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

Jon Hamilton Research on conditions like autism, schizophrenia and even brain cancer increasingly relies on clusters of human cells called brain organoids. These pea-size bits of neural tissue model aspects of human brain development as they grow for months and even years in a lab. They also make many people uneasy, in part because the brain is so closely tied to our sense of self. A group of scientists, ethicists, patient advocates and journalists met for two days in Northern California this fall to discuss how scientists, and society, should proceed. Among the questions: Is it okay to place human organoids in an animal's brain? Can organoids feel pain? Can they become conscious? Who, if anyone, should regulate this research? "We are talking about an organ that is at the seat of human consciousness. It's the seat of personality and who we are," says Insoo Hyun, a bioethicist at the Museum of Science, Boston, who attended the meeting. "So it's reasonable to be especially careful with the kind of experiments we're doing," he says. Societal issues by the sea The event was hosted by Dr. Sergiu Pașca, a prominent organoid researcher whose lab at Stanford University used the technology to develop a potential treatment for a rare cause of autism and epilepsy. © 2026 npr

Keyword: Development of the Brain
Link ID: 30065 - Posted: 01.03.2026

Jon Hamilton SCOTT SIMON, HOST: And it has been a banner year in brain science. We've learned that lifestyle changes really can keep your brain young and that electrical pulses can help with rheumatoid arthritis, and that LSD can relieve anxiety and depression. Scientists even managed to replicate a human brain network that carries pain signals. NPR science correspondent Jon Hamilton joins us. Jon, thanks so much for being with us. JON HAMILTON, BYLINE: Hi, Scott. SIMON: Well, let's start with that brain network. What does it do? HAMILTON: Well, it recreates the pathway that carries brain signals from, say, your fingertip to the part of the brain that says, you know, ouch, that hurts. And that pathway has several sort of relay stations along the way. So a team at Stanford decided to recreate those stations using brain organoids, which are these pea-sized clumps of human brain cells that can mimic different types of brain tissue. In this case, the scientists used four different organoids representing the four types of nerve cells that relay pain signals. And when they put these organoids together in a dish, they spontaneously wired up to form the entire pain pathway. SIMON: That sounds extraordinary, but I have to ask - can you tell if the organoids in a dish felt anything? HAMILTON: You can, and the way you can tell is with red hot chile peppers. The scientists took the organoid that was acting like a nerve ending, and they exposed it to chemicals like the ones in hot chile peppers, you know, that burn your mouth. Here is Dr. Sergiu Pasca explaining what happened. SERGIU PASCA: We discovered that if you start adding some of these compounds that are inducing inflammatory responses of pain, then you start seeing that information traveling. The neurons that sends these signals get activated. And they transmit that information to the next station and the next station, all the way to the cortex. HAMILTON: There's good reason for this research, too. It's part of an effort to help people with chronic pain. SIMON: Let's move on to the whole question of trying to keep your brain young. Like, can you really do that? HAMILTON: Why, yes, you can. At least according to a really big study funded by the Alzheimer's Association. This study involved about 2,000 people in their 60s and 70s, and they were all pretty sedentary, at least at the beginning. Half of these people spent two years getting aerobic exercise at the gym, eating a Mediterranean diet, watching their blood pressure and taking part in this really demanding cognitive training program. The other people - they were just told to eat better and exercise more. At the end of the study, the people in the hardcore program did better on tests of thinking and memory. And their scores were actually as good as those from people a year or two younger than they were. © 2025 npr

Keyword: Miscellaneous; Development of the Brain
Link ID: 30063 - Posted: 12.31.2025

By Ivan Amato The standard sperm-meets-egg story posits that sperm cells are hardly more than bundles of shrink-wrapped DNA with tails. Their mission is simple: Deliver a father’s genes into a mother’s egg for sexual reproduction. Just about all other aspects of a developing embryo, including its cellular and environmental components, have nothing to do with dad. Those all come from mom. But nearly two decades of studies from multiple independent labs threaten to rewrite that story. They suggest that dad’s gametes shuttle more than DNA: Within a sperm’s minuscule head are stowaway molecules, which enter the egg and convey information about the father’s fitness, such as diet, exercise habits and stress levels, to his offspring. These non-DNA transfers may influence genomic activity that boots up during and after fertilization, exerting some control over the embryo’s development and influencing the adult they will become. The findings, so far largely described in mouse models, could end up changing the way we think about heredity. They suggest “that what we do in this life affects the next generation,” said Qi Chen (opens a new tab), a reproductive and developmental biologist at the University of Utah Medical School who is among the pioneers of this research. In other words: What a father eats, drinks, inhales, is stressed by or otherwise experiences in the weeks and months before he conceives a child might be encoded in molecules, packaged into his sperm cells and transmitted to his future kid. The researchers have largely zeroed in on RNA molecules, those short-lived copies of DNA that reflect genetic activity at a given time. It’s a tantalizing notion. But the mechanistic details — how experience is encoded, how it’s transferred from sperm to egg, and whether and how it affects a developing embryo — are not easy to unpack, especially given the challenges of conducting research in human subjects. For this reason, and because of the potentially textbook-rewriting implications of the findings, researchers, including those spearheading the work, are cautious about overselling their results. © 2025 Simons Foundation

Keyword: Epigenetics; Development of the Brain
Link ID: 30061 - Posted: 12.31.2025

Amelia Hill One in 10 people in the UK aged 70 and older could have Alzheimer’s-like changes in their brain, according to the clearest, real-world picture of how common the disease’s brain changes are in ordinary, older people. The detection of the proteins linked with the disease is not a diagnosis. But the findings indicate that more than 1 million over-70s would meet Nice’s clinical criteria for anti-amyloid therapy – a stark contrast to the 70,000 people the NHS has estimated could be eligible if funding were available. Experts, including those from Alzheimer’s Research UK, have said the findings from the first-ever population-based research into the disease have huge potential for early and accurate diagnosis. “High-quality studies like this are crucial to enhancing our understanding of how blood tests for Alzheimer’s could be used in clinical practice,” said David Thomas, the head of policy and public affairs at Alzheimer’s Research UK. “We need to generate more evidence so we can use these tests in the NHS.” The lead author of the research, conducted by King’s College London, Stavanger University hospital and the University of Gothenburg, said the findings could be a “gamechanger in the understanding of the disease”. The findings also challenge some long-held assumptions about dementia, including the idea that it is mainly a disease that mainly affects women. Dag Aarsland, a professor of old age psychiatry at the Institute of Psychiatry, Psychology and Neuroscience at King’s College London and the study’s lead author, said: “In an ageing global population, the assessment and treatment of dementia presents a significant challenge. Our study used a simple blood test to establish changes that contribute to cognitive impairment in those with dementia.” © 2025 Guardian News & Media Limited

Keyword: Alzheimers; Development of the Brain
Link ID: 30057 - Posted: 12.20.2025

By Allison Parshall The human brain has 86 billion neurons connected by roughly 100 trillion synapses, making it one of the most complex objects in the known universe. Each year neuroscientists make fascinating, important and downright strange discoveries about how this resilient structure works, and 2025 didn’t disappoint. Here are 10 of the most fascinating brain discoveries of this year for your own brain to noodle on. Brain scans of thousands of people revealed that the human brain has five distinct eras, with turning points in the way it is organized occurring at age nine, 32, 66 and 83. Across each of these stages—for example, the “adolescent” period between age nine and 32—people’s brains tend to experience the same types of changes. You don’t remember being a newborn or even a toddler. Adults’ earliest memories tend to start around preschool and no earlier. But recent research suggests that your brain was making memories back then; you just don’t have access to them now. A study of the infant hippocampus, a deep-brain structure crucial for memory formation, found that it can store memories once babies are around one year old—though it’s not clear why we can’t recall them once we grow up. Untangling Alzheimer’s Researchers also discovered another oddity of newborn babies’ brain: they have very high levels of a protein that, in adults, indicates Alzheimer’s disease. Tau proteins help to stabilize brain cells’ structure, but they can undergo chemical changes that lead them to become tangled up, a process linked to Alzheimer’s. The fact that healthy newborn brains have high levels of these proteins, which later decrease, suggests that these detrimental changes in adults could be avoided or reversed. Fluorescence light micrograph of neural progenitor cells. Astrocytes have been stained orange and neural progenitor cells green. Cell nuclei are blue © 2025 SCIENTIFIC AMERICAN,

Keyword: Brain imaging; Learning & Memory
Link ID: 30054 - Posted: 12.20.2025

By Sara Talpos It’s been more than a decade since scientists first started publishing papers on neural organoids, the small clusters of cells grown in labs and designed to mimic various parts of the human brain. Since then, organoids have been used to study everything from bipolar disorder and Alzheimer’s disease, to tumors and parasitic infections. Because these new tools have the potential to reduce the use of animals in research — a goal of the current Trump administration — the field’s future may be more financially secure than other areas of scientific research. In September, for example, the federal government announced an $87 million investment into organoid research broadly. Matthew Owen brings a unique perspective to this emerging field. As a philosopher of mind, he focuses on trying to understand both what the mind is and how it relates to the body and the brain. He draws on the work of historical philosophers and applies some of their ideas to modern-day science. In 2020, as a visiting scholar in a neuroscience lab at McGill University, he was introduced to researchers working with organoids. Owen, who also does research in bioethics, wanted to help them address a perhaps unsettling question: Could these miniature cell clusters ever develop consciousness? Some experts believe that organoid consciousness is not likely to happen anytime in the near future, if at all. Still, certain experiments are prompting the question. In 2022, for example, researchers, including Brett Kagan of the Australian start-up Cortical Labs, published a paper explaining how they had taught their lab-grown brain cells to play a ping-pong-like video game. (Because the cells were placed in a single layer, the structures were not technically organoids, though they are expected to have similar capabilities.) In the process, the authors wrote, the tiny cell clusters displayed “sentience.” Undark recently spoke with Owen about this particular experiment and about his own writing on organoids.

Keyword: Consciousness; Development of the Brain
Link ID: 30048 - Posted: 12.13.2025

Alison Abbott For decades, neuroscientists focused almost exclusively on only half of the cells in the brain. Neurons were the main players, they thought, and everything else was made up of uninteresting support systems. By the 2010s, memory researcher Inbal Goshen was beginning to question that assumption. She was inspired by innovative molecular tools that would allow her to investigate the contributions of another, more mysterious group of cells called astrocytes. What she discovered about their role in learning and memory excited her even more. At the beginning, she felt like an outsider, especially at conferences. She imagined colleagues thinking, “Oh, that’s the weird one who works on astrocytes,” says Goshen, whose laboratory is at the Hebrew University of Jerusalem. A lot of people were sceptical, she says. But not any more. A rush of studies from labs in many subfields are revealing just how important these cells are in shaping our behaviour, mood and memory. Long thought of as support cells, astrocytes are emerging as key players in health and disease. “Neurons and neural circuits are the main computing units of the brain, but it’s now clear just how much astrocytes shape that computation,” says neurobiologist Nicola Allen at the Salk Institute for Biological Studies in La Jolla, California, who has spent her career researching astrocytes and other non-neuronal cells, collectively called glial cells. “Glial meetings are now consistently oversubscribed.” As far back as the nineteenth century, scientists could see with their simple microscopes that mammalian brains included two major types of cell — neurons and glia — in roughly equal numbers. © 2025 Springer Nature Limited

Keyword: Glia
Link ID: 30038 - Posted: 12.03.2025