By Siddhant Pusdekar Taste and smell are so intimately connected that a whiff of well-loved foods evokes their taste without any conscious effort. Now, brain scans and machine learning have for the first time pinpointed the region responsible for this sensory overlap in humans, a region called the insula, researchers report September 12 in Nature Communications. The findings could explain why people crave certain foods or are turned away from them, says Ivan de Araujo, a neuroscientist at Max Planck Institute for Biological Cybernetics in Tübingen, Germany. Smell and taste become associated from the moment we bite into something, says Putu Agus Khorisantono, a neuroscientist at Karolinska Institutet in Stockholm. Some food chemicals activate sweet, salty, sour, bitter or umami taste receptors on the tongue. Others travel through the roof of the mouth, activating odor receptors in the back of the nose. These “retronasal odors” are what distinguish mangoes from peaches, for example. Both taste mostly sour, Khorisantono says, “but it’s really the aroma that differentiates them.” The brain combines these signals to create our sense of flavor, but scientists have struggled to identify where this happens in the brain. In the new study, Khorisantono and colleagues gave 25 people drops of beverages designed to activate only their taste or retronasal receptors, while scanning brain activity over multiple sessions. Previously, the participants had learned to associate the combination of smells and tastes with particular flavors. © Society for Science & the Public 2000–2025.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29967 - Posted: 10.11.2025

By Jennie Erin Smith The marine whiff of ambergris. The citrusy tang of grapefruit. The must of “corked” wine. The human nose can detect a virtually infinite palette of odors, some at vanishingly low concentrations. But puzzlingly, our bodies only use about 400 receptor proteins to interpret them. Now, fragrance researchers in Switzerland have landed on a new way to study the proteins in the laboratory—and their results, they say, challenge a foundational theory of how smell works. For decades, scientists have struggled to get cells commonly used in laboratory settings to express the genes that encode olfactory receptors (ORs), proteins primarily found on neurons in our nasal cavities. Using a process they describe today in Current Biology, researchers at the Swiss fragrance and flavorings company Givaudan say they have tweaked lab-friendly cells into readily expressing ORs. The result was an in vitro system for identifying specific ORs, including those that strongly respond to molecules in ambergris, grapefruit, and corked wine. The Swiss group’s discovery, other olfaction researchers say, stands to make ORs much easier to study. But more controversially, the group also claims to have observed patterns of receptor activity that call into question combinatorial coding, a long-standing hypothesis of olfaction that helped Linda Buck and Richard Axel win a Nobel Prize in 2004. Combinatorial coding holds that multiple ORs act in concert to pick up different parts of an odorant molecule, creating patterns or codes that are recognized by the brain. Beyond that, says neuroscientist Joel Mainland of the Monell Chemical Senses Center, the model is “pretty vague on the details.” It has been hard to test, because olfactory neurons can’t be cultured in the lab. Determining which OR detects which odorant required extensive tests in rodents, and it’s not ideal “to have to sacrifice an animal each time you want to do an experiment,” says Claire de March, a chemist at CNRS, the French national research agency. As a result, investigators were left with many so-called orphan receptors whose ligands, or binding molecules, are unknown. © 2025 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Development of the Brain
Link ID: 29966 - Posted: 10.11.2025

By David Adam In February of this year, George Mentis and his colleagues published data from a small clinical trial they said showed that degraded motor neurons aren’t irreparable. In the study, electrical stimulation to the spine in three people with spinal muscular atrophy (SMA) appeared to resuscitate lost motor neurons, the authors said, as well as restore some of the cellular processes needed to activate muscle. “It was incredible,” says Mentis, professor of pathology and cell biology (in neurology) at Columbia University. “We’re unleashing or tapping on the potential of dysfunctional neurons to show plasticity.” The authors wrote that the results showed it was possible to “effectively rescue motor neuron function” and that the electrical stimulation had rebuilt neuronal circuitry and reversed—at least for a while—some degeneration. Mentis and his team think their results are coalescing into a theory, even if they don’t fully understand it yet. The researchers are essentially altering the electrical properties of the motor neurons so they start to behave better and closer to normal, says Genís Prat-Ortega, a postdoctoral associate in the Rehab Neural Engineering Labs at the University of Pittsburgh and an investigator on the study. “The motor neurons change and repair,” he says. “Somehow, we are reversing a neurodegenerative process.” Not everyone is so sure. Tim Hagenacker, professor of neurology at the University of Duisburg-Essen, says rebuilding the neural circuit is “not entirely convincing” as an explanation for the study’s results. He thinks that “other cell types play a crucial co-role” in restoring neuronal plasticity or that dysfunctional motor neurons could exist in some form of hibernation. © 2025 Simons Foundation

Keyword: ALS-Lou Gehrig's Disease ; Regeneration
Link ID: 29965 - Posted: 10.11.2025

Violeta Ruiz On 25 November 1915, the American newspaper The Review published the extraordinary case of an 11-year-old boy with prodigious mathematical abilities. Perched on a hill close to a set of railroad tracks, he could memorise all the numbers of the train carriages that sped by at 30 mph, add them up, and provide the correct total sum. What was remarkable about the case was not just his ability to calculate large numbers (and read them on a moving vehicle), but the fact that he could barely eat unassisted or recognise the faces of people he met. The juxtaposition between his supposed arrested development and his numerical facility made his mathematical feats even more impressive. ‘How can you account for it?’ asked the article’s author. The answer took the form of a medical label: the boy was what 19th-century medicine termed an ‘idiot savant’. He possessed an exceptional talent, despite a profound impairment of the mental faculties that affected both his motor and social skills. A century after The Review relayed the prodigious child’s mathematical abilities, trying to understand ‘how they do it’ still drives psychological research into savantism or ‘savant syndrome’ to this day. The SSM Health Treffert Centre in Wisconsin – named after Darold Treffert (1933-2020), one of the leading experts in the field – defines the savant phenomenon as ‘a rare condition in which persons with various developmental disorders, including autistic disorder, have an amazing ability and talent’. Today, savantism is largely comprehended through the lens of neurodivergence, since the association between savantism and autism is strong: roughly one in 10 people with autism exhibit some savant skills, while savantism in the absence of autism is much rarer. Psychological studies by Simon Baron-Cohen and Michael Lombardo, for example, have focused on the neurological basis of ‘systemising’, where exceptional mathematical or musical skills exist among people diagnosed with autism: such people are ‘hypersystemisers’, that is, they are especially good at identifying ‘laws, rules, and/or regularities’. It is believed that their brain’s systemising mechanisms are ‘tuned to very high levels’, making them acutely sensitive to sensory input and also capable of intense attentional focus and rule-learning. © Aeon Media Group Ltd. 2012-2025.

Keyword: Intelligence; Learning & Memory
Link ID: 29964 - Posted: 10.11.2025

Mohana Basu The opioid class of drugs includes heroin and morphine. Unlike those drugs, which are derived from naturally occurring opium, nitazenes are synthesized from scratch in a laboratory. The first nitazenes were developed as painkillers in the 1950s, but were never approved for medical use because they carried a high risk of dangerous side effects such loss of consciousness, coma and death. But since 2019, there has been a rise in the reported use of nitazenes, according to the World Drug Report 2025, which was released in June. In 2023, the report states, 20 different nitazenes were seized by authorities across 28 countries and reported to the United Nations Office on Drugs and Crime (UNODC) Early Warning Advisory on New Psychoactive Substances. Nitazenes can be as much as 500 times more potent than opium-derived drugs. For example, butonitazene is 2.5 times more potent than heroin, whereas isotonitazene and etonitazene are 250 and 500 times more potent, respectively. This means that just a tiny amount can be deadly. In the United Kingdom, there were 179 confirmed deaths from nitazene overdoses in the year to 31 May 2024. And reports suggest that thousands of people might have died from nitazene overdoses in the United States since 2019. In Australia, researchers note that the unpredictable presence of nitazenes in various drugs is increasing the risk of overdose in the country. Most nitazene overdoses are unintentional, says Suzanne Nielsen, an addiction researcher at Monash University in Melbourne, Australia. Overdose tends to occur when nitazenes are sold as other drugs, such as heroin, oxycodone and MDMA (also known as ecstasy). Overdoses can be treated with naloxone, a drug that has long been used to treat other opioid overdoses. More awareness of this among drug users and their families could help save lives, Nielsen adds. © 2025 Springer Nature Limited

Keyword: Drug Abuse
Link ID: 29963 - Posted: 10.11.2025

By Pam Belluck Before dawn on a March morning, Doug Whitney walked into a medical center 2,000 miles from home, about to transform from a mild-mannered, bespectacled retiree into a superhuman research subject. First, a doctor inserted a needle into his back to extract cerebral spinal fluid — “liquid gold,” a research nurse called it for the valuable biological information it contains. Then, the nurse took a sample of his skin cells. After that came an injection of a radioactive tracer followed by a brain scan requiring him to lie still for 30 minutes with a thermoplastic mask over his face. Then, another tracer injection and another brain scan. During his three-day visit to the center, at Washington University School of Medicine in St. Louis, he also had cognitive assessments, neurological evaluations and blood draws that extracted multiple tubes for analysis. For 14 years now, Mr. Whitney has been the one-person focus of exceptionally detailed scientific investigation, for which he travels periodically to St. Louis from his home in Port Orchard, Wash. It is not because he is ill. It is because he was supposed to be ill. Mr. Whitney, 76, is a scientific unicorn with potential to provide answers about one of the world’s most devastating diseases. He has a rare genetic mutation that essentially guaranteed he would develop Alzheimer’s disease in his late 40s or early 50s and would likely die within a decade. His mother and nine of her 13 siblings developed Alzheimer’s and died in the prime of their lives. So did his oldest brother, and other relatives going back generations. It is the largest family in the United States known to have an Alzheimer’s-causing mutation. “Nobody in history had ever dodged that bullet,” Mr. Whitney said. © 2025 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 29962 - Posted: 10.08.2025

Asif Ghazanfar Picture someone washing their hands. The water running down the drain is a deep red. How you interpret this scene depends on its setting, and your history. If the person is in a gas station bathroom, and you just saw the latest true-crime series, these are the ablutions of a serial killer. If the person is at a kitchen sink, then perhaps they cut themselves while preparing a meal. If the person is in an art studio, you might find resonance with the struggle to get paint off your hands. If you are naive to crime story tropes, cooking or painting, you would have a different interpretation. If you are present, watching someone wash deep red off their hands into a sink, your response depends on even more variables. How we act in the world is also specific to our species; we all live in an ‘umwelt’, or self-centred world, in the words of the philosopher-biologist Jakob von Uexküll (1864-1944). It’s not as simple as just taking in all the sensory information and then making a decision. First, our particular eyes, ears, nose, tongue and skin already filter what we can see, hear, smell, taste and feel. We don’t take in everything. We don’t see ultraviolet light like a bird, we don’t hear infrasound like elephants and baleen whales do. Second, the size and shape of our bodies determine what possible actions we can take. Parkour athletes – those who run, vault, climb and jump in complex urban environments – are remarkable in their skills and daring, but sustain injuries that a cat doing the exact same thing would not. Every animal comes with a unique bag of tricks to exploit their environment; these tricks are also limitations under different conditions. Third, the world, our environment, changes. Seasons change, what animals can eat therefore also changes. If it’s the rainy season, grass will be abundant. The amount of grass determines who is around to eat it and therefore who is around to eat the grass-eaters. Ultimately, the challenge for each of us animals is how to act in this unstable world that we do not fully apprehend with our senses and our body’s limited degrees of freedom. There is a fourth constraint, one that isn’t typically recognised. Most of the time, our intuition tells us that what we are seeing (or hearing or feeling) is an accurate representation of what is out there, and that anyone else would see (or hear or feel) it the same way. But we all know that’s not true and yet are continually surprised by it. It is even more fundamental than that: you know that seemingly basic sensory information that we are able to take in with our eyes and ears? It’s inaccurate. How we perceive elementary colours, ‘red’ for example, always depends on the amount of light, surrounding colours and other factors. In low lighting, the deep red washing down the sink might appear black. A yellow sink will make it look more orange; a blue sink may make it look violet. © Aeon Media Group Ltd. 2012-2025.

Keyword: Vision; Attention
Link ID: 29961 - Posted: 10.08.2025

By Zunnash Khan You can inherit a talent for athletics from your parents, but physical fitness—which is determined in large part by exercise and other lifestyle choices—doesn’t seem like it can be inherited. But now, a paper suggests male mice that exercise can pass their newly gained fitness on to male offspring. If the same holds true in humans, the researchers say, fathers could help improve the health of any future children by staying in shape themselves. The study is the latest example of how traits can be passed to the next generation not through the DNA in genes, but via snippets of DNA’s chemical cousin, RNA, packed as cargo into sperm cells and delivered to the embryo. “You’re having the animals exercise and then you’re getting the transmission of the phenotype to the next generation,” says Colin Conine, an epigeneticist at the University of Pennsylvania who was not involved in the work. “I think that’s interesting.” Most heritable traits are passed from parents to their offspring through the DNA in genes. (Inheriting genes for a large lung volume might increase your chances of becoming a runner, for example.) But things you experience or learn—such as the ability to make a soufflé or read Sanskrit—aren’t encoded into genes and can’t be passed on this way. Still, recent advances in biology have shown there’s more to heritability than genes. Some acquired traits can alter the chemical packaging of the DNA and affect the properties of the offspring, a phenomenon known as epigenetics. Recent research has identified so-called microRNAs (miRNAs) in sperm cells as one way epigenetic information can be passed on. For example, scientists have shown that diet, stress, and toxins can have an impact on the embryo through miRNAs. A 2021 paper suggested male mice can confer a susceptibility to depression to their offspring this way. © 2025 American Association for the Advancement of Science.

Keyword: Epigenetics
Link ID: 29960 - Posted: 10.08.2025

By Meghie Rodrigues Babies start processing language before they are born, a new study suggests. A research team in Montreal has found that newborns who had heard short stories in foreign languages while in the womb process those languages similarly to their native tongue. The study, published in August in Nature Communications Biology, is the first to use brain imaging to show what neuroscientists and psychologists had long suspected. Previous research had shown that fetuses and newborns can recognize familiar voices and rhythms and even that they prefer their native language soon after birth. But these findings come mostly from behavioral cues—sucking patterns, head turns or heart rate changes—rather than direct evidence from the brain. “We cannot say babies ‘learn’ a language prenatally,” says Anne Gallagher, a neuropsychologist at the University of Montreal and senior author of the study. What we can say, she adds, is that neonates develop familiarity with one or more languages during gestation, which shapes their brain networks at birth. The research team recruited 60 people for the experiment, all of them about 35 weeks into their pregnancy. Of those, 39 exposed their fetuses to 10 minutes of prerecorded stories in French (their native language) and another 10 minutes of the same stories in either Hebrew or German at least once every other day until birth. These languages were chosen because their acoustic and phonological properties are very distinctfrom French and from each other, explains co-lead author Andréanne René, a Ph.D. candidate in clinical neuropsychology at the University of Montreal. The other 21 participants were part of the control group; their fetuses were exposed to French in their natural environments, with no special input. © 2025 SCIENTIFIC AMERICAN

Keyword: Language; Development of the Brain
Link ID: 29959 - Posted: 10.08.2025

Natasha May Health reporter Women carry a higher genetic risk of depression, a new study has found. Claiming to be the largest genetic study to date on sex differences in major depression, the research published on Wednesday in Nature Communications has found 16 genetic variants linked to depression in women and eight in men. The study, led by Australia’s QIMR Berghofer Medical Research Institute, showed a large proportion of the variants associated with depression were shared between sexes, but there was a “higher burden of genetic risk in females which could be due to female-specific variants”. Dr Brittany Mitchell, a senior researcher at QIMR Berghofer’s genetic epidemiology lab, said “we already know that females are twice as likely to suffer from depression in their lifetime than males”. “And we also know that depression looks very different from one person to another. Until now, there hasn’t been much consistent research to explain why depression affects females and males differently, including the possible role of genetics.” The study acknowledged explanations have been put forward spanning behavioural, environmental and biological domains, including men being less likely to seek help leading to under-diagnosis, and environmental exposures such as women being more frequently exposed to sexual abuse and interpersonal violence. The study stated that together these factors highlight the need for a “multifaceted approach” to understanding the underlying mechanisms of depression but proposed that a “key component of the biological mechanisms underlying these disparities could be differences in genetics”. © 2025 Guardian News & Media Limited

Keyword: Depression; Genes & Behavior
Link ID: 29958 - Posted: 10.08.2025

By Catherine Offord Neuroscientists have been studying synapses, the fundamental junctions that allow rapid communication between neurons, for well over a century. But now, a research team has identified a different set of neuronal connections in the brain—one that might bypass synapses altogether, the group reports today in Science. Using high-resolution images of mouse and human brains, the researchers documented a network of tubes, each about 3 micrometers long and just a few hundred nanometers thick, connecting neurons to one another. In mouse cells, the team found evidence of neuron-to-neuron transfer of electrical signals via these nanotubes, and even the passage of proteins linked to Alzheimer’s disease. “We’ve been looking at the brain forever now, and every once in a while, a surprise comes along,” says Lary Walker, a neuroscientist and professor emeritus at Emory University who was not involved in the work. Although there’s still a lot to pin down about these nanotubes’ basic biology, he suggests the discovery could have wide implications for scientists’ understanding of neuronal communication and disease. Researchers already knew some cells form nanotubes. In a 2004 Science paper, a team in Germany described tiny channels that emerged spontaneously between rat kidney cells in a dish and allowed the transfer of organelles. Studies since then have documented these so-called tunneling nanotubes (TNT) in a variety of cell and tissue types, and have linked their presence to processes including organ development, tissue repair, and the spread of viruses within the body. Recent research has identified TNTs forming between neurons and microglia, the brain’s immune cells, and hinted that they have important functions in brain health and disease. But scientists have struggled to find such conduits connecting neurons to one another in the mammalian brain. The search is particularly tricky because neurons’ branching ends, or dendrites, form a tangled mass with one another, and because researchers lack molecular markers distinguishing nanotubes from other cell structures. © 2025 American Association for the Advancement of Science.

Keyword: Development of the Brain; Brain imaging
Link ID: 29957 - Posted: 10.04.2025

By Devin Effinger, Melissa Herman Psychedelics show growing promise as treatments for a variety of psychiatric diseases. Clinical trials have demonstrated rapid and persistent improvements in major depressive disorder, for example, sparking interest among both psychiatrists and neuroscientists. However, the clinical use of psychedelics is challenging; the drugs induce prolonged visual hallucinations and must be administered and monitored by trained staff, which creates barriers in terms of their availability and accessibility. Clinical trials are also challenging. Psychedelics produce profound subjective effects that make it impossible to properly placebo-control or effectively blind participants. And given the widespread cultural fascination with these drugs, it’s difficult to remove expectancy bias—if someone strongly believes a drug will work, that can influence their perception and reporting of their outcome. Moreover, these drugs are typically delivered and tested in combination with psychotherapy. Discerning whether any treatment effects stem from the drug versus the psychotherapy, as well as the role of therapy in clinical response, is a point of debate within the field. To help resolve some of these issues, we need to better understand the neurobiological mechanisms involved. Human imaging studies have shown that some psychedelics, such as psilocybin, produce long-lasting alterations in global connectivity and negative affect. But to design more effective versions of these drugs, we need to uncover their underlying mechanisms of action at greater resolution—something that is possible only through preclinical research at the level of molecular, cellular and systems neuroscience. © 2025 Simons Foundation

Keyword: Drug Abuse; Depression
Link ID: 29956 - Posted: 10.04.2025

By Ellen Barry Around the time of the pandemic, I began to notice something happening in my social circle. A close friend, then in her early 50s, got a diagnosis of attention deficit hyperactivity disorder. She described it as a profound relief, releasing her from years of self-blame — about missed deadlines and lost receipts, but also things that were deeper and more complicated, like her sensitivity to injustice. Listen to this article with reporter commentary Something similar happened to a co-worker, and a cousin in his 30s, and an increasing number of people I met covering mental health. It wasn’t always A.D.H.D. For some of them, the revelation was a diagnosis of autism spectrum disorder: After years of inarticulate unease in social situations, they felt freed by the framework of neurodivergence, and embraced by the community that came along with it. Since then I’ve heard accounts from people who received midlife diagnoses of binge eating disorder, post-traumatic stress disorder, anxiety. Nearly all of them said the diagnosis provided relief. Sometimes it led to an effective treatment. But sometimes, simply identifying the problem — putting a name to it — seemed to help. Lately, it seems as if we never stop talking about the rising rates of chronic diseases, among them autism, A.D.H.D., depression, anxiety and PTSD. Health Secretary Robert F. Kennedy Jr. has pointed to these trends as evidence that Americans are “the sickest people in the world,” and has set about upending whole swaths of our public health system in search of causes, like vaccines or environmental toxins. But much of what we’re seeing is a change in diagnostic practices, as we apply medical labels to ever milder versions of disease. There are many reasons for this: The shame that once accompanied many disorders has lifted. Screening for mental health problems is now common in schools. Social media gives us the tools to diagnose ourselves. And clinicians, in a time of mental health crisis, see an opportunity to treat illnesses early. © 2025 The New York Times Company

Keyword: ADHD; Autism
Link ID: 29955 - Posted: 10.04.2025

Gemma Conroy Whether it’s dancing the tango or playing the guitar, engaging in a creative pastime can slow brain ageing, according to a study of dancers, musicians, artists and video game players from multiple countries. The analysis used brain clocks — models that measure the difference between a person’s chronological age and the age their brain appears to be — to assess whether creative activities help to maintain neurological youth. In brain regions that are most susceptible to ageing, engaging in creative activities increased connections with different areas of the brain. Although experts had ‘younger’ brains than their less-experienced counterparts did, even learning a creative skill from scratch had an anti-ageing effect on the brain. The findings were published on 3 October in Nature Communications1. Song and dance Previous studies suggest that engaging in creative activities can help to keep the brain young and foster emotional well-being. But few have investigated the biological basis of these brain benefits or what drives them, says study co-author Agustín Ibáñez, a neuroscientist at Adolfo Ibáñez University in Santiago, Chile. “There is really poor mechanistic evidence,” he says. How fast are you ageing? Ordinary brain scans reveal the pace To address this gap, Ibáñez and his colleagues created brain clocks using neuroimaging data of brain activity taken from 1,240 participants across 10 countries. These machine-learning models used functional connectivity, a measure of how brain regions work together, to estimate brain age. The researchers then applied their brain clocks to 232 tango dancers, musicians, visual artists and video game players of different ages and experience levels to calculate their ‘brain age gap’ — the difference between their predicted brain age and their actual age. © 2025 Springer Nature Limited

Keyword: Alzheimers; Learning & Memory
Link ID: 29954 - Posted: 10.04.2025

By Keith Schneider Jane Goodall, one of the world’s most revered conservationists, who earned scientific stature and global celebrity by chronicling the distinctive behavior of wild chimpanzees in East Africa — primates that made and used tools, ate meat, held rain dances and engaged in organized warfare — died on Wednesday in Los Angeles. She was 91. Her death, while on a speaking tour, was confirmed by the Jane Goodall Institute, whose U.S. headquarters are in Washington, D.C. When not traveling widely, she lived in Bournemouth, on the south coast of England, in her childhood home. Dr. Goodall was 29 in the summer of 1963 when National Geographic magazine published her 7,500-word, 37-page account of the lives of primates she had observed in the Gombe Stream Chimpanzee Reserve in what is now Tanzania. The National Geographic Society had been financially supporting her field studies there. The article, with photographs by Hugo van Lawick, a Dutch wildlife photographer whom she later married, also described Dr. Goodall’s struggles to overcome disease, predators and frustration as she tried to get close to the chimps, working from a primitive research station along the eastern shore of Lake Tanganyika. On the scientific merits alone, her discoveries about how wild chimpanzees raised their young, established leadership, socialized and communicated broke new ground and attracted immense attention and respect among researchers. Stephen Jay Gould, the evolutionary biologist and science historian, said her work with chimpanzees “represents one of the Western world’s great scientific achievements.” On learning of Dr. Goodall’s documented evidence that humans were not the only creatures capable of making and using tools, Louis Leakey, the paleoanthropologist and Dr. Goodall’s mentor, famously remarked, “Now we must redefine ‘tool,’ redefine ‘man,’ or accept chimpanzees as humans.” © 2025 The New York Times Company

Keyword: Evolution; Animal Communication
Link ID: 29953 - Posted: 10.04.2025

By Yasemin Saplakoglu From Santiago Ramón y Cajal’s hand came branches and whorls, spines and webs. Now-famous drawings by the neuroanatomist in the late 19th and early 20th centuries showed, for the first time, the distinctiveness and diversity of the fundamental building blocks of the mammalian brain that we call neurons. In the century or so since, his successors have painstakingly worked to count, track, identify, label and categorize these cells. There is now a dizzying number of ways to put neurons in buckets, often presented in colorful, complex brain cell atlases. With such catalogs, you might organize neurons based on function by separating motor neurons that help you move from sensory neurons that help you see or number neurons that help you estimate quantities. You might distinguish them based on whether they have long axons or short ones, or whether they’re located in the hippocampus or the olfactory bulb. But the vast majority of neurons, regardless of function, form or location, fall into one of two fundamental categories: excitatory neurons that trigger other neurons to fire and inhibitory neurons that stop others from firing. Maintaining the correct proportion of excitation to inhibition is critical for keeping the brain healthy and harmonious. “Imbalances in either direction can be really catastrophic,” said Mark Cembrowski (opens a new tab), a neuroscientist at the University of British Columbia, or lead to neurological conditions. Too much excitation and the brain can produce epileptic seizures. Too little excitation can be associated with conditions such as autism. Neuroscientists are working to uncover how these two classes of cells work — and specifically, how they interact with a rarer third category of cells that influence their behavior. These insights could eventually help reveal how to restabilize networks that get out of balance, which can even occur as a result of normal aging. © 2025 Simons Foundation

Keyword: Epilepsy; Attention
Link ID: 29952 - Posted: 10.01.2025

Tobi Thomas Health and inequalities correspondent Scientists have linked the impact of living in an unequal society to structural changes in the brains of children – regardless of individual wealth – for the first time. A study of more than 10,000 young people in the US discovered altered brain development in children from wealthy and lower-income families in areas with higher rates of inequality, which were also associated with poorer mental health. The data was gathered from the Adolescent Brain Cognitive Development study and published in the journal Nature Mental Health. Researchers at King’s College London, Harvard University, and the University of York then measured inequality within a particular US state by scoring how evenly income is measured. States with higher levels of inequality included New York, Connecticut, California and Florida, while Utah, Wisconsin, Minnesota and Vermont were more equal. MRI scans were analysed to study the surface area and thickness of regions in the cortex, including those involved in higher cognitive functions including memory, emotion, attention and language. Connections between different regions of the brain were also analysed by the scans, where changes in blood flow indicate brain activity. The research found that children living in areas with higher levels of societal inequality, including socioeconomic imbalances and deprivation for example, were linked to having a reduced surface area of the brain’s cortex, and altered connections between multiple regions of the brain. The findings, the first to reveal the impact societal inequality has on the structures of the brain, also provided evidence that the impacted neurodevelopment might relate to future mental health and cognitive function. Notably, these brain changes in children were seen regardless of their economic background. © 2025 Guardian News & Media Limited

Keyword: Development of the Brain; Learning & Memory
Link ID: 29951 - Posted: 10.01.2025

By Lauren Schneider Bad news for mouse poker players: Their facial movements offer “tells” about decision-making variables that the animals track without always acting on them, according to a study published today in Nature Neuroscience. The findings indicate that “cognition is embodied in some surprising ways,” says study investigator Zachary Mainen, a researcher at the Champalimaud Center for the Unknown. And this motor activity holds promise as a noninvasive bellwether of cognitive patterns. The study builds on mounting evidence that mouse facial expressions are not solely the result of a task’s motor demands and provides a “very clear” illustration of how this movement reflects cognitive processes, says Marieke Schölvinck, a researcher at the Ernst Strüngmann Institute for Neuroscience, who was not involved with the work. For years, mouse facial movements have mostly served as a way for researchers to gauge an animal’s pain levels. Now, however, machine-learning technology has made it possible to analyze this fine motor behavior in greater detail, says Schölvinck, who has investigated how facial expressions reflect inner states in mice and macaques. Evidence that mouse facial expressions correspond to emotional states inspired the new analysis, according to Fanny Cazettes, who conducted the experiments as a postdoctoral researcher in Mainen’s lab. She says she wondered what other ways the “internal, private thoughts of animals” might manifest on their faces. Two variables shape most mouse decisions over different foraging sites, the team found: the number of failures at a site (unrewarded licks from a source of sugar water) and the site’s perceived value (the difference between reward and failure). © 2025 Simons Foundation

Keyword: Emotions; Evolution
Link ID: 29950 - Posted: 10.01.2025

By Katarina Zimmer Few mammals sleep as deeply as the ampurta. When the blonde, rat-like marsupial returns to its burrow after a night of hunting in the Australian desert, it drifts into a slumber known as torpor. While many other mammals quickly burn through their energy reserves in order to maintain stable body temperatures as they fall asleep, ampurtas allow their bodies to cool down to as low as 50 degrees Fahrenheit, saving energy critical to survival in this harsh desert environment. “I’ve held some when they’re in torpor, and they feel like they’ve been in a freezer,” says wildlife ecologist Dympna Cullen of the University of New South Wales in Sydney. Instead of using their own energy to warm up again, upon waking, the animals drag themselves to the mouths of their burrows to soak up the morning sun. Some scientists say this energy-saving trick helped the ampurta—once thought doomed to extinction—to make a comeback during a severe drought. In what they call a “rare and hopeful conservation signal,” the authors document in a new study in Biological Conservation how, during a two-year drought that lasted from 2017 to 2019—one of the region’s harshest droughts on record—the vulnerable marsupials actually significantly extended their range, reclaiming a large chunk of lost habitat. “Everything crashes during a drought,” Cullen says, “so it was quite unexpected that not only were [ampurtas] increasing in abundance but also increasing their area of occupancy by quite a significant amount during a drought.” Like many other Australian mammals, the ampurta—the Aboriginal name for Dasycercus hillieri or the crest-tailed mulgara—once seemed like it might vanish from the Earth. Rabbits brought to Australia by European colonists in the 19th century wreaked ecological havoc on the continent. They ravaged Australia’s vegetation, robbing small native herbivores of cover and food, including some of the ampurta’s prey, such as smaller mammals. The rabbit boom also fed the spread of non-native foxes and cats, which picked off ampurtas and other native wildlife. But in 1996, the Australian government released a rabbit-killing virus to quash rabbit populations, which allowed some native species populations to recover. Ampurtas were downgraded from endangered in the mid-1990s to “vulnerable” in 2013, and eventually to a species of “least concern.” © 2025 NautilusNext Inc.,

Keyword: Sleep; Evolution
Link ID: 29949 - Posted: 10.01.2025

Lynne Peeples From TikTok videos touting mouth tape and weighted blankets, to magazines ranking insomnia-curbing pillows, sleep advice is everywhere. And it’s no wonder. People all over the world complain of insomnia and not getting enough sleep, driving a market for sleep aids worth more than US$100 billion annually. But scientists warn that online hacks and pricey tools aren’t always effective. And failed attempts to remedy the situation could have negative effects, says Andrew McHill, a circadian scientist at Oregon Health & Science University in Portland. “It could discourage people from finding help, and things could get worse,” he says. Instead, researchers point to the lessons coming from circadian science, which over the past five decades has exposed a network of biological clocks throughout the body. This timekeeping machinery ensures that physiological systems are primed to do the right things at the right times — such as defend against pathogens, digest food and sleep. But circadian clocks don’t cycle precisely on their own. To stay in sync and function optimally, they need regular calibration from sunlight, daily routines and other cues. Modern life doesn’t often cooperate. People spend much of their time indoors. They eat late into the night. They shift sleep schedules between workdays and weekends, effectively jet-lagging themselves. The toll is steep. In the short term, circadian disruption and insufficient sleep can reduce cognition, mood and reaction time. In the long term, they can increase risks of infections, diabetes, depression, dementia, cancer, heart disease and premature death. For better sleep and overall health, McHill and other scientists emphasize three basics: contrasting light and dark, consolidating mealtimes and keeping sleep times consistent. “Simply taking a walk outside during the day and reducing our light exposure in the evening could have great effect,” says McHill. © 2025 Springer Nature Limited

Keyword: Sleep
Link ID: 29948 - Posted: 10.01.2025