Katie Kavanagh Why are we able to remember emotional events so well? According to a study published today in Nature1, a type of cell in the brain called an astrocyte is a key player in stabilizing memories for long-term recall. Astrocytes were thought to simply support neurons in creating the physical traces of memories in the brain, but the study found that they have a much more active role — and can even be directly triggered by repeated emotional experiences. The researchers behind the finding suggest that the cells could be a fresh target for treating memory conditions such as those associated with post-traumatic stress disorder and Alzheimer’s disease. “We provide an answer to the question of how a specific memory is stored for the long term,” says study co-author Jun Nagai, a neuroscientist at RIKEN Center for Brain Science in Wako, Japan. By studying astrocytes, Nagai said, the study identifies how the brain selectively filters important memories at the cellular level. Stable memories Nagai and his colleagues focused on the question of memory stabilization: how a short-term memory becomes more permanent in the brain. Previous research had found physical traces of memories in neuronal networks in brain regions such as the hippocampus and amygdala2. But it was unclear how these ‘engrams’ were stored in the brain as lasting memories after repeated exposure to the same stimulus. To dig deeper, the researchers developed a method for measuring activation patterns in astrocytes across a whole brain of a mouse as it completes a memory task. They measured the upregulation of a gene called Fos — an early marker of cell activity that is associated with the physical traces of memories in the brain3. © 2025 Springer Nature Limited

Keyword: Learning & Memory; Emotions
Link ID: 29975 - Posted: 10.18.2025

By Yasemin Saplakoglu The pillow is cold against your cheek. Your upstairs neighbor creaks across the ceiling. You close your eyes; shadows and light dance across your vision. A cat sniffs at a piece of cheese. Dots fall into a lake. All this feels very normal and fine, even though you don’t own a cat and you’re nowhere near a lake. You’ve started your journey into sleep, the cryptic state that you and most other animals need in some form to survive. Sleep refreshes the brain and body in ways we don’t fully understand: repairing tissues, clearing out toxins and solidifying memories. But as anyone who has experienced insomnia can attest, entering that state isn’t physiologically or psychologically simple. To fall asleep, “everything has to change,” said Adam Horowitz (opens a new tab), a research affiliate in sleep science at the Massachusetts Institute of Technology. The flow of blood to the brain slows down, and the circulation of cerebrospinal fluid speeds up. Neurons release neurotransmitters that shift the brain’s chemistry, and they start to behave differently, firing more in sync with one another. Mental images float in and out. Thoughts begin to warp. “Our brains can really rapidly transform us from being aware of our environments to being unconscious, or even experiencing things that aren’t there,” said Laura Lewis (opens a new tab), a sleep researcher at MIT. “This raises deeply fascinating questions about our human experience.” It’s still largely mysterious how the brain manages to move between these states safely and efficiently. But studies targeting transitions both into and out of sleep are starting to unravel the neurobiological underpinnings of these in-between states, yielding an understanding that could explain how sleep disorders, such as insomnia or sleep paralysis, can result when things go awry. Sleep has been traditionally thought of as an all-or-nothing phenomenon, Lewis said. You’re either awake or asleep. But the new findings are showing that it’s “much more of a spectrum than it is a category.” © 2025 Simons Foundation

Keyword: Sleep
Link ID: 29974 - Posted: 10.18.2025

Jon Hamilton In Alzheimer's, brain cells die too soon. In cancer, dangerous cells don't die soon enough. That's because both diseases alter the way cells decide when to end their lives, a process called programmed cell death. "Cell death sounds morbid, but it's essential for our health," says Douglas Green, who has spent decades studying the process at St. Jude Children's Research Hospital in Memphis, Tennessee. For example, coaxing nerve cells to live longer could help people with Alzheimer's disease, Parkinson's disease or ALS (Lou Gehrig's disease), he says, while getting tumor cells to die sooner could help people with cancer. So researchers have been searching for disease treatments that "modify or modulate the tendency of a cell to die," Green says. One of these researchers is Randal Halfmann at the Stowers Institute for Medical Research in Kansas City, Missouri. He has been studying immune cells that self-destruct when they come into contact with molecules that present a threat to the body. "They have to somehow recognize that [threat] in this vast array of other complex molecules," he says, "and then within minutes, kill themselves." They do this much the way a soldier might dive on a grenade to save others' lives. Halfmann's team has been focusing on special proteins inside cells that can trigger this process. When these proteins recognize molecules associated with a virus or some other pathogen, he says, "they implode." The proteins crumple and begin linking up with other crumpled proteins to form a structure called a "death fold" polymer. That starts a chain reaction of polymerization that ultimately kills the cell. Halfmann's team knew this process takes a burst of energy. But they couldn't locate the source. © 2025 npr

Keyword: Alzheimers; Apoptosis
Link ID: 29973 - Posted: 10.18.2025

By Michele Cohen Marill Like many first-time mothers, Lisette Lopez-Rose thought childbirth would usher in a time of joy. Instead, she had panic attacks as she imagined that something bad was going to happen to her baby, and she felt weighed down by a sadness that wouldn’t lift. The San Francisco Bay Area mother knew her extreme emotions weren’t normal, but she was afraid to tell her obstetrician. What if they took her baby away? At about six months postpartum, she discovered an online network of women with similar experiences and ultimately opened up to her primary care doctor. “About two months after I started medication, I started to feel like I was coming out of a deep hole and seeing light again,” she says. Today, Lopez-Rose works at Postpartum Support International, coordinating volunteers to help new mothers form online connections. About one in eight US women go through a period of postpartum depression, making it among the most common complications of childbirth. It typically occurs in the first few weeks after delivery, when there’s a sudden drop in the reproductive hormones estrogen and progesterone. As scientists unravel chemical and genetic changes caused by those shifting hormones, they are discovering new ways to diagnose and treat postpartum depression, and even ways to identify who is at risk for it. Graph showing a steady rise in levels of estradiol and progesterone after conception and then a very steep drop-off right after birth. The hormones estradiol (the main form of estrogen) and progesterone rise during pregnancy. In some women, their sudden drop after childbirth triggers the onset of postpartum depression. The first-ever drug for postpartum depression, containing a derivative of progesterone, received US Food and Drug Administration approval in 2019. That marked a new approach to the disorder. This winter, in another major advance, a San Diego-based startup company will launch a blood test that predicts a pregnant woman’s risk of postpartum depression with more than 80 percent accuracy. © 2025 Annual Reviews

Keyword: Depression; Hormones & Behavior
Link ID: 29972 - Posted: 10.18.2025

Vladyslav Vyazovskiy After decades of research, there is still no clearly articulated scientific consensus on what sleep is or why it exists. Yet whenever sleep comes up as a topic of discussion, it is quickly reduced to its necessity and importance. Popular media remind us of what can, and will, go wrong if we do not sleep enough, and serve up some handy tips on how to overcome insomnia. Discussed exclusively in utilitarian terms, we are force-fed the idea that sleep exists solely for our immediate benefit. Is this really all we ever want to know about a third of our existence? Sleep is perhaps the biggest blind spot, or the longest blind stretch, if you will, of our life. Naturally, the health and societal implications of sleep are huge: from technogenic disasters caused by tiredness, to sleep deprivation as a form of torture or weapon of war, and to sleep disorders, some of which inflict so much suffering that they compete with chronic pain. However, in my opinion, to say sleep is important is to miss the point entirely. Sleep is the single most bizarre experience that happens to all of us, against our will, every day. The disconnect between old questions about sleep that have remained open for centuries and new, increasingly sophisticated technologies applied to solve them is ever growing. The predominant view is that sleep provides some sort of restoration for the brain or the body: what goes awry – out of balance – in waking is almost magically recalibrated by sleep. At the centre of this narrative is the individual-who-sleeps, a lone castaway, locked in a permanent, inexorable cycle of sleeping and waking, without hope of breaking free (except in death). From the moment of opening one’s eyes, the clock starts ticking, and there is a price to pay for every minute of wakeful time, measured precisely in proportion to the transgression of staying awake. Like a snake eating its own tail, waking and sleep consume each other in an endless cycle, without beginning or end. There is no mercy, and lack of sleep can be paid back only by sleep. The image of burning a candle at both ends endures. Despite vast technological advances in recent years, exponential growth in our understanding of nature and the cosmos, and major breakthroughs in biology and medicine, there is still no unified theory of sleep. I find myself pondering whether it is time to step back and seek a different angle. Medieval manuscript illustration depicting people sleeping in three beds, with two standing figures in dialogue beside them, and an ornate floral border. © Aeon Media Group Ltd. 2012-2025.

Keyword: Sleep
Link ID: 29971 - Posted: 10.15.2025

By Grace Lindsay Neuroscientists have spent decades characterizing the types of information represented in the visual system. In some of the earliest studies, scientists recorded neural activity in anesthetized animals passively viewing stimuli—a setup that led to some of the most famous findings in visual neuroscience, including the discovery of orientation tuning by David Hubel and Torsten Wiesel. But passive viewing, whether while awake or anesthetized, sidesteps one of the more intriguing questions for vision scientists: How does the rest of the brain use this visual information? Arguably, the main reason for painstakingly characterizing the information in the visual system is to understand how that information drives intelligent behavior. Connecting the dots between how visual neurons respond to incoming stimuli and how that information is “read out” by other brain regions has proven nontrivial. It is not clear that we have the necessary experimental and computational tools at present to fully characterize this process. To get a sense for what it might take, I asked 10 neuroscientists what experimental and conceptual methods they think we’re missing. Decoding is a common approach for understanding the information present in the visual system and how it might be used. But decoding on its own—training classifiers to read out prespecified information about a visual stimulus from neural activity patterns—cannot tell us how the brain uses information to perform a task. This is because the decoders we use for data analysis do not necessarily match the downstream processes implemented by neural circuits. Indeed, there are pieces of information that can reliably be read out from the visual system but aren’t accessible to participants during tasks. Primary visual cortex contains information about the ocular origin of a stimulus, for example, but participants are not able to accurately report this information. © 2025 Simons Foundation

Keyword: Vision
Link ID: 29970 - Posted: 10.15.2025

By John Branch Photographs by Sophie Park It starts with a tingle, a tremor, a sense that something is off. Dr. Sue Goldie doesn’t recognize the symptoms at first. Maybe she ignores them, wishes them away. It is 2021. She is 59, in the prime of a long teaching career at Harvard. She has just immersed herself in the sport of triathlon. One coach notes something off with her running cadence. Another wonders why her left arm isn’t fully lifting out of the water. A trainer sees a slight tremor. The first time Sue races, she feels a strange vibration, like an internal tremble. Then Sue sees it herself: Twitching fingers on her left hand. Tests reveal it is Parkinson’s, the incurable neurological disease that robs its victims of their motor skills, and sometimes their minds, one extinguished neuron at a time. Parkinson’s doesn’t always alter life spans, but it always upends lives. The diagnosis elicits a storm of emotions, but also raises questions, both pragmatic and deep, that have consumed Sue since. At what point, if ever, do I have to say something? Who needs to know? What do I reveal and what do I conceal? And, most profoundly: Does a diagnosis have to be an identity? For nearly four years, she keeps her diagnosis from most Harvard administrators, colleagues and students, worried about what it will do to her reputation. She grows more comfortable revealing herself away from work, in the world of triathlon. “I feel very strongly that I should be able to disclose this when I want, how I want, and it’s under my control,” she tells me last year. But Parkinson’s does not wait. Maybe others don’t notice the physical signs, not yet. They don’t see her in the early morning, shuffling off-balance to the bathroom before her medications kick in, a daily reminder that Parkinson’s was not something she dreamed last night. Maybe they don’t see the pill boxes in her purse, the exposed feeling she gets when the dopamine medications wear off, the persistent worry behind her cheerful disposition. Her symptoms are worsening. Disguising them is exhausting. Starting today, she is Sue with Parkinson’s. © 2025 The New York Times Company

Keyword: Parkinsons
Link ID: 29969 - Posted: 10.15.2025

Rachel Fieldhouse During ageing, men experience a greater reduction in volume across more regions of the brain than women do, according to a longitudinal study published today in the Proceedings of the National Academy of Sciences1. The authors suggest this means that age-related brain changes do not explain why women are more frequently diagnosed with Alzheimer’s disease than men are. “It’s really important that we understand what happens in the healthy brain so that we can better understand what happens when people get these neurodegenerative conditions,” says Fiona Kumfor, a clinical neuropsychologist at the University of Sydney, Australia. This study adds to scientists’ understanding of typical brain ageing, she adds. Nearly twice as many women are diagnosed with Alzheimer’s disease as men, and ageing is the biggest risk factor for the disease. This has prompted research into age-related sex differences in the brain. “If women’s brains declined more, that could have helped explain their higher Alzheimer’s prevalence,” says co-author Anne Ravndal, a PhD student at the University of Oslo. Previous research investigating sex differences in brain ageing has shown mixed results, Ravndal adds. Several studies have found that men experience greater loss of total grey matter and hippocampus size compared with women, whereas other work has reported a sharper decline of grey matter in women. Brain scans The latest study included more than 12,500 magnetic resonance imaging (MRI) brain scans from 4,726 people — at least two scans per person, taken an average of three years apart — who did not have Alzheimer’s disease or any cognitive impairments and were control participants in 14 larger data sets. The researchers compared how the individuals’ brain structures changed over time, looking at factors including the thickness of grey matter and the size of areas that are associated with Alzheimer’s disease, such as the hippocampus, which is essential to memory. © 2025 Springer Nature Limited

Keyword: Alzheimers; Sexual Behavior
Link ID: 29968 - Posted: 10.15.2025

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