headphones can reach unsafe listening levels, “which could place some gamers at risk of sound-induced hearing loss.”

Three studies evaluated gender differences in gaming behaviours. Altogether, these indicated that boys played video games more often than girls, for longer periods of time, and at higher sound intensity levels.

The researchers acknowledge that some of the included studies date back to the early 1990s, and only 2 published in the past 10 years objectively measured average sound levels from video games or at gaming centres, although both reported high sound levels in these circumstances.

“Although the data provided in this review are limited, they suggest that some gamers, particularly those who play frequently, and at or above the average sound levels described by papers included in this review, probably exceed permissible sound exposure limits, and are thus engaging in unsafe listening practices, which could put them at risk for developing permanent hearing loss and/or tinnitus,” they nevertheless conclude.

There are also several key gaps in the available evidence, they add. For example, the impact of esports, geographic region, sex, and age, on hearing loss. Further research is essential to inform preventive measures and global policy initiatives, they suggest.

“The findings suggest that there may be a need to prioritise interventions, such as initiatives focused on education and awareness of the potential risks of gaming, that can help promote safe listening among gamers,” they suggest.

https://neurosciencenews.com/gaming-tinnitus-hearing-25470/

 

 

Inflammation and Poverty Increase Health and Mortality Risks

Summary: Recent research highlights a synergistic relationship between chronic inflammation and poverty, exacerbating health risks and reducing life expectancy in the U.S.

Analyzing data from the National Health and Nutrition Examination Survey (NHANES), researchers found that individuals suffering from both poverty and chronic inflammation face significantly worse health outcomes than those affected by either factor alone. The study used high sensitivity C-reactive protein levels to measure inflammation and considered household income against the poverty threshold.

The findings suggest that the combined effect of poverty and inflammation on mortality is not merely additive but synergistic, emphasizing the need for targeted healthcare interventions.

Key Facts:

1.      The study shows that poverty combined with chronic inflammation leads to significantly worse health outcomes than either factor alone.

2.      Data from nearly 95 million adults in NHANES was analyzed, revealing a 127% increased heart disease mortality risk and a 196% increased cancer mortality risk for those affected by both factors.

3.      The research suggests a need for healthcare professionals to screen socially disadvantaged individuals for chronic inflammation and consider appropriate treatments.

Source: Frontiers

In the US, approximately 37.9 million people, or 11.4% of the population, lived below the poverty line in 2022. It has been well demonstrated that poverty negatively affects physical and mental health. For example, people living in poverty run a greater risk of mental illness, heart disease, hypertension, and stroke, and have a higher mortality and lower life expectancy.

The mechanisms by which poverty impacts on health outcomes are manifold: for example, people experiencing poverty have reduced access to healthy food, clean water, safe housing, education, and healthcare.

Now, researchers have shown for the first time that the effects of poverty may combine in a synergistic manner with another risk factor, chronic inflammation, to reduce health and life expectancy even further. They found that health outcomes for Americans living in poverty and with chronic inflammation are significantly worse than expected from their separate health effects.

The results are published in Frontiers in Medicine.

“Here we show that clinicians need to consider the effect of inflammation on people’s health and longevity, especially on those experiencing poverty,” said lead author Dr Arch Mainous, a professor at the University of Florida.

Inflammation is a natural physiological reaction to infections or injuries, essential for healing. But chronic inflammation – caused by exposure to environmental toxins, certain diets, autoimmune disorders such as arthritis, or other chronic diseases like Alzheimer’s – is a known risk factor for disease and mortality, just like poverty.

NHANES

Mainous and colleagues analyzed data from adults aged 40 and older, enrolled between 1999 and 2002 in the National Health and Nutrition Examination Survey (NHANES), and followed them until 31 December 2019. The NHANES, conducted since 1971 by the National Center for Health Statistics, tracks the health and nutritional status of US adults and children.

The NHANES allows for estimates of the US population represented by the cohort, and this study represented nearly 95 million adults. The authors combined NHANES data with records from the National Death Index, to calculate mortality rates over a period of 15 years after enrollment.

Among other demographics, NHANES records the household income. The authors divided this by the official poverty threshold to calculate the ‘poverty index ratio’, a standard measure of poverty.

Chronic inflammation

Whether participants suffered from severe inflammation was deduced from their plasma concentration of high sensitivity C-reactive protein (hs-CRP), produced by the liver in response to the secretion of interleukins by immune and fat cells.

The concentration of hs-CRP, included among NHANES data, is a readily available, informative, and well-studied measure of inflammation: for example, elevated concentrations are known to increase the risk of cardiovascular disease and all-cause mortality.

Typically, a concentration of greater than 0.3 mg/dl hs-CRP is taken to indicate chronic systemic inflammation, but Mainous et al. also considered the more stringent threshold of 1.0 mg/dl in a separate analysis.

The authors classified participants in four groups: with or without chronic inflammation, and living below the poverty line or not. By comparing the 15-year mortality rate between these, they could thus study the effects of poverty and inflammation separately and jointly.

Synergistic effect

“We found that participants with either inflammation or poverty alone each had about a 50% increased risk in all-cause mortality. In contrast, individuals with both inflammation and poverty had a 127% increased heart disease mortality risk and a 196% increased cancer mortality risk,” said Dr Frank A. Orlando, an associate professor at the University of Florida and the study’s second author.

“If the effects of inflammation and poverty on mortality were additive, you’d expect a 100% increase in mortality for people where both apply. But since the observed 127% and 196% increases are much greater than 100%, we conclude that the combined effect of inflammation and poverty on mortality is synergistic.”

Routine screening for both risk factors?

A wide variety of treatments for systemic inflammation exists, ranging from diet and exercise to nonsteroidal anti-inflammatory drugs (NSAIDs) and steroids. The present results suggest that clinicians might consider screening socially disadvantaged people – already a medically vulnerable group – for chronic inflammation, and if necessary treat them with such anti-inflammatory drugs.

However, steroids and NSAIDS aren’t without risks when taken long-term. More research will thus be needed before patients are routinely prescribed them in clinical practice to decrease systemic inflammation.

“It’s important for guidelines panels to take up this issue to help clinicians integrate inflammation screening into their standard of care, particularly for patients who may have factors that place them at risk for chronic inflammation, including living in poverty. It is time to move beyond documenting the health problems that inflammation can cause, to trying to fix these problems,” concluded Mainous.

 https://neurosciencenews.com/poverty-inflammation-health-mortality-25461/

 

 

Brain Stimulation Unlocks Our Telepathy and Clairvoyance Powers

Summary: Researchers proposed a groundbreaking model in the study of psi phenomena, suggesting the human brain functions as a psi-inhibitory filter. They used repetitive transcranial magnetic stimulation (rTMS) to temporarily inhibit the left medial middle frontal region in healthy individuals, observing significant psi effects as a result.

The study reveals that individuals with neurological or rTMS-induced frontal lesions show enhanced mind-matter interaction abilities. This research offers a new perspective on how the brain might suppress innate psi abilities, potentially revolutionizing our understanding of these elusive phenomena.

Key Facts:

1.      The study hypothesizes that the human brain acts as a filter suppressing innate psi abilities.

2.      rTMS-induced lesions in the left medial middle frontal region led to significant psi effects.

3.      This research could fundamentally change how psi phenomena are understood and studied.

Source: BIAL Foundation

Psi is a phenomenon that includes telepathy (mind-mind connections), clairvoyance (perception of distant objects or events), precognition (perception of future events), and mind-matter interactions (psychokinesis).

There are several studies that discuss the empirical evidence for psi, including arguments against their existence as their effects are small and hard to replicate under controlled experimental conditions.

These findings support the concept that the brain serves as a filter to block psi effects and may help explain why these effects are so small and hard to replicate in healthy participants. Credit: Neuroscience News

To address this phenomenon, Dr. Morris Freedman’s team, supported by the BIAL Foundation, has developed a novel neurobiological model based upon the concept that the brain may act as a psi-inhibitory filter. In other words, humans may have innate psi abilities that are suppressed by this frontal lobe filter.

To test this hypothesis, he and his colleagues, Dr. Malcolm Binns, Dr. Jed Meltzer, Rohila Hashimi, and Dr. Robert Chen used repetitive transcranial magnetic stimulation (rTMS) to induce reversible brain lesions in the left medial middle frontal region in healthy participants.

In an article that was published online ahead of print in the scientific journal Cortex, called Enhanced mind-matter interactions following rTMS induced frontal lobe inhibition, Dr. Freedman and the researchers found a significant psi effect following rTMS inhibition of the left medial middle frontal lobe.

Healthy participants with reversible rTMS induced lesions affecting the left medial middle frontal region of the brain showed larger effects on a mind-matter interaction task compared to healthy participants without rTMS induced lesions.

These findings support the concept that the brain serves as a filter to block psi effects and may help explain why these effects are so small and hard to replicate in healthy participants.

“This study confirmed our hypothesis”, says Dr. Freedman, head of the Division of Neurology at Baycrest, adding that “individuals with neurological or reversible rTMS induced frontal lesions may represent a useful group for detection and replication of this phenomenon”.

For Dr. Freedman, these findings “are potentially transformative for the way we view interactions between the brain and seemingly random events” and may “significantly advance research in the area of psi, helping to bring this phenomenon into the realm of mainstream science”.

Learn more about the project “210/18 – Mind-matter Interactions and the Frontal Lobes of the Brain” here.

https://neurosciencenews.com/brain-stimulation-psi-telepathy-25460/

 

Autism and Beyond: Unveiling Overlapping Neurotypes

Summary: A study has uncovered significant overlaps in neurodivergent traits among children diagnosed with autism.

The research, which evaluated medical records of children referred for autism assessments, revealed that 76.2% of these children also exhibited traits associated with other neurotypes such as ADHD. Over half (55.6%) of the children assessed for autism potentially met the criteria for ADHD, indicating a high level of co-occurrence.

This study, a pioneering effort in Scotland, emphasizes the need for holistic assessments in child neurodevelopment, considering multiple neurotypes for accurate diagnosis and tailored support.

Key Facts:

1.      The study found a substantial overlap in neurodivergence, with 76.2% of autistic children displaying traits of other neurotypes, including ADHD.

2.      Over 55% of children assessed for autism might also meet the diagnostic threshold for ADHD, highlighting the necessity of holistic neurotype assessments.

3.      Despite the clinical overlap, only 26% of children with additional traits were investigated for an underlying diagnosis, stressing the need for more comprehensive evaluation methods.

Source: University of Glasgow

Three quarters of children (76.2%) who were diagnosed with autism also had traits of other neurodivergent neurotypes—including traits associated with Attention Deficit Hyperactivity Disorder (ADHD), learning and motor differences—according to a new study.

The research—led by the University of Glasgow and published in PLOS One—found that more than half (55.6%) of children referred for autism assessment may also meet the diagnostic threshold for ADHD, and certainly have at least some significant ADHD traits.

The study only looked at a small selection of possible neurotypes, suggesting the actual number of children with autism and other neurotypes may be higher.

This study is believed to be the first time the level of overlap of different neurodivergences in children has been studied in Scotland, where services aim to move away from single neurotype assessments to a more holistic assessment model, where all possible overlapping neurotypes are explored and identified.

The research showed there was a positive association between the number of neurodivergence detected and an earlier age of referral and also suggested that neurodivergent females were less likely than males to be identified before the age of five. However, despite clinical overlap and co-occurrence of neurodivergence in children, just 26% of those in the study with other traits were investigated for an additional underlying diagnosis.

For the study, the researchers evaluated anonymized medical records of children aged between two and 17 years old who were referred for an autism assessment, using validated questionnaires to assess for neurodivergent traits.

The research suggests that validated questionnaires may help clinicians identify co-occurring neurodivergence at the first assessment, allowing for earlier support and the development of whole-system insight into a child’s neurotype.

Dr. Jason Lang, Clinical Senior Lecturer in Neurodevelopment and Honorary Consultant in Child and Adolescent Psychiatry, said, “This study is extremely important, as it shows how vital it is to have a holistic approach to assessing children, to identify possible overlapping neurotypes properly. As well as a better understanding of the neurodivergent population as a whole, identifying a child’s precise ‘make and model’ will help provide better and more bespoke support for these children when needed.”

“However, it can be challenging for professionals to work across various neurotypes. As such, more work must be done to ensure services are truly holistic for overlapping traits to be properly identified. Our work suggests that one way to help is for services to use holistic questionnaires to gather this information.”

“And while this work is based in children’s services, we would also recommend that similar studies be carried out in adult populations, where current approaches remain, to a large extent, siloed in approach.”

https://neurosciencenews.com/asd-adhd-neurotypes-25456/

 

Over 200 New Depression-Related Genes Identified

Summary: A groundbreaking study has uncovered more than 200 genes linked to depression, shedding light on the complex nature of the condition. This global research effort, the first of its kind, analyzed genetic data from nearly one million participants of diverse ancestry groups.

The study identified over 50 new genetic loci and 205 novel genes associated with depression, offering potential drug targets and insights into its development. Importantly, it emphasizes the need for diverse genetic datasets to better understand and treat this widespread mental health disorder.

Key Facts:

1.      The study identified over 200 genes linked to depression, with more than 50 new genetic loci discovered.

2.      Drug repurposing potential was highlighted, as one gene encodes a protein targeted by a common diabetes drug.

3.      Diversity in genetic research is crucial, as genetic hits for depression showed less overlap across ancestry groups than expected.

Source: UCL

More than 200 genes linked to depression have been newly identified in a worldwide study led by UCL researchers.

The research, published in Nature Genetics, found more than 50 new genetic loci (a locus is a specific position on a chromosome) and 205 novel genes that are associated with depression in the first large-scale global study of the genetics of major depression in participants of diverse ancestry groups.

The study also showcases the potential for drug repurposing, as one of the identified genes encodes a protein targeted by a common diabetes drug, while also pointing to new targets for drugs that may be developed to treat depression.

Depression is very common, yet how it develops is still poorly understood. Genetic research using big data offers new avenues to understand the disease and has uncovered dozens of genes associated with depression, each of which individually confers only a small increase in risk.

It can also help find new drug targets, but so far, research has mainly focused on people of European ancestry, which the researchers say is a major shortcoming, especially for such a complex condition as depression.

The new paper involved multiple genetic research methods, including genome-wide association studies, a meta-analysis of previously published data, and a transcriptome-wide association study.

The international research team reviewed genetic data from 21 study cohorts from several countries and included nearly one million study participants of African, East Asian, South Asian, and Hispanic/Latin American descent, including 88,316 people with major depression.

The study has made major advances in identifying genes that are linked to the risk of depression, both for newly identified links and by strengthening prior evidence, and showcases some genes with potential implications for drug development, such as NDUFAF3.

The protein that NDUFAF3 encodes has been implicated previously in mood instability, and it is targeted by metformin, the first-line drug for treating type 2 diabetes. Animal studies of metformin have suggested a possible link with reduced depression and anxiety, so this latest finding further suggests that additional research into metformin and depression may be warranted.

Other genes identified in the study may have biologically plausible links with depression, such as a gene linked to a neurotransmitter involved in goal-directed behavior and genes encoding a type of protein previously linked with multiple neurological conditions.

Surprisingly, the researchers found less overlap in the genetic hits for depression across ancestry groups than expected, at about 30% (based on a new method developed by the research team to gauge the degree to which a genetic association found in one ancestry group is applicable to another ancestry group), which is less overlap than previously found for other traits and diseases.

Therefore, it is even more important to study depression in diverse samples because some of the findings might be ancestry-specific.

Lead author Professor Karoline Kuchenbaecker (UCL Psychiatry and UCL Genetics Institute) said, “Here we show beyond doubt that our understanding of such complex diseases as depression will remain incomplete until we overcome the Eurocentric bias in genetics research and look for causes in diverse people across the world.”

“Many genes previously found to be linked to the risk of depression might only actually affect depression risk in people of European origin, so in order for genetic research to contribute to new drugs that can help people of all ancestries, it is vital that our genetic datasets are suitably diverse.”

Professor Kuchenbaecker added, “This is a first-stage discovery effort, so more work will be needed to confirm these new targets, but finding them in the first place has been a huge and vital challenge, especially for a disorder where new medications are so urgently needed.”

 https://neurosciencenews.com/depression-genetics-25446/

New Neural Implant Unlocks Deep Brain Activity

Summary: Researchers create a transparent graphene-based neural implant offering high-resolution brain activity data from the surface. The implant’s dense array of tiny graphene electrodes enables simultaneous recording of electrical and calcium activity in deep brain layers.

This innovation overcomes previous implant limitations and offers insights for neuroscientific studies. The transparent design allows optical imaging alongside electrical recording, revolutionizing neuroscience research.

Key Facts:

1.      UC San Diego develops a transparent graphene-based neural implant with high-density electrodes.

2.      The implant records electrical and calcium activity, overcoming previous implant limitations.

3.      Researchers aim to scale up production and facilitate widespread adoption for neuroscience studies.

Source: UCSD

Researchers at the University of California San Diego have developed a neural implant that provides information about activity deep inside the brain while sitting on its surface.

The implant is made up of a thin, transparent and flexible polymer strip that is packed with a dense array of graphene electrodes.

The technology, tested in transgenic mice, brings the researchers a step closer to building a minimally invasive brain-computer interface (BCI) that provides high-resolution data about deep neural activity by using recordings from the brain surface.

The work was published on Jan. 11 in Nature Nanotechnology.

“We are expanding the spatial reach of neural recordings with this technology,” said study senior author Duygu Kuzum, a professor in the Department of Electrical and Computer Engineering at the UC San Diego Jacobs School of Engineering.

“Even though our implant resides on the brain’s surface, its design goes beyond the limits of physical sensing in that it can infer neural activity from deeper layers.”

This work overcomes the limitations of current neural implant technologies. Existing surface arrays, for example, are minimally invasive, but they lack the ability to capture information beyond the brain’s outer layers.

In contrast, electrode arrays with thin needles that penetrate the brain are capable of probing deeper layers, but they often lead to inflammation and scarring, compromising signal quality over time.

The new neural implant developed at UC San Diego offers the best of both worlds.

The implant is a thin, transparent and flexible polymer strip that conforms to the brain’s surface. The strip is embedded with a high-density array of tiny, circular graphene electrodes, each measuring 20 micrometers in diameter. Each electrode is connected by a micrometers-thin graphene wire to a circuit board.

In tests on transgenic mice, the implant enabled the researchers to capture high-resolution information about two types of neural activity–electrical activity and calcium activity–at the same time. When placed on the surface of the brain, the implant recorded electrical signals from neurons in the outer layers.

At the same time, the researchers used a two-photon microscope to shine laser light through the implant to image calcium spikes from neurons located as deep as 250 micrometers below the surface. The researchers found a correlation between surface electrical signals and calcium spikes in deeper layers.

This correlation enabled the researchers to use surface electrical signals to train neural networks to predict calcium activity—not only for large populations of neurons, but also individual neurons—at various depths.

“The neural network model is trained to learn the relationship between the surface electrical recordings and the calcium ion activity of the neurons at depth,” said Kuzum. “Once it learns that relationship, we can use the model to predict the depth activity from the surface.”

An advantage of being able to predict calcium activity from electrical signals is that it overcomes the limitations of imaging experiments. When imaging calcium spikes, the subject’s head must be fixed under a microscope. Also, these experiments can only last for an hour or two at a time.

“Since electrical recordings do not have these limitations, our technology makes it possible to conduct longer duration experiments in which the subject is free to move around and perform complex behavioral tasks,” said study co-first author Mehrdad Ramezani, an electrical and computer engineering Ph.D. student in Kuzum’s lab. “This can provide a more comprehensive understanding of neural activity in dynamic, real-world scenarios.”

Designing and fabricating the neural implant

The technology owes its success to several innovative design features: transparency and high electrode density combined with machine learning methods. 

“This new generation of transparent graphene electrodes embedded at high density enables us to sample neural activity with higher spatial resolution,” said Kuzum.

“As a result, the quality of signals improves significantly. What makes this technology even more remarkable is the integration of machine learning methods, which make it possible to predict deep neural activity from surface signals.”

This study was a collaborative effort among multiple research groups at UC San Diego. The team, led by Kuzum, one of the world leaders in developing multimodal neural interfaces, includes nanoengineering professor Ertugrul Cubukcu, who specializes in advanced micro- and nanofabrication techniques for graphene materials; electrical and computer engineering professor Vikash Gilja, whose lab integrates domain-specific knowledge from the fields of basic neuroscience, signal processing, and machine learning to decode neural signals; and neurobiology and neurosciences professor Takaki Komiyama, whose lab focuses on investigating neural circuit mechanisms that underlie flexible behaviors.

Transparency is one of the key features of this neural implant. Traditional implants use opaque metal materials for their electrodes and wires, which block the view of neurons beneath the electrodes during imaging experiments. In contrast, an implant made using graphene is transparent, which provides a completely clear field of view for a microscope during imaging experiments.

“Seamless integration of recording electrical signals and optical imaging of the neural activity at the same time is only possible with this technology,” said Kuzum.

“Being able to conduct both experiments at the same time gives us more relevant data because we can see how the imaging experiments are time-coupled to the electrical recordings.”

To make the implant completely transparent, the researchers used super thin, long graphene wires instead of traditional metal wires to connect the electrodes to the circuit board. However, fabricating a single layer of graphene as a thin, long wire is challenging because any defect will render the wire nonfunctional, explained Ramezani.

“There may be a gap in the graphene wire that prevents the electrical signal from flowing through, so you basically end up with a broken wire.”

The researchers addressed this issue using a clever technique. Instead of fabricating the wires as a single layer of graphene, they fabricated them as a double layer doped with nitric acid in the middle.

“By having two layers of graphene on top of one another, there’s a good chance that defects in one layer will be masked by the other layer, ensuring the creation of fully functional, thin and long graphene wires with improved conductivity,” said Ramezani.

According to the researchers, this study demonstrates the most densely packed transparent electrode array on a surface-sitting neural implant to date. Achieving high density required fabricating extremely small graphene electrodes.

This presented a considerable challenge, as shrinking graphene electrodes in size increases their impedance—this hinders the flow of electrical current needed for recording neural activity.

To overcome this obstacle, the researchers used a microfabrication technique developed by Kuzum’s lab that involves depositing platinum nanoparticles onto the graphene electrodes. This approach significantly improved electron flow through the electrodes while keeping them tiny and transparent.

Next steps

The team will next focus on testing the technology in different animal models, with the ultimate goal of human translation in the future.

Kuzum’s research group is also dedicated to using the technology to advance fundamental neuroscience research. In that spirit, they are sharing the technology with labs across the U.S. and Europe, contributing to diverse studies ranging from understanding how vascular activity is coupled to electrical activity in the brain to investigating how place cells in the brain are so efficient at creating spatial memory.

To make this technology more widely available, Kuzum’s team has applied for a National Institutes of Health (NIH) grant to fund efforts in scaling up production and facilitating its adoption by researchers worldwide.

“This technology can be used for so many different fundamental neuroscience investigations, and we are eager to do our part to accelerate progress in better understanding the human brain,” said Kuzum.

Funding: This research was supported by the Office of Naval Research (N000142012405, N000142312163 and N000141912545), the National Science Foundation (ECCS-2024776, ECCS-1752241 and ECCS-1734940) and the National Institutes of Health (R21 EY029466, R21 EB026180, DP2 EB030992, R01 NS091010A, 

https://neurosciencenews.com/deep-brain-neural-implant-25444/

 

 

The Science of Sleep: Brain’s Reset Mechanism Revealed

Summary: Sleep has long been a mystery, but a new study offers fresh insights. By tracking brain activity in sleeping rats, they propose that sleep’s primary function is to reset the brain’s computational state to achieve “criticality.” Criticality is a state that optimizes thinking and information processing by balancing order and chaos in neural activity.

This study challenges the notion that sleep merely replenishes chemicals and presents a compelling theory for the fundamental role of sleep in our lives.

Key Facts:

1.      Sleep is not just about reducing sleepiness; it serves the crucial purpose of restoring the brain’s optimal computational state.

2.      Criticality, a state balancing order and chaos, maximizes the encoding and processing of information in the brain.

3.      This multidisciplinary study bridges physics and biology, highlighting the complex, wondrous nature of the brain’s neural networks.

Source: WUSTL

Sleep is a fundamental need, just like food or water. “You’ll die without it,” said Keith Hengen, an assistant professor of biology at Washington University in St. Louis. But what does sleep actually accomplish? For years, the best researchers could say is that sleep reduces sleepiness — hardly a satisfying explanation for a basic requirement of life.

But by melding concepts from the fields of physics and biology, Hengen and a team of Arts & Sciences researchers have constructed a theory that could explain both the meaning of sleep and the complexity of the brain.

In the new paper, the team provides the first direct evidence that sleep restores the computational power of the brain. Credit: Neuroscience News

As reported in a new study published in Nature Neuroscience, they tracked the brain activity of sleeping rats to make the case that the brain needs to regularly reset its operating system to reach “criticality,” a state that optimizes thinking and processing.

“The brain is like a biological computer,” Hengen said. “Memory and experience during waking change the code bit by bit, slowly pulling the larger system away from an ideal state. The central purpose of sleep is to restore an optimal computational state.”

Co-authors of the paper include Ralf Wessel, a professor of physics; Yifan Xu, a graduate student in biology studying neuroscience; and Aidan Schneider, a graduate student in the Computational & Systems Biology program, all in Arts & Sciences.

Wessel said physicists have been thinking about criticality for more than 30 years, but they never dreamed the work would have implications for sleep. In the world of physics, criticality describes a complex system that exists at the tipping point between order and chaos.

“At one extreme, everything is completely regular. At the other extreme, everything is random,” Wessel said.

Criticality maximizes the encoding and processing of information, making it an attractive candidate for a general principle of neurobiology. In a 2019 study, Hengen and Wessel established that the brain actively works to maintain criticality.

In the new paper, the team provides the first direct evidence that sleep restores the computational power of the brain. It’s a radical departure from the long-held assumption that sleep must somehow replenish mysterious and unknown chemicals depleted during waking hours.

After their 2019 paper, Hengen and Wessel theorized that learning, thinking and being awake must push the brain away from criticality and that sleep is perfectly positioned to reset the system.

“We realized this would be a really cool and intuitive explanation for the core purpose of sleep,” Hengen said. “Sleep is a systems-level solution to a systems-level problem.”

Brain cascades

To test their theory on the role of criticality in sleep, the researchers tracked the spiking of many neurons in the brains of young rats as they went about their normal sleeping and waking routines.

“You can follow these little cascades of activity through the neural network,” Hengen said. These cascades, also called neural avalanches, reflect how information flows through the brain, he said.

“At criticality, avalanches of all sizes and durations can occur. Away from criticality, the system becomes biased toward only small avalanches or only large avalanches. This is analogous to writing a book and only being able to use short or long words.”

As predicted, avalanches of all sizes occurred in the rats that had just woken up from restorative sleep. Across the course of waking, the cascades started to shift toward smaller and smaller sizes. The researchers found they could predict when rats were about to go to sleep or wake up by tracking the distribution of avalanches. When cascade sizes were reduced to a certain point, sleep wasn’t far away.

“The results suggest that every waking moment pushes relevant brain circuits away from criticality, and sleep helps the brain reset,” Hengen said.

Physics meets biology

When physicists first developed the concept of criticality in the late 1980s, they were looking at piles of sand on a checkerboard-like grid, a scenario seemingly far removed from brains. But those sand piles provided an important insight, Wessel said. If thousands of grains are dropped on the grid following simple rules, the piles quickly reach a critical state where interesting things start happening.

Avalanches both large and small can start without warning, and piles in one square start spilling into the others. “The whole system organizes itself into something extremely complex,” he said.

The neural avalanches taking place in the brain are much like the avalanches of sand on a grid, Wessel said. In each case, the cascades are the hallmark of a system that has reached its most complex state.

According to Hengen, every neuron is like an individual grain of sand following very basic rules. Neurons are essentially on/off switches that decide whether or not to fire based on straightforward inputs. If billions of neurons can reach criticality — the sweet spot between too much order and too much chaos — they can work together to form something complex and wondrous. “Criticality maximizes a bunch of features that sound very desirable for a brain,” Hengen said.

The new study was a multidisciplinary effort. Hengen, Xu and Schneider designed the experiments and provided the data, while Wessel joined the team to implement the mathematical equations necessary to understand sleep in the framework of criticality. “It’s a beautiful collaboration between physics and biology,” Wessel said.

https://neurosciencenews.com

 

About this sleep research news

Author: Talia Ogliore
Source: 
WUSTL
Contact: Talia Ogliore – WUSTL
Image: The image is credited to Neuroscience News

Original Research: Closed access.
Sleep restores an optimal computational regime in cortical networks” by Keith Hengen et al. Nature Neuroscience


Abstract

Sleep restores an optimal computational regime in cortical networks

Sleep is assumed to subserve homeostatic processes in the brain; however, the set point around which sleep tunes circuit computations is unknown. Slow-wave activity (SWA) is commonly used to reflect the homeostatic aspect of sleep; although it can indicate sleep pressure, it does not explain why animals need sleep.

This study aimed to assess whether criticality may be the computational set point of sleep. By recording cortical neuron activity continuously for 10–14 d in freely behaving rats, we show that normal waking experience progressively disrupts criticality and that sleep functions to restore critical dynamics.

Criticality is perturbed in a context-dependent manner, and waking experience is causal in driving these effects. The degree of deviation from criticality predicts future sleep/wake behavior more accurately than SWA, behavioral history or other neural measures.

Our results demonstrate that perturbation and recovery of criticality is a network homeostatic mechanism consistent with the core, restorative function of sleep.

 

Early Riser? Anorexia Nervosa Linked to Morning Chronotype

Summary: Individuals with anorexia nervosa tend to be early risers, in contrast to many other mental disorders often associated with evening chronotypes. The study also finds a connection between anorexia nervosa and increased risk of insomnia.

Using genetic analysis, the researchers discovered a two-way association between genes related to anorexia nervosa and morning chronotype. These findings suggest a novel perspective on anorexia nervosa and could pave the way for circadian-based therapies for prevention and treatment.

Key Facts:

1.      Anorexia nervosa is associated with being an early riser, unlike other disorders often linked to evening chronotypes.

2.      The study used Mendelian Randomization to examine the relationship between anorexia nervosa, circadian genes, and sleep traits.

3.      This research could lead to new prevention and treatment strategies for anorexia nervosa, which has a high mortality rate.

Source: Mass General

New research indicates that the eating disorder anorexia nervosa is associated with being an early riser, unlike many other disorders that tend to be evening-based such as depression, binge eating disorder and schizophrenia.

The study, which is published in JAMA Network Open and led by investigators at Massachusetts General Hospital (MGH), in collaboration with University College London and the University of the Republic in Uruguay, also revealed a link between anorexia nervosa and insomnia risk.

Previous research has suggested a possible connection between eating disorders and the body’s internal clock, or circadian clock, which controls a wide range of biological functions such as sleep and affects nearly every organ in the body.

This study aimed to further understand this relationship by assessing genes associated with anorexia nervosa, the circadian clock and several sleep traits including insomnia.

The investigators used a statistical method called Mendelian Randomization to see how genes that are associated with a certain trait affect other traits of interest. For example, examining the sleep patterns of people with genetic differences that makes them more likely to have anorexia nervosa, this provides evidence on the relationship between anorexia nervosa and sleep.

They found a two-way association between genes associated with anorexia nervosa and genes associated with morning chronotype (waking early and going to bed early).

In other words, the findings suggest that being an early riser could increase the risk for having anorexia nervosa, and having anorexia nervosa could lead to an earlier wake time. The team also found an association between anorexia nervosa and insomnia.

When they further assessed the insomnia connection using the Mass General Brigham Biobank by developing a “genetic risk score” for anorexia nervosa, the scientists found that the genetic risk score was indeed associated with higher insomnia risk.

“Our findings implicate anorexia nervosa as a morning disorder in contrast to most other evening-based psychiatric diseases and support the association between anorexia nervosa and insomnia as seen in earlier studies,” says senior author Hassan S Dashti, PhD, RD, an assistant investigator in the Department of Anesthesia, Critical Care and Pain Medicine at MGH and an assistant professor of anesthesia at Harvard Medical School.

Treatments for anorexia nervosa are limited and current treatments have relapse rates of up to 52%. In addition, the cause of the disease is still unclear.

With anorexia nervosa having the second highest mortality rate of psychiatric diseases, more research is desperately needed into new prevention strategies and treatments.

“The clinical implications of our new findings are currently unclear; however, our results could direct future investigations into circadian-based therapies for anorexia nervosa prevention and treatment,” says Hannah Wilcox, lead author of the study and researcher at MGH.

Additional authors include Valentina Paz, MSc, Richa Saxena, PhD, John W. Winkelman, MD, PhD, and Victoria Garfield, PhD.

Funding: This research was supported by the National Institutes of Health.

 

Complex Sentences Fire Up Brain’s Language Centers

Summary: Researchers discovered that sentences with unusual grammar or unexpected meaning activate the brain’s language processing centers more than straightforward or nonsensical sentences. They used an artificial language network to identify sentences that drove and suppressed brain activity, finding that linguistic complexity and surprisal were key factors.

Sentences requiring cognitive effort to decipher, such as those with unusual grammar or meaning, evoked the highest brain responses. The study offers insights into how the brain processes language and has potential applications in understanding higher-level cognition.

Key Facts:

1.      MIT researchers used an artificial language network and functional MRI to study the brain’s language processing regions’ responses to different sentences.

2.      Sentences with linguistic complexity and surprisal, requiring cognitive effort, activated the language centers more strongly.

3.      The study’s findings can help improve our understanding of how the brain processes language and may have broader implications for cognitive research.

Source: MIT

With help from an artificial language network, MIT neuroscientists have discovered what kind of sentences are most likely to fire up the brain’s key language processing centers.

The new study reveals that sentences that are more complex, either because of unusual grammar or unexpected meaning, generate stronger responses in these language processing centers. Sentences that are very straightforward barely engage these regions, and nonsensical sequences of words don’t do much for them either.

For example, the researchers found this brain network was most active when reading unusual sentences such as “Buy sell signals remains a particular,” taken from a publicly available language dataset called C4. However, it went quiet when reading something very straightforward, such as “We were sitting on the couch.”

“The input has to be language-like enough to engage the system,” says Evelina Fedorenko, Associate Professor of Neuroscience at MIT and a member of MIT’s McGovern Institute for Brain Research.

“And then within that space, if things are really easy to process, then you don’t have much of a response. But if things get difficult, or surprising, if there’s an unusual construction or an unusual set of words that you’re maybe not very familiar with, then the network has to work harder.”

Fedorenko is the senior author of the study, which appears today in Nature Human Behavior. MIT graduate student Greta Tuckute is the lead author of the paper.

Processing language

In this study, the researchers focused on language-processing regions found in the left hemisphere of the brain, which includes Broca’s area as well as other parts of the left frontal and temporal lobes of the brain.

“This language network is highly selective to language, but it’s been harder to actually figure out what is going on in these language regions,” Tuckute says. “We wanted to discover what kinds of sentences, what kinds of linguistic input, drive the left hemisphere language network.”

The researchers began by compiling a set of 1,000 sentences taken from a wide variety of sources — fiction, transcriptions of spoken words, web text, and scientific articles, among many others.

Five human participants read each of the sentences while the researchers measured their language network activity using functional magnetic resonance imaging (fMRI). The researchers then fed those same 1,000 sentences into a large language model — a model similar to ChatGPT, which learns to generate and understand language from predicting the next word in huge amounts of text — and measured the activation patterns of the model in response to each sentence.

Once they had all of those data, the researchers trained a mapping model, known as an “encoding model,” which relates the activation patterns seen in the human brain with those observed in the artificial language model.

Once trained, the model could predict how the human language network would respond to any new sentence based on how the artificial language network responded to these 1,000 sentences.

The researchers then used the encoding model to identify 500 new sentences that would generate maximal activity in the human brain (the “drive” sentences), as well as sentences that would elicit minimal activity in the brain’s language network (the “suppress” sentences).

In a group of three new human participants, the researchers found these new sentences did indeed drive and suppress brain activity as predicted.

“This ‘closed-loop’ modulation of brain activity during language processing is novel,” Tuckute says. “Our study shows that the model we’re using (that maps between language-model activations and brain responses) is accurate enough to do this. This is the first demonstration of this approach in brain areas implicated in higher-level cognition, such as the language network.”

Linguistic complexity

To figure out what made certain sentences drive activity more than others, the researchers analyzed the sentences based on 11 different linguistic properties, including grammaticality, plausibility, emotional valence (positive or negative), and how easy it is to visualize the sentence content.

For each of those properties, the researchers asked participants from crowd-sourcing platforms to rate the sentences. They also used a computational technique to quantify each sentence’s “surprisal,” or how uncommon it is compared to other sentences.

This analysis revealed that sentences with higher surprisal generate higher responses in the brain. This is consistent with previous studies showing people have more difficulty processing sentences with higher surprisal, the researchers say.

Another linguistic property that correlated with the language network’s responses was linguistic complexity, which is measured by how much a sentence adheres to the rules of English grammar and how plausible it is, meaning how much sense the content makes, apart from the grammar.

Sentences at either end of the spectrum — either extremely simple, or so complex that they make no sense at all — evoked very little activation in the language network. The largest responses came from sentences that make some sense but require work to figure them out, such as “Jiffy Lube of — of therapies, yes,” which came from the Corpus of Contemporary American English dataset.

“We found that the sentences that elicit the highest brain response have a weird grammatical thing and/or a weird meaning,” Fedorenko says. “There’s something slightly unusual about these sentences.”

The researchers now plan to see if they can extend these findings in speakers of languages other than English. They also hope to explore what type of stimuli may activate language processing regions in the brain’s right hemisphere.

Funding:

The research was funded by an Amazon Fellowship from the Science Hub, an International Doctoral Fellowship from the American Association of University Women, the MIT-IBM Watson AI Lab, the National Institutes of Health, the McGovern Institute, the Simons Center for the Social Brain, and MIT’s Department of Brain and Cognitive Sciences.

https://www.oxfordlearnersdictionaries.com/definition/american_english/a_1?q=a

 

Poor Sleep Quality in Middle Age Linked to Future Cognitive Decline

 

Summary: New research suggests that disrupted sleep in one’s 30s and 40s may lead to memory and cognitive problems a decade later. While the study doesn’t establish a causal relationship, it highlights an association between sleep quality and cognitive health.

Researchers followed 526 participants for 11 years and found that those with the most disrupted sleep had over twice the odds of experiencing poor cognitive performance later in life. This emphasizes the importance of addressing sleep quality for long-term cognitive health.

Key Facts:

1.      Disrupted sleep in middle age can increase the risk of cognitive decline later in life.

2.      Sleep quality, rather than quantity, plays a significant role in cognitive health.

3.      The study highlights the need for further research to understand the connection between sleep and cognition at different life stages.

Source: AAN

Five Biological Variants of Alzheimer’s Discovered

Summary: Researchers have identified five biological variants of Alzheimer’s disease through cerebrospinal fluid analysis, shedding new light on the complexity of the condition. These variants differ in amyloid production, blood-brain barrier integrity, nerve cell growth, protein synthesis, and immune system functioning.

This breakthrough highlights the importance of personalized medicine in Alzheimer’s treatment, as a drug that works for one variant may be ineffective or even harmful for another. The study paves the way for targeted therapies tailored to specific Alzheimer’s variants, potentially improving treatment outcomes.

Key Facts:

1.      Alzheimer’s disease has five distinct biological variants, affecting amyloid production, blood-brain barrier integrity, and more.

2.      Tailored treatments based on these variants may enhance the effectiveness of Alzheimer’s drugs.

3.      Personalized medicine could lead to improved treatment outcomes and reduced risk of side effects for Alzheimer’s patients.

Source: University of Amsterdam

Dutch scientists have discovered five biological variants of Alzheimer’s disease, which may require different treatment. As a result, previously tested drugs may incorrectly appear to be ineffective or only minimally effective.

This is the conclusion of researcher Betty Tijms and colleagues from Alzheimer Center Amsterdam, Amsterdam UMC and Maastricht University.

The research results will be published on 9 January in Nature Aging.  

In those with Alzheimer’s disease, the amyloid and tau protein clump in the brain. In addition to these clumps, other biological processes such as inflammation and nerve cells growth are also involved. Using new techniques, the researchers have been able to measure these other processes in the cerebrospinal fluid of patients with amyloid and tau clumps. 

Betty Tijms and Pieter Jelle Visser examined 1058 proteins in the cerebrospinal fluid of 419 people with Alzheimer’s disease. They found that there are five biological variants within this group. The first variant is characterized by increased amyloid production. In a second type, the blood-brain barrier is disrupted and there is a reduced amyloid production and less nerve cells growth.

Furthermore, the variants differ in the degree of protein synthesis, the functioning of the immune system, and the functioning of the organ that produces cerebrospinal fluid. Patients with different Alzheimer’s variants also showed differences in other aspects of the disease. For example, the researchers found a faster course of the disease in certain subgroups. 

The findings are of great importance for drug research. It means that a drug could only work in one variant of Alzheimer’s disease. For example, medication that inhibits amyloid production may work in the variant with increased amyloid production but may be harmful in the variant with decreased amyloid production. It is also possible that patients with one variant have a higher risk of side effects, while that risk is much lower with other variants.

The next step for the research team is to show that the Alzheimer’s variants do indeed react differently to medicines, so that we can treat everyone with appropriate medicines in the future. 

https://neurosciencenews.com/alzheimers-biological-variants-25441/

People who have more disrupted sleep in their 30s and 40s may be more likely to have memory and thinking problems a decade later, according to new research published in the January 3, 2024, online issue of Neurology.

The study does not prove that sleep quality causes cognitive decline. It only shows an association.

“Given that signs of Alzheimer’s disease start to accumulate in the brain several decades before symptoms begin, understanding the connection between sleep and cognition earlier in life is critical for understanding the role of sleep problems as a risk factor for the disease,” said study author Yue Leng, PhD, of the University of California, San Francisco.

“Our findings indicate that the quality rather than the quantity of sleep matters most for cognitive health in middle age.”

The study involved 526 people with an average age of 40. They were followed for 11 years.

Researchers looked at participants’ sleep duration and quality. Participants wore a wrist activity monitor for three consecutive days on two occasions approximately one year apart to calculate their averages. Participants slept for an average of six hours.

Participants also reported bedtimes and wake times in a sleep diary and completed a sleep quality survey with scores ranging from zero to 21, with higher scores indicating poorer sleep quality. A total of 239 people, or 46%, reported poor sleep with a score greater than five.

Participants also completed a series of memory and thinking tests.

Researchers also looked at sleep fragmentation, which measures repetitive short interruptions of sleep. They looked at both the percentage of time spent moving and the percentage of time spent not moving for one minute or less during sleep. After adding these two percentages together, researchers found that participants had an average sleep fragmentation of 19%.

Researchers then divided participants into three groups based on their sleep fragmentation score.

Of the 175 people with the most disrupted sleep, 44 had poor cognitive performance 10 years later, compared to 10 of the 176 people with the least disrupted sleep.

After adjusting for age, gender, race, and education, people who had the most disrupted sleep had more than twice the odds of having poor cognitive performance when compared to those with the least disrupted sleep. There was no difference in cognitive performance at midlife for those in the middle group compared to the group with the least disrupted sleep.

“More research is needed to assess the link between sleep disturbances and cognition at different stages of life and to identify if critical life periods exist when sleep is more strongly associated with cognition,” Leng said. “Future studies could open up new opportunities for the prevention of Alzheimer’s disease later in life.”

The amount of time people slept and their own reports of the quality of their sleep were not associated with cognition in middle age.

A limitation of the study was that due to the small sample size, researchers were unable to fully investigate potential race or gender differences.

Funding: The study was funded by the National Institute on Aging and the National Heart, Lung, and Blood Institute.

 

https://neurosciencenews.com/sleeep-aging-cognition-25410/

 

 

 

Cellular Messengers of Neural Development Identified

Summary: Researchers unveil the role of cytonemes, thin cell projections, in neural development. These hair-like structures facilitate direct signal transport across cells, impacting nervous system development.

By visualizing cytonemes’ function, the researchers discovered their role in establishing signaling gradients and the transport of critical molecules like sonic hedgehog during mammalian tissue development. Compromised cytoneme function resulted in neurological defects in mouse models.

This study sheds light on previously elusive mechanisms in developmental biology, opening new avenues for research in this field.

Key Facts:

1.      Cytonemes are thin projections on cells that act as direct pathways for signal transport over long distances.

2.      The study reveals cytonemes’ role in creating signaling gradients and transporting essential molecules during neural development.

3.      Compromised cytoneme function leads to developmental defects in the neural tube, highlighting their significance in mammalian tissue development.

Source: St. Jude Children’s Research Hospital

St. Jude Children’s Research Hospital scientists found that cytonemes (thin, long, hair-like projections on cells) are important during neural development. Cytonemes connect cells communicating across vast distances but are difficult to capture with microscopy in developing vertebrate tissues.

The researchers are the first to find a way to visualize how cytonemes transport signaling molecules during mammalian nervous system development.

The findings were published in Cell.

Using their new methods, the scientists captured images of how cytonemes act as an “express” system that can skip over intervening cells to directly deliver signals to more distant ones, similar to an express subway that only stops at major stations. Credit: Neuroscience News

“We showed cytonemes are a direct express route for signal transport,” said corresponding author Stacey Ogden, PhD, St. Jude Department of Cell and Molecular Biology.

“Cells need to communicate with each other during development and tissue homeostasis and be able to reach more than just their neighbors. We’ve identified one way that signals are loaded into cytonemes for transport to responding cell populations and demonstrated that tissue patterning does not happen properly when this mode of signal dispersion is compromised.” 

Express signal delivery sets up the nervous system for success 

Researchers in Ogden’s lab were the first to visualize mammalian cytonemes in the developing nervous system by combining modern microscopy techniques with optimized sample preparations.  

“For a long time, visualizing these structures in developing mammalian tissue has been challenging,” Ogden said. “But we’ve finally found a way.” 

Using their new methods, the scientists captured images of how cytonemes act as an “express” system that can skip over intervening cells to directly deliver signals to more distant ones, similar to an express subway that only stops at major stations.

One of the major stations is the notochord, which produces a signal that plays a crucial role in organizing the developing spinal cord. Ogden’s team captured images of the transport process happening in the cytonemes originating from the notochord. 

When the researchers prevented signaling proteins from entering cytonemes, neural development was disrupted in mouse models, causing major neurological defects.  

“This is the first demonstration of these cytoneme-based transport processes occurring during the development of a complex mammalian tissue such as the neural tube,” Ogden said. “Then we showed that when we reduce cytoneme numbers or decrease the ability of cells to load signaling proteins into these structures, we get developmental defects.” 

Cytoneme transport helps establish the gradient 

Mammalian development is a carefully guided process that must be coordinated for all organs and tissues to form correctly. One way cells know when to adopt a specific fate is by responding to distinct thresholds of signaling proteins called morphogens.

Cells will respond differently to these signals across a signaling gradient, taking on different characteristics in response to high and low concentrations of a particular morphogen. A good gradient is necessary for development; a bad gradient can spell disaster.  

Despite their importance, how these patterns of morphogens are created across fields of organizing cells has remained a mystery. Simple diffusion can explain some, but not all, of these gradients.

The neurological deficits created when the scientists blocked signals from entering cytonemes provide evidence that supports a key role for cytoneme signaling during morphogen patterning.  

“These deficits are really the first direct evidence that cytoneme-based signaling plays a key role during neural tube patterning,” Ogden said.  

Transporting ‘sonic hedgehog’ through cytonemes 

The St. Jude group clarified one way that a gradient of the sonic hedgehog morphogen is formed in the neural tube. Sonic hedgehog was already known as a critical signaling molecule in neural development, but its route to reach its target cells has been difficult to ascertain.

The study identified cytonemes as key contributors to a solution that creates the sonic hedgehog signaling gradient. Correspondingly, when sonic hedgehog could not be loaded in cytonemes, its signaling function was compromised.  

“In the morphogen signaling research field, we’ve always wanted to know how a signal gets from one population of cells to spread across a receiving cell population to make a gradient,” Odgen said.

“It’s really exciting to show that cells that are producing morphogen signals are playing an active role in getting them to where they need to go through cytonemes. The signaling cell is not only making the morphogen, but it’s also helping to physically deliver the signal.” 

What remains unclear is how widespread cytoneme express transport of signaling proteins is in development.  

“Here, we’ve used sonic hedgehog as a model,” Ogden said. “But we also have evidence that these structures may be important for transporting other signals that are crucial during neural tube development. Now that we’ve developed a system to visualize these cytonemes, we can begin to uncover the true breadth of their function.” 

Authors and funding 

The study’s first author is Eric Hall of St. Jude. The study’s other authors are Miriam Dillard, Elizabeth Cleverdon, Yan Zhang, Christina Daly, Shariq Ansari, Randall Wakefield, Daniel Stewart, Shondra Pruett-Miller, Alfonso Lavado, Alex Carisey, Amanda Johnson, Yong-Dong Wang, Emma Selner, Michael Tanes, Young Sang Ryu, Camenzind Robinson and Jeffrey Steinberg, all of St. Jude. 

Funding: The study was supported by grants from the National Institutes of Health (R35GM122546 and F31HD110256), National Cancer Institute (P30CA021765 St. Jude Cancer Center Support Grant) and ALSAC, the fundraising and awareness organization of St. Jude. 

https://neurosciencenews.com/cytonemes-neurodevelopment-25407/

 

 

https://www.pinterest.com/ramzanctg60/early-to-bed-early-to-rise/

Global Genetic Insights into Problematic Alcohol Use

Summary: A new study uncovers a shared genetic basis for problematic alcohol use (PAU) across diverse ancestries. This research broadens our understanding of PAU’s genetic architecture and its consequences, including its role as a major cause of health problems and death.

The study identifies 110 risk gene regions and offers potential drug targets for future treatments. Genome-wide data may pave the way for personalized risk assessments and innovative interventions.

Key Facts:

1.      A study involving over 1 million individuals from diverse genetic backgrounds reveals shared genetic architecture for problematic alcohol use.

2.      Researchers identified 110 risk gene regions, providing insights into the biology of PAU and potential pharmacological targets.

3.      The study suggests existing medications as potential treatments for PAU and explores genetic correlations with other mental and neurological disorders.

Source: Yale

A study led by VA Connecticut Healthcare Center/Yale researchers reveals ancestries around the world possess a shared genetic architecture for problematic alcohol use (PAU)—habitual heavy drinking, accompanied by harmful consequences.

The findings, published in Nature Medicine, could help scientists understand the genetic basis of PAU, a major cause of health problems in many age groups. It is a leading cause of death in those it afflicts.

This study is the largest to date for PAU—it identified many new risk genes and uncovered a large amount of new biology. With a better understanding of PAU biology, scientists will have new possibilities in developing treatments.

Hang Zhou, Ph.D., assistant professor of psychiatry and of biomedical informatics & data science at Yale School of Medicine and VA Connecticut, and first author of the study, said, “Research with the primary focus on understanding the molecular mechanism underlying PAU and identification of gene targets for potential pharmacological studies is extremely important for future treatments and could help mitigate the consequences of excessive alcohol use.”

Researchers studied more than 1 million people with PAU and included as many genetic ancestral groups as possible, including people with European, African, Latin American, East Asian, and South Asian ancestries.

The Million Veteran Program (MVP) was a major source of data for this study—MVP data were combined with data from many other sources to create the analyses.

Compared to previous research, this work broadened the findings and demonstrated that the genetic architecture of PAU is substantially shared across these populations. There are genetic differences in different populations for PAU, but the similarities are greater. Cross-ancestry information allowed the researchers to improve the power of gene discovery.

“By leveraging the multi-ancestry information, we identified 110 gene regions and had an improved fine-mapping of the potential causal variants in each region,” Zhou said.

The researchers also used various methods to prioritize multiple genes with convergent evidence linking association to PAU with brain biology through gene expression (transcriptional-wide association study in 13 brain tissues) and chromatin interaction analyses in the brain. This work will provide valuable resources and targets for future functional analyses and drug development.

Joel Gelernter, MD, Foundations Fund Professor of Psychiatry, and professor of genetics and of neuroscience at Yale School of Medicine and VA Connecticut, was the study’s senior author.

“One of the most important products of this research is the information provided about PAU risk across the entire genome,” Gelernter said.

“The resulting data allowed us to understand the biology of PAU better, suggesting some already-approved drugs that might become tools for treating PAU in the future, with additional research. The data we produced will be shared with the research community, and this will aid greatly in future research by other scientists.”

The drug-repurposing analyses identified several existing medications as potential treatments for PAU, which are described in the published article.

One of the outputs from this study is genome-wide association data, and this kind of information can be used to compute “polygenic risk scores,” or PRS, that can be used to estimate an individual’s genetic risk for PAU.

The researchers stressed that the PRS they computed is not yet ready for use in the clinic, but they also tested the association of the PRS for PAU with hundreds of medical traits in multiple biobanks including Vanderbilt University Medical Center’s Biobank, Mount Sinai’s BioMe, the Mass General Brigham Biobank, and Penn Medicine Biobank. This analysis identified genetic correlations between PAU and many other mental and neurological disorders.

 https://neurosciencenews.com/global-genetics-aud-25397/

 

 

 

MENTAL HEALTH | OPINION

Synaptic Transistor Mirrors Human Brain Function

Summary: Researchers developed a groundbreaking synaptic transistor inspired by the human brain. This device can simultaneously process and store information, mimicking the brain’s capacity for higher-level thinking.

Unlike previous brain-like computing devices, this transistor remains stable at room temperature, operates efficiently, consumes minimal energy, and retains stored information even when powered off, making it suitable for real-world applications.

The study presents a major step forward in creating AI systems with greater energy efficiency and advanced cognitive functions.

Key Facts:

1.      The synaptic transistor combines two atomically thin materials, bilayer graphene and hexagonal boron nitride, in a moiré pattern to achieve neuromorphic functionality.

2.      It recognizes patterns and demonstrates associative learning, a form of higher-level cognition, even with imperfect input.

3.      This technology represents a significant shift away from traditional transistor-based computing, aiming to improve energy efficiency and processing capabilities for AI and machine learning tasks.

Source: Northwestern University

Taking inspiration from the human brain, researchers have developed a new synaptic transistor capable of higher-level thinking.

Designed by researchers at Northwestern University, Boston College and the Massachusetts Institute of Technology (MIT), the device simultaneously processes and stores information just like the human brain. In new experiments, the researchers demonstrated that the transistor goes beyond simple machine-learning tasks to categorize data and is capable of performing associative learning.

Although previous studies have leveraged similar strategies to develop brain-like computing devices, those transistors cannot function outside cryogenic temperatures. The new device, by contrast, is stable at room temperatures. It also operates at fast speeds, consumes very little energy and retains stored information even when power is removed, making it ideal for real-world applications.

The study will be published on Wednesday (Dec. 20) in the journal Nature.

“The brain has a fundamentally different architecture than a digital computer,” said Northwestern’s Mark C. Hersam, who co-led the research.

“In a digital computer, data move back and forth between a microprocessor and memory, which consumes a lot of energy and creates a bottleneck when attempting to perform multiple tasks at the same time.

“On the other hand, in the brain, memory and information processing are co-located and fully integrated, resulting in orders of magnitude higher energy efficiency. Our synaptic transistor similarly achieves concurrent memory and information processing functionality to more faithfully mimic the brain.”

Hersam is the Walter P. Murphy Professor of Materials Science and Engineering at Northwestern’s McCormick School of Engineering. He also is chair of the department of materials science and engineering, director of the Materials Research Science and Engineering Center and member of the International Institute for Nanotechnology. Hersam co-led the research with Qiong Ma of Boston College and Pablo Jarillo-Herrero of MIT.

Recent advances in artificial intelligence (AI) have motivated researchers to develop computers that operate more like the human brain. Conventional, digital computing systems have separate processing and storage units, causing data-intensive tasks to devour large amounts of energy. 

With smart devices continuously collecting vast quantities of data, researchers are scrambling to uncover new ways to process it all without consuming an increasing amount of power. Currently, the memory resistor, or “memristor,” is the most well-developed technology that can perform combined processing and memory function. But memristors still suffer from energy costly switching.

“For several decades, the paradigm in electronics has been to build everything out of transistors and use the same silicon architecture,” Hersam said.

“Significant progress has been made by simply packing more and more transistors into integrated circuits. You cannot deny the success of that strategy, but it comes at the cost of high power consumption, especially in the current era of big data where digital computing is on track to overwhelm the grid. We have to rethink computing hardware, especially for AI and machine-learning tasks.”

To rethink this paradigm, Hersam and his team explored new advances in the physics of moiré patterns, a type of geometrical design that arises when two patterns are layered on top of one another.

When two-dimensional materials are stacked, new properties emerge that do not exist in one layer alone. And when those layers are twisted to form a moiré pattern, unprecedented tunability of electronic properties becomes possible.

For the new device, the researchers combined two different types of atomically thin materials: bilayer graphene and hexagonal boron nitride. When stacked and purposefully twisted, the materials formed a moiré pattern.

By rotating one layer relative to the other, the researchers could achieve different electronic properties in each graphene layer even though they are separated by only atomic-scale dimensions. With the right choice of twist, researchers harnessed moiré physics for neuromorphic functionality at room temperature.

“With twist as a new design parameter, the number of permutations is vast,” Hersam said. “Graphene and hexagonal boron nitride are very similar structurally but just different enough that you get exceptionally strong moiré effects.”

To test the transistor, Hersam and his team trained it to recognize similar — but not identical — patterns. Just earlier this month, Hersam introduced a new nanoelectronic device capable of analyzing and categorizing data in an energy-efficient manner, but his new synaptic transistor takes machine learning and AI one leap further.

“If AI is meant to mimic human thought, one of the lowest-level tasks would be to classify data, which is simply sorting into bins,” Hersam said. “Our goal is to advance AI technology in the direction of higher-level thinking. Real-world conditions are often more complicated than current AI algorithms can handle, so we tested our new devices under more complicated conditions to verify their advanced capabilities.”

First the researchers showed the device one pattern: 000 (three zeros in a row). Then, they asked the AI to identify similar patterns, such as 111 or 101. “If we trained it to detect 000 and then gave it 111 and 101, it knows 111 is more similar to 000 than 101,” Hersam explained. “000 and 111 are not exactly the same, but both are three digits in a row. Recognizing that similarity is a higher-level form of cognition known as associative learning.”

In experiments, the new synaptic transistor successfully recognized similar patterns, displaying its associative memory. Even when the researchers threw curveballs — like giving it incomplete patterns — it still successfully demonstrated associative learning.

“Current AI can be easy to confuse, which can cause major problems in certain contexts,” Hersam said. “Imagine if you are using a self-driving vehicle, and the weather conditions deteriorate. The vehicle might not be able to interpret the more complicated sensor data as well as a human driver could. But even when we gave our transistor imperfect input, it could still identify the correct response.”

Funding: The study, “Moiré synaptic transistor with room-temperature neuromorphic functionality,” was primarily supported by the National Science Foundation.

https://neurosciencenews.com/synaptic-transistor-ai-25402/

 

 

 

Why Just One Sleepless Night Makes People Emotionally Fragile

Sleep loss dampens brain regions that help manage our emotions

·         By Eti Ben Simon on August 15, 2023

 

 

When I was a graduate student, my colleagues and I studied how losing one night of sleep affects a person’s ability to manage their emotions. Once a week, typically on a Friday evening, I would stay up all night to monitor our participants and ensure they followed the protocol. At about noon the next day, we would all stumble out of the lab, exhausted and eager to get home and rest.

Two months into the experiment, I was in my car at a traffic light when a silly love song started playing on the radio. Suddenly, I was crying uncontrollably. I remember feeling surprised at my reaction. It then hit me that I was not just studying sleep deprivation—I had become part of the study. Weeks of missed sleep had taken their toll, and I was no longer in control of my emotions.

That research project, and many that have followed since, demonstrated a strong and intimate link between better sleep and emotional health. In healthy individuals, good-quality sleep is linked with a more positive mood—and it takes just one night of sleep deprivation to trigger a robust spike in anxiety and depression the following morning. Moreover people who suffer from chronic sleep disruption tend to experience daily events as more negative, making it hard to escape a gloomy mindset. Indeed, in a national sleep survey, 85 percent of Americans reported mood disruption when they were not able to get enough sleep.

Studies from our lab and others are now beginning to illuminate just how a lack of sleep frays the inner fabric of our mind. One of its many impacts is to disrupt the brain’s circuitry for regulating emotions.

[Read more about healthy sleep habits]

For decades, researchers and medical professionals considered sleep loss a by-product or symptom of another, more “primary” condition, such as depression or anxiety. In other words, first comes the anxiety, and then sleep loss follows. Today we know that this order can be reversed. In fact, sleep loss and anxiety, depression or other mental health conditions may feed into one another, creating a downward spiral that is exceedingly difficult to break.

Much evidence in this area comes from chronic sleeplessness or insomnia. People who suffer from insomnia are twice as likely to develop depression or anxiety later in life, compared with individuals who sleep well. For instance, a study that followed 1,500 individuals—some with insomnia and others without—found that chronic sleeplessness was associated with a three times greater increase in the onset of depression a year later and twice the increase in the onset of anxiety. Insomnia symptoms also raise the risk of developing post-traumatic stress disorder, track closely with suicidal behavior among at-risk individuals and often precede a mood episode in people with bipolar disorder. Moreover, even after adequate treatment for depression or anxiety, people who continue to suffer from sleep difficulties are at greater risk of relapse relative to those whose sleep improves. Understanding sleep’s role in this pattern could unlock new insights for helping to prevent and treat many emotional and mental disorders.

Older research already revealed that sleep loss can precede serious mental health symptoms in otherwise healthy individuals. In studies conducted mostly in the 1960s, volunteers who stayed awake for more than two nights reported difficulties forming thoughts, finding words and composing sentences. They suffered from hallucinations, such as seeing inanimate objects move or experiencing the sensation of another’s touch despite being alone. After three days without sleep, some participants became delusional and paranoid. They believed they were secret agents or that aliens were coming to get them. (If that sounds like a psychotic episode, that’s because it is.) After five days, several participants entered a state resembling a full-blown clinical psychosis and were unable to fully comprehend their circumstances.

In one study, volunteers from the U.S. military attempted to stay awake for more than four nights. A soldier described by his friends as quiet and reserved became extremely aggressive after three nights without sleep. He provoked fights and insisted he was on a secret mission for the president. Eventually he was forcibly restrained and dismissed from the experiment. Six others exhibited outbursts of violence and persistent hallucinations. In all cases, after sleeping for an entire day, the soldiers behaved normally again and had no recollection of the earlier mayhem. Given such destructive effects, studies of prolonged sleep loss are now considered unethical, but they still offer a powerful reminder of just how sleep-dependent our minds and mental health truly are.

Even with these startling results, scientists have been skeptical about the consequences of restless nights, particularly given that (fortunately) few of us endure such extreme deprivation. That’s where the newest wave of research comes in. In recent years, a neuroscientific explanation has emerged that is beginning to illuminate what it is about sleep, or the lack of it, that seems to have a direct link to our emotions.

Whenever we face a nerve-wracking or emotionally intense challenge, a hub deep in the brain called the amygdala kicks into gear. The amygdala can trigger a comprehensive whole-body response to prepare us for the challenge or threat we face. This flight-or-fight response increases our heart rate and sends a wave of stress hormones rushing into our bloodstream. Luckily, there’s one brain region standing between us and this cascade of hyperarousal: the prefrontal cortex, an area right behind the middle of our eyebrows. Studies show that activity in this region tends to dampen, or downregulate, the amygdala, thus keeping our emotional response under control. https://www.scientificamerican.com/

 
MRI Reveals Lasting Brain Changes in Post-COVID Patients
FeaturedNeurologyNeuroscience·December 11, 2023
Summary: Researchers discovered structural differences in the brain white matter of COVID-19 patients with persisting symptoms, using advanced diffusion MRI technology. This study compares 16 men who had severe COVID-19 with healthy individuals, revealing that these differences might explain neurological problems post-COVID.
 
Diffusion MRI, more sensitive than conventional MRI, allows for a detailed understanding of microstructural changes in the brain. This research indicates a need for further exploration of long-term COVID-19 effects on the brain, potentially leading to more effective treatments for post-COVID neurological issues.
 
Key Facts:
 
Advanced diffusion MRI showed differences in brain white matter structure between COVID-19 patients with long-term symptoms and healthy individuals.
The study involved 16 men previously hospitalized for COVID-19, indicating potential neurological changes due to the virus.
This research suggests that changes in brain structure could contribute to the persisting neurological symptoms experienced by some COVID-19 survivors.
Source: Linkoping University
 
Researchers at Linköping University, Sweden, have examined the brains of 16 patients previously hospitalised for COVID-19 with persisting symptoms. They have found differences in brain tissue structure between patients with persisting symptoms after COVID-19 and healthy people.
 
Their findings, published in the journal Brain Communications, can bring insights into the underlying mechanisms of persisting neurological problems after COVID-19.
 
Several previous studies of persisting problems after COVID have involved MRI brain scanning. Although researchers have found differences compared with healthy brains, these differences are not specific to COVID-19.
 
This shows a brain
This consists mainly of nerve axons and is very important for transporting signals between the different parts of the brain and the rest of the body. Credit: Neuroscience News
“It can be frustrating for me as a doctor when I understand that the patients have problems, but I can’t find an explanation because there’s nothing in the MRI scan to explain it.
 
“To me, this underlines the importance of trying other examination technologies to understand what’s happening in the brain in patients with persisting symptoms after COVID-19,” says Ida Blystad, neuroradiologist in the Department of Radiology at Linköping University Hospital and researcher affiliated with the Department of Health, Medicine and Caring Sciences at Linköping University and the Centre for Medical Image Science and Visualization (CMIV).
 
In their current study, the researchers have therefore added a new type of MR imaging called advanced diffusion MRI. They were particularly interested in the brain’s white matter. This consists mainly of nerve axons and is very important for transporting signals between the different parts of the brain and the rest of the body.
 
“Diffusion MRI is a very sensitive technology that allows changes in how the nerve axons are organised to be detected. This is one of the reasons why we wanted to use diffusion MRI to study the effects of COVID-19 on the brain that other imaging technologies might not pick up,” says Deneb Boito, doctoral student at the Department of Biomedical Engineering at Linköping University.
 
To get an idea of what diffusion MRI is, we can imagine a big city at night. Car headlights and rear lights shine like red and white strings of pearls on the most trafficked roads. We cannot see the road itself, but we understand that it is there, as the cars can easily move about right there.
 
Similarly, doctors and researchers can get an insight into how the brain is constructed on a microscopic level through diffusion MRI. This technology builds on the fact that there is water everywhere in the brain moving in the tissue according to the law of least resistance.
 
Water molecules move more easily along the neural pathways. By measuring the movement of water molecules through the neural pathways, researchers can indirectly infer the structure of neural pathways, just as we can indirectly understand that there is a motorway where there are many cars driving.
 
Healthcare usages of diffusion MRI include diagnosing stroke and planning brain surgery. In their current study, the researchers used a more advanced version of diffusion MRI. They examined 16 men who had been hospitalised for severe COVID-19 and who are participating in the Linköping COVID-19 Study (LinCos) at the Department of Rehabilitation Medicine in Linköping.
 
They still had persisting symptoms after seven months. This group was compared with a group of healthy individuals without post-COVID symptoms who had not been hospitalised for COVID. The participants’ brains were examined with both conventional MRI and diffusion MRI.
 
“The two groups differ when it comes to brain white matter structure. This can be one of the causes of the neurological problems experienced by the group that had suffered from severe COVID-19. It’s a result that’s in line with other studies that have shown changes to the brain’s white matter.
 
“However, having examined only a small group of patients, we are cautious about drawing any major conclusions. With this technology, we’re not measuring the function of the brain, but its microstructure.
 
“To me, these findings are a sign that we must investigate long-term effects of COVID-19 in the brain using more advanced MRI technology than conventional MRI,” says Ida Blystad.
 
There are several issues that the researchers want to study further. It appears, for instance, that white matter in different parts of the brain is affected in different ways, although it is too early to draw any conclusions as to what these differences mean.
 
An upcoming study will investigate whether changes detected with diffusion MRI are in any way connected to brain activity, and how different parts of the brain communicate with each other through the brain white matter in patients suffering from post-COVID fatigue.
 
Another question is what happens over time. The MRI scan provides an image of the brain at that particular moment. As the participants were examined on one occasion only, it is not possible to know whether the differences between the two groups will disappear over time or whether they are permanent.
 
Funding: This research was funded by, among others, the Analytic Imaging Diagnostic Arena (AIDA), the ITEA/Vinnova project ASSIST, and the Wallenberg Center for Molecular Medicine at Linköping University.

Life has found a home on Earth for around 4 billion years. That's a significant fraction of the universe's 13.77 billion-year history. Presumably, if life arose here, it could have appeared anywhere. And for sufficiently broad definitions of life, it might even be possible for life to have appeared mere seconds after the Big Bang.

To explore the origins of life, first we have to define it. There are over 200 published definitions of the term, which shows just how difficult this concept is to grapple with. For example, are viruses alive? They replicate but need a host to do so. What about prions, the pathogenic protein structures? Debates continue to swirl over the line between life and nonlife. But for our purposes, we can use an extremely broad, but very useful definition: Life is everything that's subject to Darwinian evolution.

This definition is handy because we'll be exploring the origins of life itself, which, by definition, will blur the boundaries between life and nonlife. At one point, deep in the past, Earth was not alive. Then it was. This means that there was a transition period that will naturally stretch the limits of any definition you can muster. Plus, as we dig deeper into the past and explore other potential options for life, we want to keep our definition broad, especially as we explore the more extreme and exotic corners of the universe.

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Life has found a home on Earth for around 4 billion years. That's a significant fraction of the universe's 13.77 billion-year history. Presumably, if life arose here, it could have appeared anywhere. And for sufficiently broad definitions of life, it might even be possible for life to have appeared mere seconds after the Big Bang.

To explore the origins of life, first we have to define it. There are over 200 published definitions of the term, which shows just how difficult this concept is to grapple with. For example, are viruses alive? They replicate but need a host to do so. What about prions, the pathogenic protein structures? Debates continue to swirl over the line between life and nonlife. But for our purposes, we can use an extremely broad, but very useful definition: Life is everything that's subject to Darwinian evolution.

This definition is handy because we'll be exploring the origins of life itself, which, by definition, will blur the boundaries between life and nonlife. At one point, deep in the past, Earth was not alive. Then it was. This means that there was a transition period that will naturally stretch the limits of any definition you can muster. Plus, as we dig deeper into the past and explore other potential options for life, we want to keep our definition broad, especially as we explore the more extreme and exotic corners of the universe.

CLOSE

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 Summary: A new study uncovers a shared genetic basis for problematic alcohol use (PAU) across diverse ancestries. This research broadens our understanding of PAU’s genetic architecture and its consequences, including its role as a major cause of health problems and death.

 

The study identifies 110 risk gene regions and offers potential drug targets for future treatments. Genome-wide data may pave the way for personalized risk assessments and innovative interventions.

 

Key Facts:

 

A study involving over 1 million individuals from diverse genetic backgrounds reveals shared genetic architecture for problematic alcohol use.

Researchers identified 110 risk gene regions, providing insights into the biology of PAU and potential pharmacological targets.

The study suggests existing medications as potential treatments for PAU and explores genetic correlations with other mental and neurological disorders.

Source: Yale

 

A study led by VA Connecticut Healthcare Center/Yale researchers reveals ancestries around the world possess a shared genetic architecture for problematic alcohol use (PAU)—habitual heavy drinking, accompanied by harmful consequences.

 

The findings, published in Nature Medicine, could help scientists understand the genetic basis of PAU, a major cause of health problems in many age groups. It is a leading cause of death in those it afflicts.

 

This study is the largest to date for PAU—it identified many new risk genes and uncovered a large amount of new biology. With a better understanding of PAU biology, scientists will have new possibilities in developing treatments.

 

Hang Zhou, Ph.D., assistant professor of psychiatry and of biomedical informatics & data science at Yale School of Medicine and VA Connecticut, and first author of the study, said, “Research with the primary focus on understanding the molecular mechanism underlying PAU and identification of gene targets for potential pharmacological studies is extremely important for future treatments and could help mitigate the consequences of excessive alcohol use.”

 

Researchers studied more than 1 million people with PAU and included as many genetic ancestral groups as possible, including people with European, African, Latin American, East Asian, and South Asian ancestries.

 

The Million Veteran Program (MVP) was a major source of data for this study—MVP data were combined with data from many other sources to create the analyses.

 

Compared to previous research, this work broadened the findings and demonstrated that the genetic architecture of PAU is substantially shared across these populations. There are genetic differences in different populations for PAU, but the similarities are greater. Cross-ancestry information allowed the researchers to improve the power of gene discovery.

 

“By leveraging the multi-ancestry information, we identified 110 gene regions and had an improved fine-mapping of the potential causal variants in each region,” Zhou said.

 

The researchers also used various methods to prioritize multiple genes with convergent evidence linking association to PAU with brain biology through gene expression (transcriptional-wide association study in 13 brain tissues) and chromatin interaction analyses in the brain. This work will provide valuable resources and targets for future functional analyses and drug development.

 

Joel Gelernter, MD, Foundations Fund Professor of Psychiatry, and professor of genetics and of neuroscience at Yale School of Medicine and VA Connecticut, was the study’s senior author.

 

“One of the most important products of this research is the information provided about PAU risk across the entire genome,” Gelernter said.

 

“The resulting data allowed us to understand the biology of PAU better, suggesting some already-approved drugs that might become tools for treating PAU in the future, with additional research. The data we produced will be shared with the research community, and this will aid greatly in future research by other scientists.”

 

The drug-repurposing analyses identified several existing medications as potential treatments for PAU, which are described in the published article.

 

One of the outputs from this study is genome-wide association data, and this kind of information can be used to compute “polygenic risk scores,” or PRS, that can be used to estimate an individual’s genetic risk for PAU.

 

The researchers stressed that the PRS they computed is not yet ready for use in the clinic, but they also tested the association of the PRS for PAU with hundreds of medical traits in multiple biobanks including Vanderbilt University Medical Center’s Biobank, Mount Sinai’s BioMe, the Mass General Brigham Biobank, and Penn Medicine Biobank. This analysis identified genetic correlations between PAU and many other mental and neurological disorders.

https://neurosciencenews.com/global-genetics-aud-25397/https://neurosciencenews.com/global-genetics-aud-25397/

`If an elephant’s brain is bigger than ours, why are they not smarter?

This is a good question, because the answer teaches us a lot about the nature of intelligence itself. The average human brain weighs about a kilogram and a half, which is remarkably small really. The sum of all consciousness is housed within that little scoop of nervous tissue. On the other hand, within the cranium of an African bush elephant sits a brain well over twice the size of ours.

It’s clear that there’s more to intelligence than just brain size. The baleen whales of the oceans have brains weighing 7 kilograms, well over quadruple the mass of ours. However, their behaviour is much less complex and sophisticated than that of humans, or indeed of elephants. Baleen whales aren’t stupid - their songs are a rich and advanced form of communication, and they’ve been known to display altruism - but their intelligence definitely isn’t proportional to their massive brain size. যদি একটি হাতির মস্তিষ্ক আমাদের চেয়ে বড় হয় তবে তারা কেন স্মার্ট নয়?

যাইহোক, তাদের আচরণ মানুষের বা প্রকৃতপক্ষে হাতির তুলনায় অনেক কম জটিল এবং পরিশীলিত বেলেন তিমিরা বোকা নয় - তাদের গানগুলি যোগাযোগের একটি সমৃদ্ধ এবং উন্নত রূপ, এবং তারা পরার্থপরতা প্রদর্শন করতে পরিচিত - তবে তাদের বুদ্ধিমত্তা অবশ্যই তাদের বিশাল মস্তিষ্কের আকারের সমানুপাতিক নয়

This is of course because their brains are tiny relative to their bodies. A blue whale’s brain makes up as little as 0.005% of its total body mass! Our brains, by comparison, are about 2.5% of our bodyweight. So is brain-to-body mass ratio the true decider of intellect? It’s certainly a better metric to compare between animals, but still one which is deeply flawed.

It turns out that, all else being equal, brain mass does not scale linearly with body mass. After all, there is a minimum number of neurons an animal needs to function, a concept known as the “grey floor”. Smaller animals tend to have much higher brain-to-body mass ratios, without necessarily seeming any more intelligent. A humble shrew, for example, has a brain which constitutes one tenth of the size of its body! If the metric were reliable, the shrew would be taming us!

While we’re on the topic, I should mention that the species with the lowest brain-to-body mass ratio of all vertebrates on this Earth is the magnificently named bony-eared assfish. Brains consume huge amounts of precious energy, so in the incredibly barren environment of the deep sea, the bony-eared assfish has done away with most of its grey matter.

 

For a fish with such an unflattering name, it is hauntingly beautiful!

Anyway, it’s clear that raw brain-to-body mass ratio is far from a perfect measure of intelligence; it is too harsh on big animals, and too kind to small animals. Scientists have studied the relative brain sizes of mammals, and come up with a formula that adjusts for this problem. Applying this formula gives a new, more refined metric: encephalisation quotient, or EQ for short.

এটি অবশ্যই কারণ তাদের মস্তিষ্ক তাদের শরীরের তুলনায় ক্ষুদ্র একটি নীল তিমির মস্তিষ্ক তার মোট শরীরের ভরের 0.005% এর মতোই কম করে! আমাদের মস্তিষ্ক, তুলনা করে, আমাদের শরীরের ওজনের প্রায় 2.5% তাহলে কি মস্তিষ্ক-থেকে-শরীরের ভরের অনুপাতই বুদ্ধির প্রকৃত নির্ধারক? প্রাণীদের মধ্যে তুলনা করার জন্য এটি অবশ্যই একটি ভাল মেট্রিক, তবে এখনও একটি যা গভীরভাবে ত্রুটিযুক্ত

দেখা যাচ্ছে যে, অন্য সব কিছু সমান হওয়ায়, মস্তিষ্কের ভর শরীরের ভরের সাথে রৈখিকভাবে স্কেল করে না সর্বোপরি, একটি প্রাণীর কাজ করার জন্য ন্যূনতম সংখ্যক নিউরন প্রয়োজন, একটি ধারণা যা "ধূসর ফ্লোর" নামে পরিচিত ছোট প্রাণীদের মস্তিষ্ক থেকে শরীরের ভর অনুপাত অনেক বেশি থাকে, অগত্যা আরও বুদ্ধিমান বলে মনে হয় না উদাহরণস্বরূপ, একজন নম্র শ্রুয়ের একটি মস্তিষ্ক রয়েছে যা তার শরীরের আকারের এক দশমাংশ গঠন করে! মেট্রিক নির্ভরযোগ্য হলে, বুদ্ধিমান আমাদের taming করা হবে!

যখন আমরা বিষয়টি নিয়ে আছি, তখন আমার উল্লেখ করা উচিত যে এই পৃথিবীতে সমস্ত মেরুদণ্ডী প্রাণীর মধ্যে সর্বনিম্ন মস্তিষ্ক-থেকে-শরীরের ভরের অনুপাতের প্রজাতির নাম হল অস্থি-কানযুক্ত অ্যাসফিশ মস্তিষ্ক প্রচুর পরিমাণে মূল্যবান শক্তি খরচ করে, তাই গভীর সমুদ্রের অবিশ্বাস্যভাবে অনুর্বর পরিবেশে, অস্থি-কানযুক্ত অ্যাসফিশ তার বেশিরভাগ ধূসর পদার্থকে সরিয়ে ফেলেছে

 

যেমন একটি অপ্রস্তুত নামের একটি মাছের জন্য, এটা খুব সুন্দর!

যাই হোক, এটা পরিষ্কার যে কাঁচা মস্তিষ্ক-থেকে-শরীরের ভর অনুপাত বুদ্ধিমত্তার নিখুঁত পরিমাপ থেকে অনেক দূরে; এটা বড় প্রাণীদের জন্য খুব কঠোর, এবং ছোট প্রাণীদের জন্য খুব দয়ালু বিজ্ঞানীরা স্তন্যপায়ী প্রাণীদের আপেক্ষিক মস্তিষ্কের আকার অধ্যয়ন করেছেন এবং একটি সূত্র নিয়ে এসেছেন যা এই সমস্যার জন্য সামঞ্জস্য করে এই সূত্রটি প্রয়োগ করা একটি নতুন, আরও পরিমার্জিত মেট্রিক দেয়: এনসেফালাইজেশন ভাগফল, বা সংক্ষেপে EQ

In other words, EQ is the ratio of actual brain size to predicted brain size. When we compare different animals’ EQ values, the results line up a lot more with what we would expect, intelligence-wise. Humans have the highest score of any animal, at about 7.6. The tucuxi, a very interesting type of freshwater dolphin from the rivers of South America, takes second place. It measures only 1.5 metres in length, and has a bright pink underbelly!

Manta rays have one of the highest EQs among fish, octopuses triumph among invertebrates, and corvids outperform their feathered friends. These results are all exactly what we would predict based on behavioural signs of intelligence. So, is encephalisation quotient really the answer? Probably not. Once again, this method seems to fall short of being perfect.

On average, birds have much lower EQs than mammals, but there is ample evidence to suggest that birds are incredibly smart. In fact, all the dinosaurs, not just birds, have surprisingly low encephalisation values. If estimated EQ is to be believed, Tyrannosaurus rex was less intelligent than a slug. Believe it or not, the sauropod dinosaurs have the lowest score of any animal in history ever measured, at as low as 0.01!

                                         

There are several likely reasons for this. The formula for encephalisation quotient was based only on data from mammalian species, so in general it probably shouldn’t be used to compare mammals to non-mammals. Bird/dinosaur cells are much smaller than mammalian cells. For its size, a typical avian brain has twice as many neurons as a standard mammal brain!

Raw brain size, brain-to-body mass ratio, EQ… all these metrics share a fundamental problem: they’re all based on overall brain mass in some way, and there’s a lot of stuff inside brains that has nothing to do with intelligence. For example, a large portion of whales’ and dolphins’ brain mass is just insulating blubber! There are all kinds of factors like this that really muddy the waters. Perhaps it’s better to just focus on the part of the brain that actually does the thinking.

 

The cerebral cortex is thought to be the seat of intelligence in mammals. This grooved and convoluted outer layer of tissue is responsible for processing our senses, finely controlling our movement, abstract thought, and much more. Non-mammal animals don’t have a cerebral cortex per se, but they always have an equivalent brain region - for example, birds have their dorsoventricular ridge, or DVR.

 

So far, the single best predictor of intelligence we have found is the number of cortical neurons; that is, the total number of nerve cells within the cerebral cortex (or equivalent area). Humans have at least 16 billion, which is exceptional! Elephants, despite having a brain twice as large, have about a third as many cortical neurons. However, the real world champion is the orca, believe it or not, with an absolutely astonishing 43 billion cortical neurons!

 

In fact, by this measure, humans sit at humble fifth place. There are four species of dolphins with more cortical neurons, the most of all belonging to the orca. Some might be quick to discredit this method as soon as they hear that it doesn’t put humans on top, and I would encourage those people to keep an open mind. If we’re so, so sure that orcas are less smart than us, perhaps we’re looking at intelligence in the wrong way.

কাঁচা মস্তিষ্কের আকার, মস্তিষ্ক-থেকে-শরীরের ভরের অনুপাত, EQ... এই সমস্ত মেট্রিক্স একটি মৌলিক সমস্যা ভাগ করে: এগুলি সবই কোনও না কোনওভাবে সামগ্রিক মস্তিষ্কের ভরের উপর ভিত্তি করে এবং

But that’s a more philosophical discussion for another answer. Anyway, for centuries, humans have been trying to put a number on intelligence, to find some way to quantify it. None of the metrics we’ve come up with are perfect, but for now, the best we have is the number of cortical neurons. It doubtless has its discrepancies, but overall it seems to be an extremely useful way of comparing animal acumen.

So, going back to your question, if an elephant’s brain is bigger than ours, why isn’t it smarter? Because the size of a brain, as we’ve seen, has little to do with intelligence. Apologies if this answer was long-winded, though I think we visited some interesting places on our journey through animal minds! Thank you everyone for reading, I hope you enjoyed, and have a great day.

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তবে এটি অন্য উত্তরের জন্য আরও দার্শনিক আলোচনা যাইহোক, বহু শতাব্দী ধরে, মানুষ বুদ্ধিমত্তার উপর একটি সংখ্যা স্থাপন করার চেষ্টা করছে, এটি পরিমাপ করার কিছু উপায় খুঁজে বের করার জন্য আমরা যে মেট্রিকগুলি নিয়ে এসেছি তার কোনওটিই নিখুঁত নয়, তবে আপাতত, আমাদের কাছে সেরাটি হল কর্টিকাল নিউরনের সংখ্যা নিঃসন্দেহে এটির অসঙ্গতি রয়েছে, তবে সামগ্রিকভাবে এটি প্রাণী বুদ্ধির তুলনা করার একটি অত্যন্ত দরকারী উপায় বলে মনে হচ্ছে

সুতরাং, আপনার প্রশ্নে ফিরে যাচ্ছি, যদি একটি হাতির মস্তিষ্ক আমাদের চেয়ে বড় হয় তবে কেন এটি স্মার্ট নয়? কারণ মস্তিষ্কের আকার, যেমনটি আমরা দেখেছি, বুদ্ধিমত্তার সাথে খুব কম সম্পর্ক রয়েছে এই উত্তরটি দীর্ঘস্থায়ী হলে ক্ষমাপ্রার্থী, যদিও আমি মনে করি আমরা প্রাণীদের মনের মাধ্যমে আমাদের যাত্রায় কিছু আকর্ষণীয় স্থান পরিদর্শন করেছি! পড়ার জন্য সবাইকে ধন্যবাদ, আমি আশা করি আপনি উপভোগ করেছেন, এবং আপনার দিনটি দুর্দান্ত কাটবে

On the other hand, Stephen Hawking used to think that the universe was created entirely from nothing without the intervention of infinity, but quantum mechanics proves that energy exists even in nothing.

Noted that in 2011, despite the objections of world-renowned scientists including Hawking, when CERN announced through their Opera Project that neutrino is at least 60 nanoseconds faster than light - in the same year (2011), Stephen Hawking returned from his "Null theory" of the universe" and declared: "For the creation of the universe there is no need to lighting an infinite being, the universe arose from gravity."

 

Global Genetic Insights into Problematic Alcohol Use

FeaturedGeneticsNPLAY SOUND

 
https://neurosciencenews.com/long-covid-brain-changes-25345/
 
https://www.iqrasense.com/death-and-after-life/the-journey-of-a-muslim-believer-after-death-islamic-beliefs-according-to-hadith.html?awt_a=8lp.&awt_l=DH9Ki&awt_m=kCEI.buhMEBWmp.
 
https://www.iqrasense.com/death-and-after-life/islamic-beliefs-on-afterlife-questions-asked-after-a-persons-death.html
 

Global Genetic Insights into Problematic Alcohol Use

FeaturedGeneticsN

 

Childhood Brain Growth Linked to Gut Microbiome

Summary: A new study uncovers the significant influence of the gut microbiome on cognitive function and brain structure in healthy children. Analyzing data from 381 children in The RESONANCE cohort, the research identifies specific microbial species linked to higher cognitive abilities, while others correlate with lower cognitive scores.
 
This study utilizes advanced machine learning models to demonstrate the potential of gut microbial profiles in predicting cognitive performance and brain development. This novel research highlights the gut-brain-microbiome axis’s crucial role in early childhood development and opens doors for future interventions.
 
Key Facts:
 
The study found a correlation between specific gut microbial species and cognitive function in children.
Advanced machine learning models showed gut microbial profiles could predict brain structure and cognitive performance.
The research provides a new understanding of the gut-brain-microbiome axis in normal neurocognitive development among healthy children.
Source: Wellesley College
 
Emerging evidence implicates the gut microbiome in cognitive outcomes and neurodevelopmental disorders, but the influence of gut microbial metabolism on typical neurodevelopment has not been explored in detail. 
 
Researchers from Wellesley College, in collaboration with other institutions, have demonstrated that differences in the gut microbiome are associated with overall cognitive function and brain structure in healthy children.
 
This shows a child.
This research is the first to examine the gut-brain-microbiome axis in normal neurocognitive development among healthy children. Credit: Neuroscience News
This study – published today in Science Advances – is a part of the Environmental Influences on Child Health Outcome (ECHO) Program funded by the National Institutes of Health.
 
This study investigates this relationship in 381 healthy children, all part of The RESONANCE cohort in Providence, Rhode Island, offering novel insights into early childhood development. 
 
 Key Findings:
 
The research reveals a connection between the gut microbiome and cognitive function in children. Specific gut microbial species, such as Alistipes obesi and Blautia wexlerae, are associated with higher cognitive functions. Conversely, species like Ruminococcus gnavus are more prevalent in children with lower cognitive scores.
The study emphasizes the role of microbial genes, particularly those involved in the metabolism of neuroactive compounds like short-chain fatty acids, in influencing cognitive abilities.
Advanced machine learning models demonstrated the capability of gut microbial profiles to predict variations in brain structure and cognitive performance, highlighting the potential for early detection and intervention strategies in neurodevelopment.
This study represents an important first step in the understanding of the relationship between the gut biome and cognitive function in children. The corresponding author Vanja Klepac-Ceraj notes, “This research on a single cohort offers exciting hypotheses that we now want to test in additional settings.”
What Makes This Research Novel?
 
This research is the first to examine the gut-brain-microbiome axis in normal neurocognitive development among healthy children. The integration of multivariable linear and machine learning models to analyze the complex relationship between gut microbiome profiles and neurodevelopment is innovative.
 
These models not only established the association of gut microbiota with cognitive function but also predicted future cognitive performance based on early-life microbial profiles.
 
Public Health Relevance:
 
The findings pave the way for developing biomarkers for neurocognition and brain development.
 
This research could lead to early detection of developmental issues and interventions, potentially mitigating long-term cognitive challenges. It highlights the importance of gut health in early childhood, suggesting dietary and lifestyle considerations for parents and healthcare providers.
 
Furthermore, this study marks the first step in formulating hypotheses that can be tested experimentally and in animal models.
 
Contribution of Wellesley College:
 
Wellesley College played a crucial role in this research. The Klepac-Ceraj Lab at the Department of Biological Sciences provided essential expertise in microbiome analysis and cognitive assessment.
 
The lead author of this study, Dr. Kevin Bonham together with Dr. Guilherme Fahur Bottino spearheaded the data analyses. The college’s dedication to interdisciplinary collaboration was instrumental in conducting this complex study.
https://neurosciencenews.com/microbiome-brain-development-25393/
 

Spinal Stimulation Shows Promise As Depression Treatment

Summary: Researchers conducted a pilot clinical trial showing that spinal cord stimulation (SCS) is a feasible and well-tolerated method with potential to treat major depressive disorder. The trial involved 20 patients undergoing three weekly 20-minute SCS sessions over eight weeks.
 
Results revealed that those who received active stimulation exhibited a greater decrease in depressive symptom severity compared to the control group. This innovative approach suggests that modulating brain-body neural pathways through SCS can significantly impact mood regulation and offers a novel direction in treating psychiatric disorders.
 
Key Facts:
 
The study showed spinal cord stimulation to be a promising treatment for depression, well-tolerated by patients.
Participants receiving active stimulation experienced a significant reduction in depressive symptoms.
The research opens possibilities for further trials and development of a portable SCS device for psychiatric disorder treatment.
Source: University of Cincinnati
 
A pilot clinical trial led by University of Cincinnati researchers at the Lindner Center of HOPE found electrical stimulation of the spinal cord is feasible, well-tolerated and shows therapeutic potential to treat depression.
 
The results of the trial were published in the journal Molecular Psychiatry on Dec. 20.
 
Research background
Principal investigator Francisco Romo-Nava, MD, PhD, said his research focuses on how brain-body communication is involved in psychiatric disorders.
 
This shows a spinal cord.
Patients that received the active stimulation had a greater decrease in the severity of their depressive symptoms compared to the control group, but Romo-Nava cautioned the study was limited by its small sample size. Credit: Neuroscience News
“We think that the connection between the brain and the body is essential for psychiatric disorders,” said Romo-Nava, associate professor in the Department of Psychiatry and Behavioral Neurosciences at UC, associate chief research officer for the Research Institute at the Lindner Center of HOPE and a UC Health physician scientist.
 
“Many of the symptoms of mood disorders or eating disorders or anxiety disorders have to do with what one could interpret as dysregulation in this brain-body interaction.”
 
Romo-Nava said pathways of neurons located in the spinal cord convey information from the body to regions of the brain that are involved in the emotional experience we know as mood. When functioning properly, the brain uses this information to constantly make adjustments to help regulate a person’s mood.
 
While major depressive disorder can have many different causes, one contributor could be this pathway being overloaded with information.
 
“For example, chronic stress could lead to a hyperactive brain-body circuit that eventually burns the system out and prevents it from adjusting itself in an effective and optimal way,” Romo-Nava said.
 
The research team looked at different ways to modulate this interaction between the brain and body and developed a novel approach through noninvasive spinal cord stimulation. Romo-Nava obtained a patent in 2020 for the stimulation method used after working with UC’s Office of Innovation.
 
The spinal cord stimulation is designed to decrease the flow of information in the brain-body circuit so that the brain is better able to readjust and regulate itself.
 
“Spinal cord stimulation is thought to help the brain modulate itself as it should by decreasing the noise or decreasing the hyperactive signaling that may be in place during a depressive syndrome,” Romo-Nava said.
 
The investigational device that was used is no larger than a shoe box, with the active electrode placed on the patient’s back and the return electrode placed on their right shoulder.
 
Trial details
With funding through a Brain & Behavior Research Foundation NARSAD Young Investigator Award, Romo-Nava designed the pilot study to test the feasibility and tolerability of spinal cord stimulation for patients with major depressive disorder.
 
A total of 20 patients were enrolled in the trial, with half randomized to receive the active version of the spinal cord stimulation and half receiving a different version of current that was not expected to have much of an effect.
 
Patients went to the Lindner Center of HOPE for three 20-minute sessions a week for eight weeks, for a total of 24 spinal stimulation sessions.
 
Trial results
Romo-Nava said like with most pilot studies, the primary focus of the study was the feasibility and safety of the intervention and how well patients tolerated the stimulation. The study was designed so that the dose of stimulation could be decreased if needed, but Romo-Nava said all patients tolerated the initially prescribed dose well.
 
“We used a current that is so small that it’s about 10 times smaller than the one known to induce tissue damage, so that’s also pretty encouraging because there’s a lot to explore in terms of what is the optimal dose and session frequency,” he said.
 
Side effects of the treatment were mild, including skin redness at the site of stimulation and brief non-painful itching or burning sensations that only lasted during the treatment sessions. The skin redness typically did not last more than 20 minutes after a session, Romo-Nava said.
 
A virtual reconstruction of how the current from the device moves through the body showed the current reaches spinal gray matter in the spinal cord, but does not reach the brain itself.
 
“That supports our hypothesis that it is the modulation of these pathways of information that then may induce an effect on the mood-relevant areas in the brain,” he said. “So it is not the current that reaches the brain, it is the change in the signal that then has an effect. This study is not sufficient to prove all of these components of the hypothesis, but we think it’s a great start.”
 
Patients that received the active stimulation had a greater decrease in the severity of their depressive symptoms compared to the control group, but Romo-Nava cautioned the study was limited by its small sample size. These results will need to be replicated in much larger studies to be confirmed.
 
“We need to be cautious when we interpret these results because of the pilot nature and the small sample size of the study,” he said. “While the primary outcome was positive and it shows therapeutic potential, we should acknowledge all the limitations of the study.”
 
Data showed participants’ resting blood pressure did not change over the course of the eight weeks, but their diastolic blood pressure (the bottom number of a blood pressure reading) decreased for a short time after each session in a cumulative way during the study.
 
“That may mean that we may be actually inducing a form of plastic effect on the brain-body interaction circuit that is also involved in autonomic functions like blood pressure and heart rate,” Romo-Nava said. “This is very preliminary, but it is also another signal that is in the right direction.”
 
Moving forward, Romo-Nava said the research team is seeking additional funding to put together an expanded trial and develop a portable version of the spinal cord stimulation device.
 
If further studies confirm the stimulation is safe and effective to treat psychiatric disorders, future work will also be needed to find the optimal dose, frequency and conditions it can be used for. https://neurosciencenews.com/spinal-stimulation-depression-25388/
 

Human Brain’s Unique Parallel Pathways

Summary: Researchers discovered a unique feature of the human brain’s communication networks: the transmission of information via multiple parallel pathways, a trait not observed in macaques or mice.
 
This finding emerged from a study using diffusion and functional MRI data, combined with information and graph theory. The team mapped “brain traffic” to compare signal transmission in different mammalian brains.
 
Their research indicates that these parallel pathways in humans might contribute to our advanced cognitive abilities and could have implications for understanding brain evolution and potential medical applications.
 
Key Facts:
 
The EPFL study found that human brains uniquely transmit information through multiple parallel pathways, unlike macaques and mice.
This discovery was made using a novel combination of diffusion MRI, functional MRI, information theory, and graph theory.
The research suggests that these parallel pathways could contribute to higher cognitive functions and offer new insights into brain resilience and neurorehabilitation.
Source: EPFL
 
In a study comparing human brain communication networks with those of macaques and mice, EPFL researchers found that only the human brains transmitted information via multiple parallel pathways, yielding new insights into mammalian evolution.
 
When describing brain communication networks, EPFL senior postdoctoral researcher Alessandra Griffa likes to use travel metaphors. Brain signals are sent from a source to a target, establishing a polysynaptic pathway that intersects multiple brain regions “like a road with many stops along the way.”
 
This shows a brain.
The DWI scans allowed the scientists to reconstruct the brain “road maps”, and the fMRI scans allowed them to see different brain regions light up along each “road”, which indicated that these pathways were relaying neural information. Credit: Neuroscience News
She explains that structural brain connectivity pathways have already been observed based on networks (“roads”) of neuronal fibers. But as a scientist in the Medical Image Processing Lab (MIP:Lab) in EPFL’s School of Engineering, and a research coordinator at CHUV’s Leenaards Memory Centre, Griffa wanted to follow patterns of information transmission to see how messages are sent and received. In a study recently published in Nature Communications, she worked with MIP:Lab head Dimitri Van de Ville and SNSF Ambizione Fellow Enrico Amico to create “brain traffic maps” that could be compared between humans and other mammals.
 
To achieve this, the researchers used open-source diffusion (DWI) and functional magnetic resonance imaging (fMRI) data from humans, macaques, and mice, which was gathered while subjects were awake and at rest.
 
The DWI scans allowed the scientists to reconstruct the brain “road maps”, and the fMRI scans allowed them to see different brain regions light up along each “road”, which indicated that these pathways were relaying neural information.
 
They analyzed the multimodal MRI data using information and graph theory, and Griffa says that it is this novel combination of methods that yielded fresh insights.
 
“What’s new in our study is the use of multimodal data in a single model combining two branches of mathematics: graph theory, which describes the polysynaptic ‘roadmaps’; and information theory, which maps information transmission (or ‘traffic’) via the roads.
 
“The basic principle is that messages passed from a source to a target remain unchanged or are further degraded at each stop along the road, like the telephone game we played as children.”
 
The researchers’ approach revealed that in the non-human brains, information was sent along a single “road”, while in humans, there were multiple parallel pathways between the same source and target. Furthermore, these parallel pathways were as unique as fingerprints, and could be used to identify individuals.
 
“Such parallel processing in human brains has been hypothesized, but never observed before at a whole-brain level,” Griffa summarizes.
 
Potential insights for evolution and medicine
 
Griffa says that the beauty of the researchers’ model is its simplicity, and its inspiration of new perspectives and research avenues in evolution and computational neuroscience. For example, the findings can be linked to the expansion of human brain volume over time, which has given rise to more complex connectivity patterns.
 
“We could hypothesize that these parallel information streams allow for multiple representations of reality, and the ability to perform abstract functions specific to humans.”
 
She adds that although this hypothesis is only speculative, as the Nature Communications study involved no testing of subjects’ computational or cognitive ability, these are questions that she would like to explore in the future.
 
“We looked at how information travels, so an interesting next step would be to model more complex processes to study how information is combined and processed in the brain to create something new.”
 
As a memory and cognition researcher, she is especially interested in using the model developed in the study to investigate if parallel information transmission could confer resilience to brain networks, and potentially play a role in neurorehabilitation after brain injury, or in the prevention of cognitive decline in pathologies of advanced age.
 
“Some people age healthily, while others experience cognitive decline, so we’d like to see if there is a relationship between this difference and the presence of parallel information streams, and whether they could be trained to compensate neurodegenerative processes.”
https://neurosciencenews.com/brain-pathways-neuroscience-25384/
 
 Innovative Brain Cell Chips Unlock New Horizons in Speech Recognition
FeaturedNeuroscience·December 12, 2023
 
 
Summary: In a revolutionary study, researchers created a hybrid system called Brainoware, which integrates human brain cell networks, or organoids, with a computer chip.
 
This innovative setup demonstrates capabilities in processing, learning, and memory, and has achieved basic speech recognition skills by decoding audio clips of Japanese vowels. The organoid-AI system, though less accurate than artificial neural networks, improved its speech recognition accuracy to about 78% with training.
 
This research opens new possibilities in biocomputing, showcasing the potential of brain organoids in complex computational tasks.
 
Key Facts:
 
Brainoware is a pioneering hybrid system combining brain organoids with a computer chip, capable of processing information and learning.
The system has shown potential in speech recognition, successfully decoding audio signals into electrical impulses interpreted by the brain cells.
While initially less accurate, Brainoware’s speech recognition capabilities improved significantly with training, highlighting the adaptability of the brain cell networks.
Source: Neuroscience News
 
In a groundbreaking research initiative, neuroscientists have successfully integrated human brain cell networks, known as brain organoids, with electronic chips to perform elementary computational operations.
 
This landmark study, spearheaded by Feng Guo and his team at Indiana University Bloomington, marks a significant step in the realm of biocomputing.
 
The research group cultivated a brain organoid from stem cells and ingeniously connected it to a computer chip, forming a unique setup named “Brainoware.” This setup was further linked to an AI tool, leading to intriguing outcomes.
 
This shows a computer chip.
The team discovered that the organoid-AI combination could interpret these audio signal patterns, equating to a rudimentary form of speech recognition. Credit: Neuroscience News
The brain-cell-and-chip hybrid demonstrated capabilities in processing, learning, and memory retention. Remarkably, it exhibited basic skills in speech recognition.
 
The findings, featured in today’s issue of Nature Electronics, hint at future bio-computer models that could surpass traditional computers in efficiency.
 
For many years, scientists have been exploring the possibility of building computers modeled on complex biological systems. Guo’s vision of these biological computers is to overcome certain limitations of traditional silicon-based computing, such as data processing bottlenecks.
 
Standard computers excel in numerical tasks, but the human brain outperforms them in handling intricate information with minimal energy consumption. Guo notes that this is the inaugural demonstration of employing brain organoids in computing. He expresses enthusiasm about the future prospects of organoids in the biocomputing sector.
 
The Brainoware project aimed to utilize real brain cells for sending and receiving data. Upon stimulating the brain-cell-chip hybrid electrically, Brainoware reacted, indicating neural network adaptations. This response implies that the system processed information and might potentially execute computing operations autonomously.
 
In testing Brainoware’s practical capabilities, Guo’s team engaged it in various tasks. They challenged it with mathematical problems and a speech recognition test involving 240 audio clips of Japanese vowels spoken by eight individuals.
 
The audio was transformed into electrical signals, which then interacted with the brain organoid’s neural networks. These interactions were decoded using an AI tool.
 
The team discovered that the organoid-AI combination could interpret these audio signal patterns, equating to a rudimentary form of speech recognition. Guo acknowledges the system’s initial low accuracy rate, which, however, improved with training to about 78% accuracy. Yet, it still trailed behind the efficiency of artificial neural networks.
 
Lena Smirnova, an assistant professor of public health at Johns Hopkins University, points out that while brain organoids cannot truly perceive speech, they respond to the electrical impulses from the audio clips.
 
She also notes the study didn’t confirm whether Brainoware could sustain information processing and learning over an extended period or handle multiple tasks simultaneously. Cultivating and maintaining brain cell cultures for computational purposes is a formidable challenge.
 
Despite these hurdles, Smirnova acknowledges the study as a compelling demonstration of brain organoids’ potential. This research not only opens new avenues in biocomputing but also underscores the intricate relationship between neuroscience and technology.
https://neurosciencenews.com/brain-cell-chips-speech-recognition-25352/
 

Infant Brain Study Links Enlarged Brain Spaces to Autism Risk

Summary: Researchers uncovered a potential early marker for autism in infants: abnormally enlarged perivascular spaces (PVS) in the brain.
 
The study found that infants with enlarged PVS had a 2.2 times greater chance of developing autism compared to those with the same genetic risk. The researchers followed infants with a higher likelihood of autism due to having an older sibling with the condition.
 
Additionally, these infants showed an association between enlarged PVS and sleep problems later in life, suggesting a long-term impact of these early brain abnormalities.
 
Key Facts:
 
Infants with enlarged perivascular spaces have over double the risk of developing autism.
30% of infants who later developed autism showed enlarged PVS by 12 months.
The study links CSF abnormalities in infancy to later sleep disturbances and potentially other developmental disabilities.
Source: UNC
 
Throughout the day and night, cerebrospinal fluid (CSF) pulses through small fluid-filled channels surrounding blood vessels in the brain, called perivascular spaces, to flush out neuroinflammation and other neurological waste. A disruption to this vital process can lead to neurological dysfunction, cognitive decline, or developmental delays.
 
For the first time, researchers Dea Garic, Ph.D., and Mark Shen, Ph.D., both at the UNC School of Medicine’s Department of Psychiatry, discovered that infants with abnormally enlarged perivascular spaces have a 2.2 times greater chance of developing autism compared to infants with the same genetic risk. Their research also indicated that enlarged perivascular spaces in infancy are associated with sleep problems seven to 10 years after diagnosis.
 
This shows a baby.
The researchers studied infants at increased likelihood for developing autism, because they had an older sibling with autism. Credit: Neuroscience News.
“These results suggest that perivascular spaces could serve as an early marker for autism,” said Garic, assistant professor of psychiatry and a member of the Carolina Institute for Developmental Disabilities (CIDD).
 
The researchers studied infants at increased likelihood for developing autism, because they had an older sibling with autism. They followed these infants from 6-24 months of age, before the age of autism diagnosis.
 
Their study, published in JAMA Network Open, found that 30% of infants who later developed autism had enlarged perivascular spaces by 12 months. By 24 months of age, nearly half of the infants diagnosed with autism had enlarged perivascular spaces.
 
The importance of cerebrospinal fluid and sleep
Starting ten years ago, there has been a resurgence of research on the important functions of CSF in regulating brain health and development. Shen’s lab was the first to report that excessive volume of CSF was evident at 6 months of age in infants who would later develop autism. The current study showed that excessive CSF volume at 6 months was linked to enlarged perivascular spaces at 24 months.
 
Every six hours, the brain expels a wave of CSF that flows through perivascular spaces to remove potentially harmful neuroinflammatory proteins, such as amyloid beta, from building up in the brain. The CSF cleansing process is especially efficient when we are asleep, as the majority of CSF circulation and clearance occurs during sleep.
 
Disrupted sleep, however, can reduce CSF clearance from perivascular spaces, leading to dilation or enlargement, but this has previously only been studied in animal studies or in human studies of adults. This is the first study of its kind in children.
 
Shen, senior author of the JAMA Network Open paper, and Garic hypothesized that CSF abnormalities in infancy would be related to later sleep problems, based on Shen’s earlier research. The current sleep analysis revealed children who had enlarged perivascular spaces at two years of age had higher rates of sleep disturbances at school age.
 
“Since autism is so highly linked with sleep problems, we were in this unique position to examine CSF dynamics and sleep,” said Garic, who is the first author of the paper. “It was really striking to observe such a strong association separated by such a long period of time over childhood. But it really shows how perivascular spaces not only have an effect early in life, but they can have long-term effects, too.”
 
New clinical relevance in infancy
The research was done in conjunction with the Infant Brain Imaging Study (IBIS), a nationwide network of researchers investigating brain development, autism, and related developmental disabilities. The network consists of five universities, of which the University of North Carolina-Chapel Hill is the lead site.
 
For their study, Garic and Shen analyzed 870 MRIs from IBIS to measure excessive CSF volume and enlarged perivascular spaces. MRIs were obtained from babies during natural sleep at six, 12, and 24 months of age to observe changes over time.
 
The infant’s brain undergoes rapid development over this period. Previously, measurement of perivascular spaces was only thought to be clinically relevant for disorders of aging in older adults, such as in dementia. These findings suggest that younger populations may need to be considered and monitored for these types of brain abnormalities.
 
“Our findings were striking, given that neuroradiologists typically view enlarged perivascular spaces as a sign of neurodegeneration in adults, but this study reported it in toddlers,” said Garic. “This is an important aspect of brain development in the first years of life that should be monitored.”
 
Future studies and possibilities
Garlic and Shen hypothesize that excess CSF volume is stagnant or clogged and not circulating through the brain as efficiently as it should. For their next research endeavor, the researchers are planning to once again use MRIs to measure CSF in a sleeping infant’s brain, but this time focusing on the physiology and speed of CSF flow throughout the brain.
 
The research team is also working with other collaborators to quantify the size of perivascular spaces and the severity of behavioral outcomes. The team also plans to extend their research to neurogenetic syndromes associated with autism, such as Fragile X syndrome and Down syndrome.
 
“Collectively, our research has shown that CSF abnormalities in the first year of life could have downstream effects on a variety of outcomes, including later autism diagnosis, sleep problems, neuroinflammation, and possibly other developmental disabilities,” said Shen.
https://neurosciencenews.com/asd-brain-space-25385/
 
ফজলু ভাইয়ের অআম্মা গুরুতর অসুস্থ, শুধু বুকের শ্বাস-উঠা-নামা , নিথর দেহ, লিকুইড দেয়া হলে গাল বেয়ে বেরিয়ে অআসে। সবাই অজানা ..চিন্তায় বিভোর। ডাক্তারের করণীয় শেষ, বাড়ীতে কেবল অপেক্ষমান থাকা। হঠাৎ শাহীনুর বলে ডেকে উঠেএবং বলেনঃ অআমি নামাজ পড়বো। পরবর্তীতে বলেনঃ অআমাকে তছবীহ দাও... গুরুতরর অসুস্থতার সংবাদে প্রথম দুই রাকাত নামাজ পড়লাম, দ্রুত জানিয়ে দিলাম ধার্মিক ভাইদের কাছে। এর পর দোয়া চলতে থাকে। ডাক্তারের বাড়ীতে পাঠিয়ে দেয়া, সবাই একরকম অআশা ছেড়ে দেয়া, পাশাপাশি দোওআ কালাম অচিন্তনীয়ভাবে সুস্থ হয়ে উঠা...এর মধ্যে বাতিল হঠাৎ জ্বলে উঠার মধ্যে সম্পর্ক কি? ফজলু ভাইয়ের বর্ণনা তারিখঃ ২৮ জুলাই, ২০২৩,  মুহররম ১৪৪৫, জুমাবার।
 
হযরত দাঊদ  ইয়াহইয়া (আঃ) এর মধ্যবর্তী সময়ে আগমনকারী ব্যক্তিদের মধ্যে উযাইর (আঃ) ছিলেন অন্যতম। উযাইর (আঃ) কি নবী ছিলেন নাকি নবী ছিলেন না তা নিয়ে মতভেদ রয়েছে। অনেকে বলেন, তিনি বনী ইসরাঈলের নবীগণের মধ্যে অন্যতম একজন নবী ছিলেন। অনেকে আবার বলেন, তিনি নবী ছিলেন না বরং একজন জ্ঞানী  পুণ্যবান লোক ছিলেন।Uzair (A.S.) was one of those who came between Dawood and Yahya (A.S.). There is a difference of opinion as to whether Uzair (a.s.) was a prophet or not. Many say that he was one of the prophets of Bani Israel. Many people say that he was not a prophet but a wise and virtuous man. দাউদ  ইয়াহিয়া (.)-এর মধ্যে যারা এসেছিল তাদের মধ্যে উজাইর (.) ছিলেন একজন। উযাইর (আঃ) নবী ছিলেন কি না তা নিয়ে মতভেদ রয়েছে। অনেকে বলেন, তিনি ছিলেন বনী ইসরাঈলের নবীদের একজন। অনেকে বলেন, তিনি নবী ছিলেন না বরং একজন জ্ঞানী  গুণী ব্যক্তি ছিলেন
 
একদা তিনি তাঁর ক্ষেত-খামার  বাগ-বাগিচা দেখার জন্যে ঘর থেকে বের হন। সেখান থেকে প্রত্যাবর্তনকালে দ্বিপ্রহরের সময় একটা বিধ্বস্ত বাড়িতে বিশ্রাম নেন। তাঁর বাহন গাধার পিঠ থেকে নিচে অবতরণ করেন। বিশ্রামের উদ্দেশ্যে চিত হয়ে শুয়ে পড়েন।  অবস্থায় তিনি বিধ্বস্ত ঘরগুলোর প্রতি লক্ষ্য করলেন, যার অধিবাসীরাও ধ্বংস হয়ে গিয়েছে। Once he came out of the house to see his fields and gardens. On his way back from there he rested in a ruined house at afternoon. He dismounted from the back of his vehicle, a donkey. He lay down to rest. In this situation, he noticed the destroyed houses, whose inhabitants were also destroyed. একবার বাড়ি থেকে বের হয়ে তার ক্ষেত-বাগান দেখতে পান। সেখান থেকে ফেরার পথে দুপুর দুইটার দিকে তিনি একটি ধ্বংসপ্রাপ্ত বাড়িতে বিশ্রাম নেন। তিনি তার গাড়ির পিছন থেকে নামলেন, একটি গাধা। তিনি বিশ্রাম নিতে শুয়ে পড়লেন। এই অবস্থায়, তিনি ধ্বংস হওয়া বাড়িগুলি লক্ষ্য করলেন, যার বাসিন্দারাও ধ্বংস হয়ে গেছে
তিনি অনেকগুলো পুরাতন হাড় দেখতে পেয়ে মনে মনে ভাবলেন, মৃত্যুর পর আল্লাহ কিরূপে এগুলোকে জীবিত করবেন? আল্লাহ যে জীবিত করবেন, এতে তার আদৌ কোন সন্দেহ ছিল না।  কথাটি তিনি কেবল অবাক বিস্ময়ের সাথে ভেবেছিলেন। অতঃপর আল্লাহ মৃত্যুর ফেরেশতাকে পাঠিয়ে তাঁর রূহ কবজ করান এবং একশ বছর পর্যন্ত মৃত অবস্থায় রেখে দেন।He saw many old bones and thought to himself, how will God revive them after death? He had no doubt that God would bring him back to life. He thought of this only with amazement. Then Allah sent the angel of death to charm his soul and keep him dead for a hundred years. সে অনেক বৃদ্ধ হাড় দেখে মনে মনে ভাবল, মৃত্যুর পর আল্লাহ কিভাবে তাদের জীবিত করবেন? তার কোন সন্দেহ ছিল না যে ঈশ্বর তাকে জীবিত করবেন। তিনি কেবল বিস্ময়ের সাথে এটি ভেবেছিলেন। অতঃপর আল্লাহ তার আত্মাকে মোহিত করার জন্য এবং তাকে একশত বছর মৃত রাখার জন্য মৃত্যুর ফেরেশতা পাঠান
একশ বছর পূর্ণ হলে আল্লাহ উযাইরের নিকট ফেরেশতা পাঠিয়ে দেন। ফেরেশতা এসে উযাইরের অন্তর  চক্ষুদ্বয় জীবিত করলেন, যাতে কিভাবে আল্লাহ মৃতকে জীবিত করবেন তা স্বচক্ষে দেখেন  অন্তর দিয়ে উপলব্ধি করেন। এরপর ফেরেশতা আল্লাহর নির্দেশে উযাইরের বিক্ষিপ্ত হাড়গুলো একত্রিত করে তাতে গোশত লাগালেন, চুল পশম যথাস্থানে সংযুক্ত করলেন এবং চামড়া দ্বারা সমস্ত শরীর আবৃত করলেন।When one hundred years were completed, Allah sent an angel to Wazir. The angel came and revived the heart and eyes of Uzair, so that he could see with his own eyes and understand with his heart how God would bring the dead back to life. Then the angel assembled the scattered bones of Wazir by Allah's command and put flesh on them, attached the hair and fur in its proper place and covered the whole body with skin. একশ বছর পূর্ণ হলে আল্লাহ উজিরের কাছে ফেরেশতা পাঠালেন। ফেরেশতা এসে উজাইরের হৃদয়  চোখকে পুনরুজ্জীবিত করলেন, যাতে তিনি নিজের চোখে দেখতে পারেন এবং হৃদয় দিয়ে বুঝতে পারেন কিভাবে ঈশ্বর মৃতদেরকে জীবিত করবেন। অতঃপর ফেরেশতা আল্লাহর হুকুমে উজিরের ছড়িয়ে ছিটিয়ে থাকা হাড়গুলো একত্র করে তার উপর গোশত বসিয়ে চুল  পশম যথাস্থানে লাগিয়ে সারা শরীর চামড়া দিয়ে ঢেকে দেন
 
সবশেষে তার মধ্যে রূহ প্ৰবেশ করালেন। তার দেহ এভাবে তৈরি হচ্ছে তা তিনি প্ৰত্যক্ষ করছিলেন এবং অন্তর দিয়ে আল্লাহর কুদরত উপলব্ধি করছিলেন। উযাইর উঠে বসলেন। ফেরেশতা জিজ্ঞেস করলেন, আপনি  অবস্থায় কতদিন অবস্থান করলেন? তিনি বললেন, এক দিন অথবা এক দিনেরও কিছু কম। ফেরেশতা জানালেন, না বরং আপনি একশ বছর এভাবে অবস্থান করেছেন। At last the Spirit entered him. He was witnessing his body being formed in this way and he was realizing the power of Allah through his heart. Uzair sat up. The angel asked, how long did you stay in this situation? He said, a day or less than a day. The angel said, no, you have stayed like this for a hundred years. অবশেষে আত্মা তার মধ্যে প্রবেশ করল। এভাবে নিজের শরীর গঠন হতে দেখেন এবং হৃদয় দিয়ে আল্লাহর কুদরত উপলব্ধি করছিলেন। উজাইর উঠে বসল। ফেরেশতা জিজ্ঞেস করলেন,  অবস্থায় কতদিন অবস্থান করেছিলেন? তিনি বলেন, একদিন বা একদিনের কম। ফেরেশতা বললেন, না, আপনি একশ বছর এভাবেই থেকেছেন
 

 

আপনার খাদ্য সামগ্ৰী  পানীয় বস্তুর প্রতি লক্ষ্য করুন। এখানে খাদ্য বলতে তাঁর শুকনা রুটি এবং পানীয় বলতে পেয়ালার মধ্যে আঙ্গুর নিংড়ানো রস বুঝানো হয়েছে। দেখা গেল,  দুটির একটিও নষ্ট হয়নি। রুটি  রসের মত তাঁর আঙ্গুর এবং ডুমুরও টাটকা রয়েছে। এর কিছুই নষ্ট হয়নি। উযাইর ফেরেশতার মুখে একশ বছর অবস্থানের কথা শুনে এবং খাদ্য সামগ্রী অবিকৃত দেখে দ্বিধা-দ্বন্দ্বের মধ্যে পড়ে যান। Watch your food and drink. Here the food is his dry bread and the drink is the grape juice in the cup. As it turned out, none of these two were destroyed. His grapes and figs are fresh as are bread and juice. Nothing was wasted. Uzair was in dilemma after hearing the hundred years stay in the angel's mouth and seeing the food items uncorrupted. আপনার খাদ্য এবং পানীয় দেখুন. এখানে খাবার তার শুকনো রুটি এবং পানীয় হল কাপে আঙুরের রস। দেখা গেল, এই দুটির একটিও ধ্বংস হয়নি। তার আঙ্গুর এবং ডুমুর রুটি এবং রস হিসাবে তাজা. কিছুই নষ্ট হয়নি। ফেরেশতার মুখে একশত বছর থাকার কথা শুনে এবং খাদ্যদ্রব্য অবিকৃত দেখে উজাইর দ্বিধায় পড়ে যান
তাই ফেরেশতা তাকে বললেন, আপনি আমার কথায় সন্দেহ করছেন? তাহলে আপনার গাধাটির প্রতি লক্ষ্য করুন। উযাইর লক্ষ্য করে দেখলেন যে, তার গাধাটি মরে পচে গলে প্ৰায় নিশ্চিহ্ন হয়ে গিয়েছে। হাড়গুলো পুরাতন হয়ে যত্রতত্র বিক্ষিপ্ত হয়ে পড়ে রয়েছে। অতঃপর ফেরেশতা হাড়গুলোকে আহ্বান করলেন। সঙ্গে সঙ্গে হাড়গুলো চতুর্দিক থেকে এসে একত্রিত হয়ে গেল এবং ফেরেশতা সেগুলো পরস্পরের সাথে সংযুক্ত করে দিলেন। উযাইর তা তাকিয়ে দেখছিলেন। So the angel said to him, you doubt my words? Then watch your donkey. Uzair noticed that his donkey had died and rotted and almost disappeared. The bones are old and scattered everywhere. Then the angel called the bones. Immediately the bones came together from all quarters and the angel joined them together. Uzair was eagerly looking at it.
 তারপর ফেরেশতা উক্ত কংকালে রগ, শিরা-উপশিরা সংযোজন করলেন। গোশত দ্বারা আচ্ছাদিত করলেন এবং চামড়া  পশম দ্বারা তা আবৃত করলেন। সবশেষে তার মধ্যে রূহ প্রবেশ করালেন। ফলে গাধাটি মাথা  কান খাড়া করে দাঁড়াল এবং কিয়ামত আরম্ভ হয়ে গিয়েছে ভেবে চীৎকার করতে লাগল। যখন উযাইর (আঃ) এর নিকট  বিষয়টি সুস্পষ্ট হয়ে গেল তখন তিনি বলে উঠলেন, আমি জানি যে, আল্লাহ সর্ববিষয়ে সর্বশক্তিমান। মৃতকে জীবিত করা সহ যে কোন কাজ করতে তিনি সম্পূর্ণ সক্ষম।Then the angel added veins, veins and tendons to the skeleton. covered it with flesh and covered it with skin and fur. At last the Spirit entered him. As a result, the donkey raised its head and ears and started shouting thinking that the doomsday had begun. When this matter became clear to Uzair (a.s.), he said, "I know that Allah/God is all-powerful in all matters." He is fully capable of doing anything including bringing the dead back to life.

 

 

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অতঃপর উযাইর (আঃ) উক্ত গাধার পিঠে আরোহণ করে নিজ এলাকায় চলে যান কিন্তু সেখানে কোন লোকই তিনি চিনতে পারছেন না আর তাকেও দেখে কেউ চিনতে পারছে না নিজের বাড়ি-ঘরও তিনি সঠিকভাবে চিনে উঠতে পারছিলেন না অবশেষে ধারনার বশে নিজের মনে করে এক বাড়িতে উঠলেন সেখানে অন্ধ পঙ্গু এক বৃদ্ধাকে পেলেন তার বয়স ছিল একশ বিশ বছর এই বৃদ্ধা ছিল উযাইর পরিবারের দাসী একশ বছর পূর্বে তিনি যখন বাড়ি থেকে বের হয়ে যান, তখন এই বৃদ্ধার বয়স ছিল বিশ বছর এবং উযাইরকে সে চিনত বৃদ্ধ বয়সে উপনীত হলে সে অন্ধ পঙ্গু হয়ে যায় উযাইর জিজ্ঞেস করলেনঃ হে বৃদ্ধা, এটা কি উযাইরের বাড়ি? বৃদ্ধা বললঃ হ্যাঁ, এটা উযাইরের বাড়ি বৃদ্ধা মহিলাটি কেঁদে ফেলল এবং বলল, এতগুলো বছর কেটে গেল কেউ তার নামটি উচ্চারণও করে না, সবাই তাকে ভুলে গিয়েছে উযাইর নিজের পরিচয় দিয়ে বললেন, আমিই সেই উযাইর আল্লাহ আমাকে একশ বছর মৃত অবস্থায় রেখে পুনরায় জীবিত করেছেন বৃদ্ধা বলল, কী আশ্চর্য আমরাও তো তাকে একশ বছর পর্যন্ত পাচ্ছি না, সবাই তার নাম ভুলে গিয়েছে কেউ তাকে স্মরণ করে না তিনি বললেন, আমিই সেই উযাইর বৃদ্ধা বলল, আপনি যদি সত্যিই উযাইর হন তাহলে উযাইরের দোয়া আল্লাহ কবুল করতেন কোন রোগী বা বিপদগ্রস্তের জন্যে দোয়া করলে আল্লাহ তাকে নিরাময় করতেন এবং বিপদ থেকে মুক্তি দিতেন সুতরাং আপনি আমার জন্য দোয়া করুন, আল্লাহ আমার দৃষ্টিশক্তি ফিরিয়ে দিলে আপনাকে দেখব এবং আপনি উযাইর হলে আমি চিনব তখন উযাইর দোয়া করলেন এবং বৃদ্ধার চোখে হাত বুলিয়ে দিলেন এতে তার অন্ধত্ব দূর হয়ে গেল

 

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তারপর তিনি বৃদ্ধার হাত ধরে বললেন, আল্লাহর হুকুমে তুমি উঠে দাঁড়াও সাথে সাথে তার পঙ্গুত্ব বিদূরিত হল, সে উঠে দাঁড়ালো তারপর উযাইরের দিকে তাকিয়ে দেখে বলে উঠল, আমি সাক্ষ্য দিচ্ছি আপনিই উযাইর এরপর বৃদ্ধা বনী ইসরাঈলের মহল্লায় চলে গেল সে দেখল তারা এক আসরে জমায়েত হয়েছে সে আসরে উযাইরের এক বৃদ্ধ পুত্ৰও উপস্থিত ছিল, যার বয়স একশ আঠার বছর পুত্রদের পুত্ররাও তথায় উপস্থিত ছিল তারাও আজ প্রৌঢ় বৃদ্ধা মহিলা এক পাশে দাড়িয়ে মজলিশের লোকদের ডেকে বলল, উযাইর তোমাদের মধ্যে আবার ফিরে এসেছেন কিন্তু বৃদ্ধার কথা তারা হেসে উড়িয়ে দিল তারা বলল, তুমি মিথ্যুক বৃদ্ধা নিজের পরিচয় দিয়ে বলল, আমি অমুক, তোমাদের বাড়ির দাসী উযাইর এসে আমার জন্যে আল্লাহর নিকট দোয়া করেছেন তিনি আমার দৃষ্টিশক্তি ফিরিয়ে দিয়েছেন এবং পঙ্গু পা সুস্থ করে দিয়েছেন উযাইর বলেছেন, আল্লাহ তাঁকে একশ বছর মৃত অবস্থায় রেখে আবার জীবিত করে দিয়েছেন

 

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কথা শোনার পর লোকজন উঠে উযাইরের বাড়িতে গেল এবং তাকে ভাল করে দেখল উযাইরের বৃদ্ধ পুত্র বলল, আমার পিতার দুই কাঁধের মাঝে একটি কাল তিল ছিল সুতরাং সে কাঁধের কাপড় উঠিয়ে তিল দেখে তাকে চিনতে পারল এবং বলল, ইনিই আমার পিতা উযাইর তখন বনী ইসরাঈলের লোকজন উযাইরকে বলল, আমরা শুনেছি আপনি ব্যতীত অন্য কোন লোকের তাওরাত কিতাব মুখস্থ ছিল না দিকে বুখত নসর এসে লিখিত তাওরাতের সমস্ত কপি আগুনে জ্বালিয়ে দিয়েছে একটি অংশও অবশিষ্ট নেই সুতরাং আপনি আমাদের জন্যে একখানা তাওরাত লিখে দিন বুখত নসরের আক্রমণকালে উযাইরের পিতা সারূখা তাওরাতের একটি কপি মাটির নিচে পুঁতে রেখেছিলেন কিন্তু সেই স্থানটি কোথায় উযাইর ব্যতীত আর কেউ তা জানত না সুতরাং তিনি উপস্থিত লোকদেরকে সাথে নিয়ে সেই স্থানে গেলেন এবং মাটি খুঁড়ে তাওরাতের কপি বের করলেন কিন্তু এতদিনে তাওরাতের পাতাগুলো নষ্ট হয়ে সমস্ত লেখা মুছে গিয়েছে এরপর তিনি একটি বৃক্ষের নিচে গিয়ে বসলেন, বনী ইসরাঈলের লোকজনও তাঁর পাশে গিয়ে ঘিরে বসল কিছুক্ষণের মধ্যে আকাশ থেকে দুটি নক্ষত্র এসে তার পেটের মধ্যে প্রবেশ করল এতে গোটা তাওরাত কিতাব তাঁর স্মৃতিতে ভেসে উঠলো তখন বনী ইসরাঈলের জন্যে তিনি নতুনভাবে তাওরাত লিখে দিলেন

 

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সকল কারণে অর্থাৎ নক্ষত্রদ্বয়ের অবতরণ, তাওরাত কিতাব নতুনভাবে লিখন বনী ইসরাঈলের নেতৃত্ব গ্রহণের কারণে ইহুদীদের একদল পথভ্রষ্ট লোক উযাইরকেআল্লাহর পুত্রহিসেবে আখ্যায়িত করে

 

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আল্লাহ তায়ালা হযরত উযাইর (আঃ)-কে মানব জাতির জন্যে নিদর্শন বানাবার উদ্দেশ্যে এরূপ করেছিলেন উযাইর (আঃ) যখন বনী ইসরাঈলের নিকট ফিরে এসেছিলেন তখন তাঁর পুত্ৰগণ সবাই ছিল বৃদ্ধ, অথচ তিনি যুবক কেননা যখন তাঁর মৃত্যু হয়েছিল তখন তাঁর বয়স ছিল চল্লিশ বছর একশ বছর পর আল্লাহ যখন তাঁকে জীবিত করলেন তখন (প্রথম) মৃত্যুকালের যৌবন অবস্থার উপরেই জীবিত করেছিলেন তাই তাঁর মাথার চুল কালই ছিল, কিন্তু এর পূর্বেই তাঁর পুত্র পৌত্রের চুল পেকে সাদা হয়ে গিয়েছিল তিনি ছিলেন যুবক অথচ তাঁর পুত্র ছিলেন বৃদ্ধ, লাঠির উপর ভর দিয়ে চলাফেরা করতেন পিতার বয়স চল্লিশ বছর আর পুত্রের বয়স নব্বই বছর অতিক্রম করেছে আল্লাহু আকবার আল্লাহ সকল বিষয়ের উপর ক্ষমতাবান

সূত্রঃআল বিদায়া ওয়ান নিহায়াকিতাব থেকে সংগৃহীত সংক্ষেপিতhttps://umarbinkhattab.medium.com//একশ-বছর-মৃত-থাকার-পর-উযাইর-আঃ-এর-পুনরায়-জীবিত-হওয়ার-ইতিহাস-cda0d8374091

 

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