Rachel Fieldhouse A group of specialized cells play a crucial part in clearing toxic proteins from inside the brain1. But in people with Alzheimer’s disease, these cells malfunction, leading to the build up of tau proteins — a hallmark of the disease. Tanycytes, specialized cells that line the third ventricle of the brain, are unique because they are in direct contact with both the bloodstream and the cerebrospinal fluid (CSF). This means that they can circumvent the blood–brain barrier to allow molecules into and out of the brain. “Tanycytes are highways for the brain,” says Vincent Prévot, a neuroendocrinologist based in Paris at Inserm, the French National Institute of Health and Medical Research. Although it was known that tanycytes transport molecules into the CSF, Prévot and his colleagues are the first to show that tanycytes also transport molecules out of the CSF. In particular, they move tau proteins from the CSF surrounding the brain into the bloodstream. The findings are fascinating, says Amy Brodtmann, a cognitive neurologist and researcher at Monash University in Melbourne, Australia. “No one has looked at these cells before” in relation to Alzheimer’s disease, she adds. The works shows a potential explanation for how abnormal tau proteins accumulate in the brain, she adds. Tau proteins usually help to support the internal structure of cells and make them stronger, including cells in the brain. But in people with Alzheimer’s disease, the protein stops working properly. Brodtmann says tau then becomes “sticky”, forming clumps in the cells and causing them to die. These tau tangles tend to accumulate in regions of the brain that are involved in memory. © 2026 Springer Nature Limited

Keyword: Alzheimers; Glia
Link ID: 30152 - Posted: 03.07.2026

By Dana G. Smith Many people’s brains deteriorate as they age, becoming riddled with malfunctioning proteins that result in cell death and the loss of memory and cognition. But other people’s brains remain almost perfectly intact, their thinking as sharp at 80 as it was in their 50s. A paper published Wednesday in the journal Nature provides a new potential explanation for this discrepancy, and it taps into one of the hottest debates in neuroscience: whether human brains can grow new neurons in adulthood, a phenomenon called neurogenesis. The study found that so-called super-agers — people 80 and up who have the memory ability of someone 30 years younger — had roughly twice as many new neurons as older adults with normal memory for their age, and 2.5 times more than people with Alzheimer’s disease. The research focused on an area of the brain called the hippocampus, which is important for learning and memory and is thought to be the primary birthplace of new neurons. “This paper shows biological proof that the aging brain is plastic,” even into a person’s 80s, said Tamar Gefen, an associate professor of psychiatry and behavioral sciences at the Northwestern University Feinberg School of Medicine, who contributed to the research. To look for neurogenesis in older adults, the scientists first tried to detect signs of it in the autopsied brains of young adults, age 20 to 40, who died with normal cognition. They identified genetic markers for three key types of cells: neural stem cells, neuroblasts and immature neurons. © 2026 The New York Times Company

Keyword: Neurogenesis; Alzheimers
Link ID: 30144 - Posted: 02.28.2026

Mariana Lenharo Adults whose brains still have strong neuron production seem to have better memory and cognitive function than do those in whom the ability wanes, finds a study published today in Nature1. The authors examined brain samples from deceased donors ranging from young adults to ‘super agers’ — people older than 80 with exceptional memory. She lived to 117: what her genes and lifestyle tell us about longevity They found that young and old adults with healthy cognition generated neurons, a process called neurogenesis, at high levels for their age. The team estimated that the new neurons made up only a small fraction — 0.01% — of those in the hippocampus, a brain region that’s essential for memory. By contrast, in people experiencing cognitive decline, including individuals with Alzheimer’s disease, neurogenesis seems to falter: the researchers spotted fewer developing, or immature, neurons in those brain samples. Surprisingly, a group of ‘super agers’ had an even higher number of immature neurons than did other groups, and significantly more than did those with Alzheimer’s. However, the group sizes were small, so the findings were not all statistically significant. Maura Boldrini Dupont, a neuroscientist and psychiatrist at Columbia University in New York City, says that the small size of the groups — each had ten or fewer individuals — is a reason to take the results with a grain of salt. Understanding the tools that the brain uses to generate neurons and maintain cognitive function in old age could help researchers to develop drugs that induce neurogenesis in people with cognitive decline, says co-author Orly Lazarov, a neuroscientist at the University of Illinois Chicago. © 2026 Springer Nature Limited

Keyword: Neurogenesis; Alzheimers
Link ID: 30143 - Posted: 02.28.2026

By Nora Belblidia To the naked eye, Annie Kathuria’s experiments look a bit like tiny tufts of cotton floating in pink Petri dishes. These unassuming orbs are clusters of millions of human brain cells called brain organoids — brainstem organoids in this case — cultured in a lab in East Baltimore. Roughly a month old, the tufts are each around a millimeter wide, smaller than a coarse grain of salt. “We have about maybe 500 to 600 organoids growing,” said Kathuria, an assistant professor of biomedical engineering and neurosurgery at Johns Hopkins University. In addition to the brainstem organoids, her lab is also growing other types that correspond to different parts of the nervous system: cortical organoids, which mimic a brain’s developing cortex, and spinal cord organoids, to model the spinal nerve tissue that connects to the brain. Each of these clumps of neural tissue functions similarly to specific regions of the human brain. That similarity has led to some media coverage referring to them as “mini-brains” or “brains in a dish” — now irksome terms to many researchers in the field, some of whom also prefer the term neural organoids to brain organoids. Annie Kathuria, assistant professor of biomedical engineering and neurosurgery, in her lab at Johns Hopkins University in Baltimore. Visual: Nora Belblidia for Undark “Whatever else they are, they aren’t brains. They aren’t organized like brains. They aren’t big enough,” said Hank Greely, a Stanford University professor and expert in law and biosciences who works with researchers in the field. “But more importantly, they don’t have the right architecture.” By that he means organoids are basic parts of a whole, similar to how a broom closet or stairwell would never be considered a skyscraper.

Keyword: Development of the Brain
Link ID: 30141 - Posted: 02.28.2026

Rachel Fieldhouse Alzheimer’s disease is about to become a big problem for China. Nearly 30% of all people with the condition or related forms of dementia already live in the country. And with its ageing population and falling birth rate, the burden on health and social welfare is expected to multiply dramatically in the coming decades. The Chinese government has responded with programmes and funding that are aimed at improving screening, diagnosis and treatment of Alzheimer’s disease by 2030. And the research has started to take off. Scientists have been working on new drugs and innovative — if controversial — surgical techniques. The government has also encouraged the development of drugs derived from traditional Chinese medicine. And researchers are accelerating the search for biological markers that precede the onset of Alzheimer’s disease, including genetic contributors, which could explain how the condition develops and reveal the best way to identify it early. Although the investments don’t yet match the level of funding in the United States, the improving quality and quickening pace of clinical and preclinical research has attracted attention from researchers around the world. “Maybe China is the next place that will take the lead,” says John Hardy, a neurogeneticist at the UK Dementia Research Institute in London, who is also affiliated with the Hong Kong Center for Neurodegenerative Diseases. Treating the root of the problem Nearly 17 million people in China had Alzheimer’s disease and related dementias in 2021 — about 9 in 1,000, according to a report published last year1. Projections suggest that this number could reach as high as 66 million by 2050 (see ‘Dementia’s rise’) or even exceed 100 million by then2,3. The problem is compounded by China’s low fertility rate, which means that there will be fewer people of working age to support the growing population of older individuals with debilitating conditions. © 2026 Springer Nature Limited

Keyword: Alzheimers
Link ID: 30139 - Posted: 02.25.2026

Heidi Ledford A simple blood test might one day serve as a molecular ‘clock’ that predicts not only whether someone will develop Alzheimer’s disease — but when. Blood tests are now approved for Alzheimer’s: how accurate are they? The test, published in Nature Medicine on 19 February1, is based on an abnormal form of a protein called tau that circulates in the blood, and begins to accumulate in the brains of people with Alzheimer’s well before symptoms such as memory loss appear. If validated in larger studies, the test could provide a way to intervene in the neurodegenerative disease at an earlier stage, when treatment is more likely to be effective. It could also provide a measurable biological marker, or ‘biomarker’, to make clinical trials of potential Alzheimer’s disease treatments easier and cheaper. “Predicting if and when patients are likely to develop Alzheimer’s symptoms could be useful in designing trials of interventions to prevent or delay symptom onset,” says Howard Fink, a physician at the Minneapolis Veterans Affairs Health Care System in Minnesota. But until further studies are done, people should not take the test themselves, says Suzanne Schindler, a neurologist at Washington University School of Medicine in St. Louis, Missouri, and lead author of the study. (In-home blood tests for the form of tau that the study focuses on are available to consumers.) “At this point, we do not recommend that any cognitively unimpaired individuals have any Alzheimer’s disease biomarker test,” Schindler adds. Abnormal tau proteins can form tangled fibres that disrupt communication among the brain’s nerve cells. Brain-imaging tests that detect tangled tau are sometimes used when diagnosing Alzheimer’s, and preliminary studies suggest that such tests might also be able to predict when a person’s Alzheimer’s symptoms will appear2,3. © 2026 Springer Nature Limited

Keyword: Alzheimers
Link ID: 30130 - Posted: 02.21.2026

Jon Hamilton A little brain training today may help stave off Alzheimer's disease and other forms of dementia for at least 20 years. That's the conclusion of a study of older adults who participated in a cognitive exercise experiment in the 1990s that was designed to increase the brain's processing speed. The federally funded study of 2,802 people found that those who did eight to 10 roughly hourlong sessions of cognitive speed training, as well as at least one booster session, were about 25% less likely to be diagnosed with dementia over the next two decades. "We now have a gold-standard study that tells us that there is something we can do to reduce our risk for dementia," says Marilyn Albert, an author of the study and a professor of neurology at Johns Hopkins University School of Medicine. "It's super-exciting to see that these effects are still holding 20 years out," says Jennifer O'Brien, an associate professor of psychology at the University of South Florida who was not involved in the research. The study appears in the journal Alzheimer's & Dementia: Translational Research & Clinical Interventions. The result is good news for people like George Kovach, 74, who started doing cognitive speed training a decade ago. This illustration shows a pink human brain with stick legs and stick arms. The pink stick arms are holding up a black barbell with black disk-shaped weights on each end. © 2026 npr

Keyword: Alzheimers; Learning & Memory
Link ID: 30127 - Posted: 02.18.2026

By Lauren Schneider Microglia may be a key mediator between maternal immune activation and a pup’s memory of contextual fear conditioning in early infancy, a new mouse study reports. The findings sharpen the picture of memory formation in early life, but the study’s approach to microglia has raised questions. That scrutiny comes as scientists reevaluate concepts such as synaptic pruning, through which microglia may shape neuronal circuits in early life and beyond. Humans and rodents are unable to recall some of the earliest memories formed after birth. This period of infantile amnesia offers researchers a window to test conditions that may alter the survival of engrams, the changes in the brain tied to memory formation. “Development is an experiment that nature does for you,” says study investigator Tomás Ryan, professor in neuroscience at Trinity College Dublin. Activation of the immune system during pregnancy in mice leads to autism-like behaviors in their pups and reduces infantile amnesia, according to a previous study by Ryan’s team. Blocking microglial activity allows some infantile memories to persist in mice, Ryan and his colleagues report in the new paper, published 20 January in PLOS Biology. Administering minocycline in water daily starting one day before foot-shock conditioning at postnatal day 17 led to greater fear memory at postnatal day 25, after the typical onset of infantile amnesia. This recall was accompanied by a reactivation of associated engrams in the basolateral amygdala and central amygdalar nucleus. © 2026 Simons Foundation

Keyword: Glia; Development of the Brain
Link ID: 30122 - Posted: 02.14.2026

Andrew Gregory Health editor Reading, writing and learning a language or two can lower your risk of dementia by almost 40%, according to a study that suggests millions of people could prevent or delay the condition. Dementia is one of the world’s biggest health threats. The number of people living with the condition is forecast to triple to more than 150 million globally by 2050, and experts say it presents a big and rapidly growing threat to future health and social care systems in every community, country and continent. US researchers found that engaging in intellectually stimulating activities throughout life, such as reading, writing or learning a new language, was associated with a lower risk of Alzheimer’s disease, the most common form of dementia, and slower cognitive decline. The study author Andrea Zammit, of Rush University Medical Center in Chicago, said the discovery suggested cognitive health in later life was “strongly influenced” by lifelong exposure to intellectually stimulating environments. “Our findings are encouraging, suggesting that consistently engaging in a variety of mentally stimulating activities throughout life may make a difference in cognition. Public investments that expand access to enriching environments, like libraries and early education programs designed to spark a lifelong love of learning, may help reduce the incidence of dementia.” Researchers tracked 1,939 people with an average age of 80 who did not have dementia at the start of the study. They were followed for an average of eight years. Participants completed surveys about cognitive activities and learning resources during three stages. © 2026 Guardian News & Media Limited

Keyword: Alzheimers; Learning & Memory
Link ID: 30121 - Posted: 02.14.2026

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 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

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 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