By Amber Dance Real estate agents will tell you that a home’s most important feature is “location, location, location.” It’s similar in neuroscience: “Location is everything in the brain,” said Bosiljka Tasic (opens a new tab), a self-described “biological cartographer.” Brain injury in one spot could knock out memory; damage in another could interfere with personality. Neuroscientists and doctors are lost without a good map. Researchers have been mapping the brain for more than a century. By tracing cellular patterns that are visible under a microscope, they’ve created colorful charts and models that delineate regions and have been able to associate them with functions. In recent years, they’ve added vastly greater detail: They can now go cell by cell and define each one by its internal genetic activity. But no matter how carefully they slice and how deeply they analyze, their maps of the brain seem incomplete, muddled, inconsistent. For example, some large brain regions have been linked to many different tasks; scientists suspect that they should be subdivided into smaller regions, each with its own job. So far, mapping these cellular neighborhoods from enormous genetic datasets has been both a challenge and a chore. Recently, Tasic, a neuroscientist and genomicist at the Allen Institute for Brain Science, and her collaborators recruited artificial intelligence for the sorting and mapmaking effort. They fed genetic data from five mouse brains — 10.4 million individual cells with hundreds of genes per cell — into a custom machine learning algorithm. The program delivered maps that are a neuro-realtor’s dream, with known and novel subdivisions within larger brain regions. Humans couldn’t delineate such borders in several lifetimes, but the algorithm did it in hours. The authors published their methods (opens a new tab) in Nature Communications in October. © 2026 Simons Foundation

Keyword: Brain imaging; Development of the Brain
Link ID: 30117 - Posted: 02.11.2026

By Holly Barker Synaptic proteins degrade more slowly in aged mice than in younger mice, a new study finds. Microglia appear to unburden the neurons of the excess proteins, but that accumulation may turn toxic, the findings suggest. To function properly, cells need to clear out old and damaged proteins periodically, but that process stalls with age: Protein turnover is about 20 percent slower in the brains of older rodents than in youthful ones, according to an analysis of whole-brain samples. The new study is the first to probe protein clearance specifically in neurons in living animals. “Neurons face unique challenges to protein turnover,” says study investigator Ian Guldner, a postdoctoral fellow in Tony Wyss-Coray’s lab at Stanford University. For instance, their longevity prevents them from distributing old proteins among daughter cells. And unlike other proteins on the path to degradation, neuronal components must first navigate the axon—sometimes traveling as far as 1 meter, Guldner says. In the new study, Guldner and his colleagues engineered mice to express a modified version of aminoacyl-tRNA synthetase—a component of the protein synthesis machinery—in excitatory neurons. Every day for one week, mice of different ages received injections of chemically altered amino acids compatible only with that mutant enzyme. Neurons used the labeled amino acids to replenish proteins, enabling the group to track how quickly those proteins degraded over the subsequent two weeks. “The achievement lies in the technical advance, namely by being able to look at protein degradation and aggregation specifically in neuronal cells,” says F. Ulrich Hartl, director of the Max Planck Institute of Biochemistry, who was not involved in the study. © 2026 Simons Foundation

Keyword: Development of the Brain; Glia
Link ID: 30114 - Posted: 02.11.2026

Ian Sample Science editor People who have a couple of teas or coffees a day have a lower risk of dementia and marginally better cognitive performance than those who avoid the drinks, researchers say. Health records for more than 130,000 people showed that over 40 years, those who routinely drank two to three cups of caffeinated coffee or one to two cups of caffeinated tea daily had a 15-20% lower risk of dementia than those who went without. The caffeinated coffee drinkers also reported slightly less cognitive decline than those who opted for decaf and performed better on some objective tests of brain function, according to a report published in the Journal of the American Medical Association. The findings suggest habitual tea and coffee drinking is good for the brain, but the research cannot prove it, as caffeine drinkers may be less prone to dementia for other reasons. A similar link would arise if poor sleepers, who appear to have a greater risk of cognitive decline, steered clear of caffeine to get a better night’s rest. “Our study alone can’t prove causality, but to our knowledge, it is the best evidence to date looking at coffee and tea intake and cognitive health, and it is consistent with plausible biology,” said the lead author, Yu Zhang, who studies nutritional epidemiology at Harvard University. Coffee and tea contain caffeine and polyphenols that may protect against brain ageing by improving vascular health and reducing inflammation and oxidative stress, where harmful atoms and molecules called free radicals damage cells and tissues. Substances in the drinks could also work by improving metabolic health. Caffeine, for example, is linked to lower rates of type 2 diabetes, a known risk factor for dementia. © 2026 Guardian News & Media Limited

Keyword: Drug Abuse; Alzheimers
Link ID: 30113 - Posted: 02.11.2026

By Nora Bradford For more than a century, psychologists thought that the infant experience was, as the psychologist and philosopher William James famously put it, a “blooming, buzzing confusion.” But new research suggests babies are born with a surprisingly sophisticated neurological toolkit that can organize the visual world into categories and pick out the beat in a song. In the first of two new studies, neuroscientists managed a rare feat: performing functional MRI (fMRI) scans on more than 100 awake 2-month-old infants to see how their brains categorize visual objects. fMRI requires near-stillness, which makes scanning babies notoriously difficult. While the infants lay in the machines, images of animals, food, household objects and other familiar items appeared above their heads like “an IMAX for babies,” says Cliona O’Doherty, a developmental neuroscientist at Stanford University who conducted the work at Trinity College Dublin. “MRI is difficult even under ‘ideal’ circumstances when research participants can follow instructions to hold still,” says Scott Johnson, a developmental psychologist at UCLA who was not involved in the study. “Babies can’t take instruction, so these researchers must have the patience of saints.” The imaging showed that a brain region called the ventral visual cortex, responsible for recognizing what we see, already responded similarly to that of adults, O’Doherty and colleagues report February 2 in Nature Neuroscience. In both adults and 2-month olds, the ventral visual cortex’s activity is distinct for different categories of objects, pushing back against the traditional view that the brain gradually learns to distinguish between categories throughout development. © Society for Science & the Public 2000–2026

Keyword: Hearing; Development of the Brain
Link ID: 30111 - Posted: 02.07.2026

Peter Lukacs Popular wisdom holds we can ‘rewire’ our brains: after a stroke, after trauma, after learning a new skill, even with 10 minutes a day on the right app. The phrase is everywhere, offering something most of us want to believe: that when the brain suffers an assault, it can be restored with mechanical precision. But ‘rewiring’ is a risky metaphor. It borrows its confidence from engineering, where a faulty system can be repaired by swapping out the right component; it also smuggles that confidence into biology, where change is slower, messier and often incomplete. The phrase has become a cultural mantra that is easier to comprehend than the scientific term, neuroplasticity – the brain’s ability to change and form new neural connections throughout life. But what does it really mean to ‘rewire’ the brain? Is it a helpful shorthand for describing the remarkable plasticity of our nervous system or has it become a misleading oversimplification that distorts our grasp of science? After all, ‘rewiring your brain’ sounds like more than metaphor. It implies an engineering project: a system whose parts can be removed, replaced and optimised. The promise is both alluring and oddly mechanical. The metaphor actually did come from engineering. To an engineer, rewiring means replacing old and faulty circuits with new ones. As the vocabulary of technology crept into everyday life, it brought with it a new way of thinking about the human mind. Medical roots of the phrase trace back to 1912, when the British surgeon W Deane Butcher compared the body’s neural system to a house’s electrical wiring, describing how nerves connect to muscles much like wires connect appliances to a power source. By the 1920s, the Harvard psychologist Leonard Troland was referring to the visual system as ‘an extremely intricate telegraphic system’, reinforcing the comparison between brain function and electrical networks. © Aeon Media Group Ltd. 2012-2026.

Keyword: Learning & Memory; Development of the Brain
Link ID: 30108 - Posted: 02.04.2026

By Marla Vacek Broadfoot Nearly 1 in 8 dementia cases — about half a million nationwide — may be linked to insomnia. The new findings, reported December 27 in the Journals of Gerontology: Series A, add weight to growing evidence that sleep is a modifiable risk factor for dementia, akin to hearing loss and hypertension. The study does not establish a direct cause-and-effect relationship between insomnia and dementia for individuals, says Yuqian Lin, a data analyst at Massachusetts General Hospital in Boston. Rather, she says, it looks at the overall extent to which insomnia may contribute to dementia across the population. Lin and her colleagues analyzed data from the National Health and Aging Trends Study, or NHATS, a long-running survey of 5,900 U.S. adults ages 65 and older. Participants reported whether they had difficulty falling asleep, staying asleep or both. Dementia was identified using standard research tools that rely on cognitive testing and reports from family members or caregivers. To estimate the impact of insomnia on the population, Lin and her team calculated the proportion of dementia cases that could theoretically be prevented if insomnia-related sleep disturbances were eliminated. The calculation combined the prevalence of insomnia and dementia in the NHATS population with relative risk estimates drawn from recent large meta-analyses linking insomnia to dementia later in life. © Society for Science & the Public 2000–2026.

Keyword: Sleep; Alzheimers
Link ID: 30105 - Posted: 02.04.2026

By Ingrid Wickelgren The human brain is a vast network of billions of neurons. By exchanging signals to depress or excite each other, they generate patterns that ripple across the brain up to 1,000 times per second. For more than a century, that dizzyingly complex neuronal code was thought to be the sole arbiter of perception, thought, emotion, and behavior, as well as related health conditions. If you wanted to understand the brain, you turned to the study of neurons: neuroscience. But a recent body of work from several labs, published as a trio of papers in Science in 2025, provides the strongest evidence yet that a narrow focus on neurons is woefully insufficient for understanding how the brain works. The experiments, in mice, zebra fish, and fruit flies, reveal that the large brain cells called astrocytes serve as supervisors. Once viewed as mere support cells for neurons, astrocytes are now thought to help tune brain circuits and thereby control overall brain state or mood — say, our level of alertness, anxiousness, or apathy. Astrocytes, which outnumber neurons in many brain regions, have complex and varied shapes, and sometimes tendrils, that can envelop hundreds of thousands or millions of synapses, the junctions where neurons exchange molecular signals. This anatomical arrangement perfectly positions astrocytes to affect information flow, though whether or how they alter activity at synapses has long been controversial, in part because the mechanisms of potential interactions weren’t fully understood. In revealing how astrocytes temper synaptic conversations, the new studies make astrocytes’ influence impossible to ignore. “We live in the age of connectomics, where everyone loves to say [that] if you understand the connections [between neurons], we can understand how the brain works. That’s not true,” said Marc Freeman (opens a new tab), the director of the Vollum Institute, an independent neuroscience research center at Oregon Health and Science University, who led one of the new studies. “You can get dramatic changes in firing patterns of neurons with zero changes in [neuronal] connectivity.” © 2026 Simons Foundation

Keyword: Glia; Learning & Memory
Link ID: 30103 - Posted: 01.31.2026

By Azeen Ghorayshi Health Secretary Robert F. Kennedy Jr. has overhauled a panel that helps the federal government set priorities for autism research and social services, installing several members who have said that vaccines can cause autism despite decades of research that has failed to establish such a link. The panel, the Interagency Autism Coordinating Committee, was established in 2000 and has historically included autistic people, parents, scientists and clinicians, as well as federal employees, who hold public meetings to debate how federal funds should best be allocated to support people with autism. The 21 new public members selected by Mr. Kennedy include many outspoken activists, among them a former employee of a super PAC that supported Mr. Kennedy’s presidential campaign, a doctor who has been sued over dangerous heavy metal treatments for a young child with autism, a political economist who has testified against vaccines before a congressional committee, and parents who have spoken publicly about their belief that their children’s autism was caused by vaccines. The group, which also includes 21 government members across many federal agencies, will advise the federal government on how to prioritize the $2 billion allocated by Congress toward autism research and services over the next five years. Though it’s not yet clear what the committee will do — or what it can do, given that it serves only an advisory function — many longtime autism advocates and researchers said they were alarmed by the fact that the committee seemed stacked to advance Mr. Kennedy’s priorities on vaccines. “The new committee does not represent the autism community,” said Alison Singer, who served on the committee from 2007 to 2019. Ms. Singer, whose 28-year-old daughter has profound autism, is the head of the Autism Science Foundation. “It disproportionately, excruciatingly so, represents an extremely small subset of families who believe vaccines cause autism.” © 2026 The New York Times Company

Keyword: Autism
Link ID: 30100 - Posted: 01.31.2026

By Jackie Flynn Mogensen Everyone who menstruates and lives long enough experiences menopause in one form or another. Yet despite that, research into what happens during this natural cessation of menstruation and why is limited. Scientists know that menopause can cause a myriad of neurological symptoms, from hot flashes to poor sleep to depression. But what is going on in people’s brain during this period is still murky. Now new research offers clues to a link between menopause and changes in the brain’s gray matter, as well as anxiety and depression. Using brain scans from 10,873 people in the U.K., the researchers found that postmenopausal participants showed lower volumes of gray matter in the entorhinal cortex and hippocampus, which are involved in storing and retrieving memories, and in the anterior cingulate, which is involved in emotional regulation. The researchers also looked at whether hormone replacement therapy (HRT), a frontline but still rarely prescribed treatment for symptoms of menopause, might ameliorate some of these changes. Barbara Sahakian, a psychiatry professor at the University of Cambridge and an author of the study, explains that she and her colleagues theorized HRT might influence people’s experiences, tamping down their neurological symptoms, for instance. “That was the hypothesis,” she says, “but it didn’t seem to pan out completely that way.” They found that people who were treated with HRT for menopause showed lower volumes of gray matter in some areas of the brain than those who did not receive HRT. The HRT group also showed higher rates of anxiety and depression—importantly, Sahakian says their work doesn’t find that HRT treatment causes brain changes or menopause symptoms. Previous research suggests HRT prescribed during the run-up to menopause and early postmenopause can reduce anxiety, depending on the kind of HRT and dose, in at least some women. And a subsequent analysis found that participants who were prescribed HRT were more likely to have reported anxiety and depression before HRT treatment, the study explains. © 2025 SCIENTIFIC AMERICAN,

Keyword: Hormones & Behavior; Development of the Brain
Link ID: 30097 - Posted: 01.28.2026

Jon Hamilton At a press conference in late 2025, federal officials made some big claims about leucovorin, a prescription drug usually reserved for people on cancer chemotherapy. "We're going to change the label to make it available [to children with autism spectrum disorder]," said Dr. Marty Makary, commissioner of the Food and Drug Administration. "Hundreds of thousands of kids, in my opinion, will benefit." The Trump administration has suggested that leucovorin, a drug used in cancer treatment, might have some benefit for children with autism. Many researchers and families aren't so sure. The FDA still hasn't made that label change. Since Makary's remarks, though, more than 25,000 people have joined a Facebook group called Leucovorin for Autism. Most members appear to be parents seeking the drug for their autistic children. Also since the press conference, some doctors have begun writing off-label prescriptions for autistic children, against the advice of medical groups including the American Academy of Pediatrics. The buzz about leucovorin has led to a shortage of the drug. In response, the FDA is temporarily allowing imports of tablets that are made in Spain and sold in Canada, but not approved in the U.S. All of this is part of a familiar cycle for Dr. Paul Offit, who directs the vaccine education center at Children's Hospital of Philadelphia. Offit says he realized years ago that leucovorin's popularity was far ahead of the science. Jason Mazzola walks to work at The Residence at Natick South, an LCB Senior Living community in Natick, MA. August 22, 2024. © 2026 npr

Keyword: Autism
Link ID: 30095 - Posted: 01.28.2026

By Yasemin Saplakoglu On a remote island in the Indian Ocean, six closely watched bats took to the star-draped skies. As they flew across the seven-acre speck of land, devices implanted in their brains pinged data back to a group of sleepy-eyed neuroscientists monitoring them from below. The researchers were working to understand how these flying mammals, who have brains not unlike our own, develop a sense of direction while navigating a new environment. The research, published in Science, reported that the bats used a network of brain cells (opens a new tab) that informed their sense of direction around the island. Their “internal compass” was tuned by neither the Earth’s magnetic field nor the stars in the sky, but rather by landmarks that informed a mental map of the animal’s environment. These first-ever wild experiments in mammalian mapmaking confirm decades of lab results and support one of two competing theories about how an internal neural compass anchors itself to the environment. “Now we’re understanding a basic principle about how the mammalian brain works” under natural, real-world conditions, said the behavioral neuroscientist Paul Dudchenko (opens a new tab), who studies spatial navigation at the University of Stirling in the United Kingdom and was not involved in the study. “It will be a paper people will be talking about for 50 years.” Follow-up experiments that haven’t yet been published show that other cells critical to navigation encode much more information in the wild than they do in the lab, emphasizing the need to test neurobiological theories in the real world. Neuroscientists believe that a similar internal compass, composed of neurons known as “head direction cells,” might also exist in the human brain — though they haven’t yet been located. If they are someday found, the mechanism could shed light on common sensations such as getting “turned around” and quickly reorienting oneself. It might even explain why some of us are so bad at finding our way. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30094 - Posted: 01.24.2026

Heidi Ledford For decades, researchers have noted that cancer and Alzheimer’s disease are rarely found in the same person, fuelling speculation that one condition might offer some degree of protection from the other. Now, a study in mice provides a possible molecular solution to the medical mystery: a protein produced by cancer cells seems to infiltrate the brain, where it helps to break apart clumps of misfolded proteins that are often associated with Alzheimer’s disease. The study, which was 15 years in the making, was published on 22 January in Cell1 and could help researchers to design drugs to treat Alzheimer’s disease. “They have a piece of the puzzle,” says Donald Weaver, a neurologist and chemist at the Krembil Research Institute at the University of Toronto in Canada, who was not involved in the study. “It’s not the full picture by any stretch of the imagination. But it’s an interesting piece.” Alzheimer’s mystery Weaver has been interested in that puzzle ever since he began his medical training, when a senior pathologist made an offhand comment: “If you see someone with Alzheimer’s disease, they’ve never had cancer.” The remark stuck with Weaver over the years as he diagnosed thousands of people with Alzheimer’s disease. “I can’t remember a single one that has had cancer,” he says. Epidemiological data do not draw such a clear divide, but a 2020 meta-analysis of data from more than 9.6 million people found that cancer diagnosis was associated with an 11% decreased incidence of Alzheimer’s disease2. It has been a difficult relationship to unpick: researchers must control for a variety of external factors. For example, people might die of cancer before they are old enough to develop symptoms of Alzheimer’s disease, and some cancer treatments can cause cognitive difficulties, which could obscure an Alzheimer’s diagnosis. © 2026 Springer Nature Limited

Keyword: Alzheimers; Stress
Link ID: 30092 - Posted: 01.24.2026

By Pria Anand I loved literature before I loved medicine, and as a medical student, I often found that my textbooks left me cold, their medical jargon somehow missing the point of profound diseases able to rewrite a person’s life and identity. I was born, I decided, a century too late: I found the stories I craved, not in contemporary textbooks, but in outdated case reports, 18th- and 19-century descriptions of how the diseases I was studying might shape the life of a single patient. These reports were alive with vivid details: how someone’s vision loss affected their golf game or their smoking habit, their work or their love life. They were all tragedies: Each ended with an autopsy, a patient’s brain dissected to discover where, exactly, the problem lay, to inch closer to an understanding of the geography of the soul. To write these case studies, neurologists awaited the deaths and brains of living patients, robbing their subjects of the ability to choose what would become of their own bodies—the ability to write the endings of their own stories—after they had already been sapped of agency by their illnesses. Among these case reports was one from a forbidding state hospital in the north of Moscow: the story of a 19th-century Russian journalist referred to simply as “a learned man.” The journalist suffered a type of alcoholic dementia because of the brandy he often drank to cure his writer’s block and he developed a profound amnesia. He could not remember where he was or why. He could win a game of checkers but would forget that he had even played the minute the game ended. In the place of these lost memories, the journalist’s imagination spun elaborate narratives; he believed he had written an article when in fact he had barely begun to conceive it before he became sick, would describe the prior day’s visit to a far-off place when in actuality he had been too weak to get out of bed, and maintained that some of his possessions—kept in a hospital safe—had been taken from him as part of an elaborate heist. Sacks’ journals suggest he injected his own experiences into the stories of his patients. © 2026 NautilusNext Inc.,

Keyword: Attention; Learning & Memory
Link ID: 30089 - Posted: 01.21.2026

By Erin Garcia de Jesús A deck brush can be a good tool for the right task. Just ask Veronika, the Brown Swiss cow. Veronika uses both ends of a deck brush to scratch various parts of her body, researchers report January 19 in Current Biology. It’s the first reported tool use in a cow, a species that is often “cognitively underestimated,” the researchers say. Cows usually rub against trees, rocks or wooden planks to scratch, but Veronika’s handy tool allows her to reach parts of her body that she couldn’t otherwise, says Antonio Osuna-Mascaró, a cognitive biologist at the Messerli Research Institute of the University of Veterinary Medicine, Vienna. It’s unclear how the cow figured it out, but “somehow Veronika learned to use tools, and she’s doing something that other cows simply can’t.” Veronika, a pet cow that lives in a pasture on a small Austrian farm, picks up the brush by its handle with her tongue and twists her neck to place the brush where she needs it. Setting the brush in front of her in different orientations showed that she uses the hard, bristled end to target most areas, including the tough, thick skin on her back. She also uses the nonbristled end, slowly moving the handle over softer body parts such as her belly button and udder. Veronika uses different parts of a deck brush to reach various parts of her body. She uses the brush end to scratch large areas such as her thigh (top left) and back (top right). She uses the handle to scratch more delicate areas such as her navel flap (bottom left) and anus (bottom right). © Society for Science & the Public 2000–2026.

Keyword: Learning & Memory; Evolution
Link ID: 30088 - Posted: 01.21.2026

By Azeen Ghorayshi A scientific review of 43 studies on acetaminophen use during pregnancy concluded that there was no evidence that the painkiller increased the risk of autism or other neurodevelopmental disorders. “We found no clinically important increase in the risk of autism, A.D.H.D. or intellectual disability,” Dr. Asma Khalil, a professor of obstetrics and maternal fetal medicine at St. George’s Hospital, University of London, and the lead author of the report, said at a news briefing. The study was published on Friday in the British medical journal The Lancet. Acetaminophen, the active ingredient in Tylenol, remains “the first-line treatment that we would recommend if the pregnant women have pain or fever in pregnancy,” Dr. Khalil said. Studies that have examined a possible link between acetaminophen in pregnancy and a risk of neurodevelopmental disorders have produced conflicting data, with some finding no connection and others finding small increases in risk. The new review comes after President Trump told pregnant women during a news conference in September to “tough it out” and “fight like hell” not to take Tylenol, because he said the painkiller could cause autism in children. The message was delivered as part of a broader campaign by Health Secretary Robert F. Kennedy Jr. to try to identify the causes behind rising autism rates among children in the United States, zeroing in on the unproven risks of acetaminophen and long-discredited theories that vaccines cause autism. Medical groups worldwide, including the American College of Obstetricians and Gynecologists, quickly disputed the president’s statements. They argued that doctors already advised their pregnant patients to use acetaminophen judiciously, and cautioned that untreated fevers during pregnancy could cause health problems for the mother and the baby © 2026 The New York Times Company

Keyword: Autism
Link ID: 30085 - Posted: 01.17.2026

Lynne Peeples Sometimes the hardest part of doing an unpleasant task is simply getting started — typing the first word of a long report, lifting a dirty dish on the top of an overfilled sink or removing clothes from an unused exercise machine. The obstacle isn’t necessarily a lack of interest in completing a task, but the brain’s resistance to taking the first step. Now, scientists might have identified the neural circuit behind this resistance, and a way to ease it. In a study1 published today in Current Biology, researchers describe a pathway in the brain that seems to act as a ‘motivation brake’, dampening the drive to begin a task. When the team selectively suppressed this circuit in macaque monkeys, goal-directed behaviour rebounded. “The change after this modulation was dramatic,” says study co-author Ken-ichi Amemori, a neuroscientist at Kyoto University in Japan. The motivation brake, which can be particularly stubborn for people with certain psychiatric conditions, such as schizophrenia and major depressive disorder, is distinct from the avoidance of tasks driven by risk aversion in anxiety disorders. Pearl Chiu, a computational psychiatrist at Virginia Tech in Roanoke, who was not involved in the study, says that understanding this difference is essential for developing new treatments and refining current ones. “Being able to restore motivation, that’s especially exciting,” she says. Motivated macaques Previous work on task initiation has implicated a neural circuit connecting two parts of the brain known as the ventral striatum and ventral pallidum, both of which are involved in processing motivation and reward2,3,4. But attempts to isolate the circuit’s role have fallen short. Electrical stimulation, for example, inadvertently activates downstream regions, affecting motivation, but also anxiety. © 2026 Springer Nature Limited

Keyword: Learning & Memory; Emotions
Link ID: 30079 - Posted: 01.14.2026

By Sujata Gupta Chimps ages 2 to 5 are more likely than older chimps to free-fall from tree limbs in the forest canopies or leap wildly from branch to branch, researchers report January 7 in iScience. Past age 5, those dangerous canopy behaviors decrease by roughly 3 percent each year. Among humans, teens are the real daredevils. They are, for instance, more likely than other children to break bones and die from injuries. But human toddlers might behave as recklessly as chimp toddlers were it not for parents and caregivers putting the kibosh on all the fun — and broken bones, says biologist Lauren Sarringhaus of James Madison University in Harrisonburg, Va. “If humans scaled back their oversight, our kids would be way more daredevilish.” Humans and chimpanzees show markedly different caregiving patterns, say Sarringhaus and others. Chimp moms largely parent alone. Dads don’t help. Nor, typically, do grandmothers, older siblings or other group members. Chimpanzees cling to their moms for the first five years of life, but by age 2 or so, they begin to explore more independently. Moms can’t readily help kids swinging high up in the air. By comparison, the presence of alloparents, or caregivers beyond the parents, are a defining feature of human groups, Sarringhaus says. In modern times, alloparents have come to include teachers and coaches for a plethora of supervised after-school activities. Nowadays, many developmental experts in the Western world have been decrying the rise of intensive or helicopter parenting in which kids spend less time unsupervised and playing outside than those in generations past. “It’s a really exciting avenue of research of how caregiving influences risk-taking behavior. There’s not a lot of research out there addressing this point,” says Lou Haux, a psychologist and primatologist at the Max Planck Institute for Human Development in Berlin, who was not involved with the study. © Society for Science & the Public 2000–2026

Keyword: Development of the Brain; Evolution
Link ID: 30078 - Posted: 01.14.2026

By Azeen Ghorayshi Academic research labs across the country are working to find biological markers that can predict whether a child is at risk of developing autism. And companies are rushing to turn the findings into commercial tests, despite limited evidence to back their validity, raising concerns that their results could mislead desperate parents. They include one test that examines a strand of hair to rule out an autism diagnosis in babies as young as one month old. Two other tests just entered the market. One promises to predict autism risk based on skin cells collected as early as days after birth. Another looks for the presence of certain antibodies in a mother’s blood to determine whether her children, or babies that she might have in the future, are at risk of developing autism. For decades, clinicians and parents have hoped for a biological test that could help determine if a child has autism. The push to commercialize investigators’ early research has accelerated as Health Secretary Robert F. Kennedy Jr. has elevated the neurodevelopmental disorder into a national political priority, creating new funding for autism research and reviving long-discredited theories about autism and vaccines. But the new tests, largely aimed as a screening tool for the general population, are not yet reliable enough to be offered commercially, outside scientists familiar with the tests say, especially in a landscape where families are already inundated with incorrect or unverified information about autism. None of the tests has gone through large experimental trials or had its validity evaluated by a regulatory agency. “All of these tests are interesting hypotheses,” said Joseph Buxbaum, a neuroscientist at the Icahn School of Medicine at Mount Sinai who studies the genetics of autism. But they are “absolutely not at a point for any kind of clinical use,” he said. © 2026 The New York Times Company

Keyword: Autism
Link ID: 30076 - Posted: 01.10.2026

Ian Sample Science editor New therapies for Alzheimer’s disease should target a particular gene linked to the condition, according to researchers who said most cases would never arise if its harmful effects were neutralised. The call to action follows the arrival of the first wave of drugs that aim to treat Alzheimer’s patients by removing toxic proteins from the brain. While the drugs slow the disease down, the benefits are minor, and they have been rejected for widespread use by the UK’s National Institute for Health and Care Excellence (Nice). In searching for alternative therapies, scientists at UCL say drug developers should focus on two risk-raising variants of a gene named Apoe. Therapies designed to block the variants’ impact have “vast potential” for preventing the disease, they claim. Dr Dylan Williams, a genetic epidemiologist at UCL, said: “Most Alzheimer’s disease cases would not arise without the contribution of just this single gene: Apoe. We need to think about it as a direct target. Almost all potential Alzheimer’s cases could benefit from Apoe-related interventions.” More than half a million people in the UK, and more than 40 million worldwide, are living with Alzheimer’s disease, the most common form of dementia. Several genes contribute to Alzheimer’s risk and lifestyle is important too: smoking, obesity, diabetes, high blood pressure and cholesterol all make the disease more likely. Williams and his colleagues analysed medical records from more than 450,000 people of European ancestry to calculate how much Alzheimer’s disease arose due to different variants of the Apoe gene. People inherit two copies of the gene – one from each parent – and there are three main variants: Apoe2, 3 and 4. © 2026 Guardian News & Media Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 30074 - Posted: 01.10.2026

By Holly Barker In early life, astrocytes help to mold neural pathways in response to the environment. In adulthood, however, those cells curb plasticity by secreting a protein that stabilizes circuits, according to a mouse study published last month in Nature. “It’s a new and unique take on the field,” says Ciaran Murphy-Royal, assistant professor of neuroscience at Montreal University, who was not involved in the study. Most research focuses on how glial cells drive plasticity but “not how they apply the brakes,” he says. Astrocytes promote synaptic remodeling during the development of sensory circuits by secreting factors and exerting physical control—in humans, a single astrocyte can clamp onto 2 million synapses, previous studies suggest. But the glial cells are also responsible for shutting down critical periods for vision and motor circuits in mice and fruit flies, respectively. It has been unclear whether this loss of plasticity can be reversed. Some evidence hints that modifying the neuronal environment—through matrix degradation or transplantation of young neurons—can rekindle flexibility in adult brains. The new findings confirm that in adulthood, plasticity is only dormant, rather than lost entirely, says Nicola Allen, professor of molecular neurobiology at the Salk Institute for Biological Studies and an investigator on the new paper. “Neurons don’t lose an intrinsic ability to remodel, but that process is controlled by secreted factors in the environment,” she says. Specifically, astrocytes orchestrate that dormancy by releasing CCN1, a protein that stabilizes circuits by prompting the maturation of inhibitory neurons and glial cells, Allen’s team found. The findings suggest that astrocytes have an active role in stabilizing adult brain circuits. © 2026 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 30069 - Posted: 01.07.2026