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

By Pam Belluck A recently recognized form of dementia is changing the understanding of cognitive decline, improving the ability to diagnose patients and underscoring the need for a wider array of treatments. Patients are increasingly being diagnosed with the condition, known as LATE, and guidelines advising doctors how to identify it were published this year. LATE is now estimated to affect about a third of people 85 and older and 10 percent of those 65 and older, according to those guidelines. Some patients who have been told they have Alzheimer’s may actually have LATE, dementia experts say. “In about one out of every five people that come into our clinic, what previously was thought to maybe be Alzheimer’s disease actually appears to be LATE,” said Dr. Greg Jicha, a neurologist and an associate director of the University of Kentucky’s Sanders-Brown Center on Aging. “It can look like Alzheimer’s clinically — they have a memory problem,” Dr. Jicha said. “It looks like a duck, walks like a duck, but then it doesn’t quack, it snorts instead. ” On its own, LATE, shorthand for Limbic-predominant age-related TDP-43 encephalopathy, is usually less severe than Alzheimer’s and unfolds more slowly, said Dr. Pete Nelson, an associate director of the Sanders-Brown Center, who helped galvanize efforts to identify the disorder. That can be reassuring to patients and their families. But there is no specific treatment for LATE. Also, many older people have more than one type of dementia pathology, and when LATE occurs in conjunction with Alzheimer’s, it exacerbates symptoms and speeds decline, he said. © 2025 The New York Times Company

Keyword: Alzheimers
Link ID: 30033 - Posted: 11.29.2025

By Angie Voyles Askham Rats, like people, jump at the chance to repeat a task that rewards them handsomely, but they are less eager when the reward is paltry: They learn from past experience and update their behavior accordingly. That learning is shaped by the hormone estradiol, according to a new study. And when estradiol levels peak during the estrus cycle, female rats adapt their behavior in response to reward size more quickly than they do during other phases—and faster than males overall. The female rats also have a larger release of dopamine in response to an unexpected reward, along with reduced expression of dopamine transporters in a reward center of their brain after the hormone peaks, the new work shows. “It’s giving mechanistic insight into how estrogen modulates reinforcement learning—all the way down to the molecular mechanism,” says Ilana Witten, professor of neuroscience at Princeton University and Howard Hughes Medical Institute investigator, who was not involved in the study. The team behind the new work used a task that measures how much an animal values an anticipated reward: Thirsty rats poke their nose into a central port and then listen for a tone that indicates how much water one of two side ports will dispense. The animals choose to either hold out at the cued location for the reward or to abandon the trial and start a new one by poking their nose into the other side. Rats learn to initiate their next trial more quickly when the experiment is doling out large rewards and to hold off on initiating new trials when rewards are small, previous work from the group has shown. “It takes a lot of energy to initiate a trial, so if there are small rewards, it’s not as motivating,” says study investigator Carla Golden, a postdoctoral researcher in Christine Constantinople’s lab at New York University. © 2025 Simons Foundation

Keyword: Hormones & Behavior; Attention
Link ID: 30028 - Posted: 11.26.2025

Hannah Devlin Science correspondent Scientists have identified five major “epochs” of human brain development in one of the most comprehensive studies to date of how neural wiring changes from infancy to old age. The study, based on the brain scans of nearly 4,000 people aged under one to 90, mapped neural connections and how they evolve during our lives. This revealed five broad phases, split up by four pivotal “turning points” in which brain organisation moves on to a different trajectory, at around the ages of nine, 32, 66 and 83 years. “Looking back, many of us feel our lives have been characterised by different phases. It turns out that brains also go through these eras,” said Prof Duncan Astle, a researcher in neuroinformatics at Cambridge University and senior author of the study. “Understanding that the brain’s structural journey is not a question of steady progression, but rather one of a few major turning points, will help us identify when and how its wiring is vulnerable to disruption.” The childhood period of development was found to occur between birth until the age of nine, when it transitions to the adolescent phase – an era that lasts up to the age of 32, on average. In a person’s early 30s the brain’s neural wiring shifts into adult mode – the longest era, lasting more than three decades. A third turning point around the age of 66 marks the start of an “early ageing” phase of brain architecture. Finally, the “late ageing” brain takes shape at around 83 years old. The scientists quantified brain organisation using 12 different measures, including the efficiency of the wiring, how compartmentalised it is and whether the brain relies heavily on central hubs or has a more diffuse connectivity network. From infancy through childhood, our brains are defined by “network consolidation”, as the wealth of synapses – the connectors between neurons – in a baby’s brain are whittled down, with the more active ones surviving. During this period, the study found, the efficiency of the brain’s wiring decreases. © 2025 Guardian News & Media Limited

Keyword: Development of the Brain; Brain imaging
Link ID: 30027 - Posted: 11.26.2025

By Gina Kolata Hopes were high. In retrospect, perhaps too high. On Monday, Novo Nordisk announced that two large studies failed to find any effect of the drug semaglutide on cognition and functioning in people with mild cognitive impairment — an early stage of Alzheimer’s — or with dementia. The participants were randomly assigned to take a pill of semaglutide, the compound at the heart of the weight-loss injections Ozempic and Wegovy, or a placebo for two years. “Today we announced that our efforts to slow down the progression of Alzheimer’s disease has come to an end,” said Maziar Mike Doustdar, chief executive at Novo Nordisk, in a video posted on LinkedIn. He added, “Based on the indicative data points we had, this is not the outcome we had hoped for.” The studies, involving 1,855 people in one trial and 1,953 in the other, seemed to stem an initial phase of optimism. The drugs appeared miraculous in their treatment of obesity, diabetes, heart disease and kidney disease. Alzheimer’s and other brain illnesses looked like the next frontier. But there had been other recent warnings, in two smaller studies of brain diseases. One, done by researchers in Britain, asked if a similar drug could help with Parkinson’s disease. That drug had no effect. Another study found that semaglutide did not help with cognitive impairment in people with major depression, a severe form of the disease. The company will present more detailed results from its Alzheimer’s study at a conference on Dec. 3, and another in March of 2026. Novo Nordisk’s stock was down nearly 6 percent on Monday, deepening a monthslong slump for the once-surging company. “We always knew there would be a low likelihood of success, but it was important to determine if semaglutide could take on one of medicine’s most challenging frontiers,” Mr. Doustdar said. © 2025 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 30026 - Posted: 11.26.2025

By Meghan Rosen Taking just a few thousand steps daily could potentially stave off Alzheimer’s disease. People with the disease tend to experience debilitating cognitive challenges, like memory loss and difficulty communicating, that worsen over time. But physical activity may slow that steady downward march. In an observational study of people at risk for Alzheimer’s, researchers linked walking between 3,000 and 5,000 steps per day to a three-year delay in cognitive decline, compared with sedentary individuals. For people who walked between 5,000 and 7,500 steps per day, the reprieve appeared to last even longer — seven years, Harvard Medical School behavioral neurologist Jasmeer Chhatwal and his colleagues report November 3 in Nature Medicine. The association still needs to be tested in a clinical trial, Chhatwal says, but his team’s results hint at something important. Quality of life for people with Alzheimer’s and their families often plummets in the later stages of the disease. “If the disease can be delayed,” he says, “that can have a very big impact on people’s lives.” Previous studies have reported links between physical activity and delayed Alzheimer’s progression, says Deborah Barnes, an epidemiologist who studies dementia at the University of California, San Francisco, and who was not part of the research team. But the new study pinpoints the step count where people begin to see benefits. It also “helps to explain how,” she says. Chhatwal’s team reported a connection between exercise and less accumulation of certain Alzheimer’s proteins in the brain. It’s a mechanism that illustrates how physical activity probably works to slow Alzheimer’s progression, Barnes says. © Society for Science & the Public 2000–2025

Keyword: Alzheimers
Link ID: 30025 - Posted: 11.26.2025

On 19 November 2025, the U.S. Centers for Disease Control and Prevention changed language on a “vaccine safety” page on its website to assert that the statement “vaccines do not cause autism” is not evidence based. The updated CDC page now incorrectly suggests that a link between infant vaccination and autism exists, and it casts doubt on a wealth of research that has produced evidence to the contrary. The updated language contradicts decades of research findings that show vaccines do not cause autism. The move has also prompted backlash from multiple groups, including the Coalition of Autism Scientists and the Autism Science Foundation. “These sort of claims have been repeatedly debunked by good science and multiple independent replications of negative studies, and for years no scientist has opined that more research is needed,” Eric Fombonne, professor emeritus of psychiatry at Oregon Health & Science University, told The Transmitter. He noted several problems with the arguments presented on the CDC website, including the citation of “fringe studies executed by uncredentialed authors with poor methodologies and published in low-quality journals.” Fombonne described the authors of the page as having “cherry pick[ed data] … in support of their preconceived beliefs” and mischaracterizing well-conducted and replicated research. Experts The Transmitter spoke with raised many concerns about the agency’s statements, including how those statements could confuse families and whether they indicate shifts in priorities that threaten solid scientific research. “Families deserve honest answers,” says David Mandell, professor of psychiatry at the University of Pennsylvania and director of the Penn Center for Mental Health. © 2025 Simons Foundation

Keyword: Autism; Neuroimmunology
Link ID: 30020 - Posted: 11.22.2025

By Oliver Whang Owen Collumb was paralyzed in 1993, when he was 21 years old. A tire on his motorbike blew out and he fell into a ravine, breaking a single bone in his spine. When he recovered, he couldn’t move his legs and could control only the biceps in his arms, meaning that he could lift his hands but, to put them down, he had to twist his shoulders and let gravity unbend his elbows. He spent years in an assisted living home before petitioning to move to his own place in Dublin, with the help of home aides. Living alone was liberating; he could choose what he ate and when he woke in the morning. He began working multiple jobs for foundations and advocating for people with disabilities. One of his assistants, Sylwia Filipiek, a Polish immigrant to Ireland, had been employed at a printing factory. She had no experience with home care and struggled to help Mr. Collumb into his wheelchair at first. But, over the years, they learned how to work together, and grew close. In the summer of 2024, Mr. Collumb and Ms. Filipiek flew to Bath, England, to train for the Cybathlon, an international competition run every four years to encourage the development of assistive technologies. The competition, hosted in Switzerland by the university ETH Zurich, consists of eight races for teams and their pilots (which is what the primary competitors, with varying disabilities, are called), each targeting different innovations, such as arm prostheses, leg prostheses and vision assistance. Each race consists of remote tasks that are supposed to simulate everyday life for the pilots: walking across a room, picking up a grocery bag, throwing a ball. One of Cybathlon’s founders, Roland Sigrist, compared it to Formula 1. Teams are encouraged to develop prototypes toward the ultimate goal of “the independence of people with disabilities,” but the competition is straightforward and real, with all its accompaniments: nerves, heartbreak, glory. The pilots are the ones that put themselves on the line. “They’re the masters of the technology, and not the other way around,” Mr. Sigrist said. © 2025 The New York Times Company

Keyword: Robotics
Link ID: 30018 - Posted: 11.19.2025

By Lauren Schenkman The purported autism-microbiome connection is having a moment. It’s the focus of a new $50-million call for proposals from Wellcome Leap—a research initiative of the Wellcome Trust—and a 2024 Netflix documentary portrays fecal microbiota transplants as a promising treatment for autism-related traits. “It seems to have captured the public’s imagination,” says Kevin Mitchell, associate professor of genetics and neuroscience at Trinity College in Dublin. But Mitchell says he has long been skeptical. Eventually, he and some colleagues “collectively got exasperated enough by this that we felt that we had to say something about it,” Mitchell says. Today, they published a comprehensive review in Neuron of more than 30 studies on the autism-microbiome connection, including preclinical experiments in mice, human observational studies and clinical trials. After accounting for statistical, technical and conceptual flaws, the team reached a clear conclusion: “There’s nothing there,” Mitchell says. Research projects that include the keywords “autism” and “microbiome” have netted about $20 million to $25 million in U.S. federal funding annually since 2018, Mitchell’s team found using the funding database NIH RePORTER. It’s worrying that funders assume “there’s a solid foundation of work,” Mitchell says. “It’s just this huge amount of scientific effort and funding going into exploring these ideas.” Mitchell spoke with The Transmitter about the problems he sees with studies that claim to show a microbiome-autism link, and how neuroscientists can read them with an analytical eye. © 2025 Simons Foundation

Keyword: Autism
Link ID: 30015 - Posted: 11.19.2025