Tobi Thomas Health and inequalities correspondent Scientists have linked the impact of living in an unequal society to structural changes in the brains of children – regardless of individual wealth – for the first time. A study of more than 10,000 young people in the US discovered altered brain development in children from wealthy and lower-income families in areas with higher rates of inequality, which were also associated with poorer mental health. The data was gathered from the Adolescent Brain Cognitive Development study and published in the journal Nature Mental Health. Researchers at King’s College London, Harvard University, and the University of York then measured inequality within a particular US state by scoring how evenly income is measured. States with higher levels of inequality included New York, Connecticut, California and Florida, while Utah, Wisconsin, Minnesota and Vermont were more equal. MRI scans were analysed to study the surface area and thickness of regions in the cortex, including those involved in higher cognitive functions including memory, emotion, attention and language. Connections between different regions of the brain were also analysed by the scans, where changes in blood flow indicate brain activity. The research found that children living in areas with higher levels of societal inequality, including socioeconomic imbalances and deprivation for example, were linked to having a reduced surface area of the brain’s cortex, and altered connections between multiple regions of the brain. The findings, the first to reveal the impact societal inequality has on the structures of the brain, also provided evidence that the impacted neurodevelopment might relate to future mental health and cognitive function. Notably, these brain changes in children were seen regardless of their economic background. © 2025 Guardian News & Media Limited

Keyword: Development of the Brain; Learning & Memory
Link ID: 29951 - Posted: 10.01.2025

By Azeen Ghorayshi As a child, Jodie Singer barely spoke. She could repeat words that people said to her or recite the book “Madeline” from beginning to end, but she could not answer yes or no when her mother asked if she wanted juice. Sometimes she hurt herself, compulsively tearing at the skin and hair on the nape of her neck. She threw tantrums, thrashing and refusing to be comforted. When she was almost 3, Jodie was given a diagnosis of autism. Now 28, she still speaks only in short, repetitive phrases and requires round-the-clock care, including help eating, getting dressed and using the toilet. At the time Jodie’s diagnosis was first made, the definition of autism was expanding, as it would continue to do over the next 25 years. Once primarily limited to severely disabled people, autism began to be viewed as a spectrum that included far less impaired children and adults. Along the way, it also became an identity, embraced by college graduates and even by some of the world’s most successful people, like Elon Musk and Bill Gates. That broadening of the diagnosis, autism experts believe, along with the increasing awareness of the disorder, is largely responsible for the steep rise in autism cases that Health Secretary Robert F. Kennedy Jr. has called “an epidemic” and has attributed to theories of causality that mainstream scientists reject, like vaccines and, more recently, Tylenol. And the diagnostic expansion has now become a flashpoint in a long-running debate over how autism should defined, one that has divided parents and activists, ignited social media battles and grown fiercer with Mr. Kennedy’s laser focus on autism. Speaking of autistic children in the spring, Mr. Kennedy said, “These are kids who will never pay taxes, they’ll never hold a job, they’ll never play baseball, they’ll never write a poem, they’ll never go out on a date.” His words drew a swift backlash from many autistic adults, who called his characterization of their lives false and dehumanizing. But Jodie’s mother, Alison Singer, said that, though she disagrees with Mr. Kennedy’s views on the causes of autism, his words about the harsh realities of living with the disorder spoke to families like her own. © 2025 The New York Times Company

Keyword: Autism
Link ID: 29947 - Posted: 10.01.2025

Heidi Ledford After a mouse received treatment to eliminate immune cells called microglia, it was injected with human progenitor cells that developed into human immune cells (green, pink and blue) in the animal’s brain.Credit: M. M.-D. Madler et al./Nature A fresh supply of the immune cells that keep the brain tidy might one day help to treat a host of conditions, from ultra-rare genetic disorders to more familiar scourges, such as Alzheimer’s disease. In the past few months, a spate of new studies have highlighted the potential of a technique called microglia replacement and explored ways to make it safer and more effective. “This approach is very promising,” says Pasqualina Colella, who studies gene and cell therapy at Stanford University School of Medicine in California. “But the caveat is the toxicity of the procedure.” Microglia are immune cells that patrol the brain, gobbling up foreign invaders, damaged cells and harmful substances. They can help to protect neurons — cells that transmit and receive messages to and from other tissues — during seizures and strokes, and they prune unneeded connections between neurons during normal brain development. “Microglia do a lot of important things,” says Chris Bennett, a psychiatrist who studies microglia at the Children’s Hospital of Philadelphia in Pennsylvania. “So, it’s not surprising that they are involved in the pathogenesis of many diseases.” Those diseases include a suite of rare disorders caused by genetic mutations that directly affect microglia. Malfunctioning microglia have also been implicated in more familiar conditions with complex causes, such as Alzheimer’s disease and Parkinson’s disease, as well as ageing, says Bo Peng, a neuroscientist at Fudan University in Shanghai, China. © 2025 Springer Nature Limited

Keyword: Development of the Brain; Glia
Link ID: 29944 - Posted: 09.27.2025

By Roni Caryn Rabin Women who are pregnant, planning a pregnancy or breastfeeding should be screened for cannabis use and strongly discouraged from it, the American College of Obstetricians and Gynecologists said in new clinical guidelines published on Friday. Cannabis use during pregnancy has been rising for years. Many women rely on the drug to cope with nausea and other pregnancy symptoms. But the college warned that mounting evidence linked cannabis to preterm births, low birth weights and a greater need for neonatal intensive care, as well as neurocognitive and behavioral problems in children. “Patients are often using cannabis to help with some kind of medical ailment, not recreationally — in their mind, they think it’s a more natural way to deal with a medical problem,” said Dr. Melissa Russo, an author of the new guidance. “But there are lots of natural things that are not safe,” Dr. Russo said. There are no studies demonstrating that cannabis is effective for pregnant or lactating women, she added, “and research now shows there are potential adverse effects.” The college warned against blood or urine tests for cannabis screening. Instead, it urged physicians to talk with women about their habits, and to encourage them to stop using marijuana as soon as possible while offering alternative therapies for medical ailments. The screening should be universal in an effort to avoid bias and racism, the college said. It noted that pregnant Black and Hispanic women are four to five times as likely as white women to be tested for drug use. Black women are almost five times as likely to be reported to child protective services for suspected drug use. The new guidelines say that cannabis should be discouraged among breastfeeding women, but that breastfeeding should continue even with use of the drug because the benefits most likely outweigh the potential risks. © 2025 The New York Times Company

Keyword: Drug Abuse; Development of the Brain
Link ID: 29942 - Posted: 09.24.2025

Jon Hamilton In a White House press conference Monday, President Trump and several deputies said the Food and Drug Administration would be updating drug labeling to discourage the use of acetaminophen by pregnant women, suggesting a link between the common painkiller and autism. Federal officials also said they would be changing the label for leucovorin, a form of vitamin B typically used in conjunction with cancer treatment, to enable its use as a treatment for autism. And they added that state Medicaid programs, in partnership with the federal Centers for Medicare & Medicaid Services, would cover this use. The suite of changes was announced despite a notable lack of clear scientific evidence to support these moves. The changes were presented as part of what the administration said was its commitment to identify the root causes of autism, diagnoses of which have increased in recent years. Flanked by Health and Human Services Secretary Robert F. Kennedy Jr. and Centers for Medicare and Medicaid head Dr. Mehmet Oz, President Trump pinned substantial blame for rising autism rates on the common painkiller, which is also known by its brand name, Tylenol. "Taking Tylenol is not good — I'll say it: It's not good," he said, suggesting without evidence that communities without access to the medicine have "no autism," while in others, autism now affects 1 in 12 boys. (An estimated 1 in 31 children in the U.S. are diagnosed with autism.) Trump discouraged giving acetaminophen to babies, as well. (He also suggested that vaccines and their frequency may be a culprit in causing autism, an oft-repeated claim that has been debunked by decades of research.) © 2025 npr

Keyword: Autism
Link ID: 29941 - Posted: 09.24.2025

By Christina Caron Dr. Marty Makary, the commissioner of the Food and Drug Administration, announced on Monday that the agency would be modifying the label of a relatively obscure medicine so that “it can be available for children with autism.” He was referring to leucovorin, or folinic acid, a modified version of vitamin B9, also known as folate — which is naturally found in beans, leafy greens, eggs, beets and citrus. Folate helps the body make red blood cells and is important for cell growth. It’s especially crucial during early pregnancy to lower the risk of major birth defects in a baby’s brain or spine. Studies suggest that folate levels can affect our health in various ways, and scientists are researching what role folate plays in depression, dementia, heart disease and autism. Some people have antibodies that interfere with how folate is transported within the body, and small studies suggest that a number of people with autism — in some cases up to 75 percent — may have these antibodies. In a Federal Register notice filed on Monday, the F.D.A. said it was approving leucovorin tablets for people with “cerebral folate deficiency,” based on a review of studies from 2009 to 2024 that found that they “improve certain symptoms.” The agency, noting that more studies were needed, cited one study that compared 40 people on the medication and 40 on a placebo; those who took the medication showed “substantial improvement” of the deficiency symptoms. The medicine has been used off-label to treat people diagnosed with cerebral folate deficiency for about two decades. Symptoms of cerebral folate deficiency usually begin to show up around the age of 2 when children start to experience speech difficulties, intellectual disabilities and, in some cases, seizures. They may also have tremors and difficulty controlling their muscle movements. © 2025 The New York Times Company

Keyword: Autism
Link ID: 29940 - Posted: 09.24.2025

Rachel Fieldhouse Last week, a study involving more than nine million pregnancies reported that children whose mothers had gestational diabetes during pregnancy had a higher chance of developing attention deficit–hyperactivity disorder (ADHD) and autism than did children whose mothers didn’t have the condition. The study, presented at the European Association for the Study of Diabetes in Vienna, is under review at a peer-reviewed journal. It is not the first to link gestational diabetes to neurodevelopmental disorders in children, but it is one of the largest. Researchers pooled results from 48 studies across 20 countries, finding that children born to people with gestational diabetes had lower IQ scores, a 36% higher risk of ADHD and a 56% higher risk of autism spectrum disorders. Estimates suggest the prevalence of autism in the general population is one in 127 people1 and between 3-10%2 of children and teenagers have ADHD. The latest results mirror those of another meta-analysis3 published in The Lancet Diabetes & Endocrinology journal in June, which included 56 million mother–child pairs and found that all types of diabetes in pregnancy, including type 1, type 2 and gestational diabetes, increase the risk of the baby developing ADHD and autism. But none of these studies have been able to show that diabetes during pregnancy causes these conditions. “There’s no doubt that there is a signal here, but certainly further research is required,” says Alex Polyakov, an obstetrician and researcher at the University of Melbourne in Australia. Long a topic of research, the causes of autism have been thrust into the spotlight by the administration of US President Donald Trump. On Sunday, while speaking at the memorial for conservative activist Charlie Kirk, Trump said: “I think we found an answer to autism. How about that?” © 2025 Springer Nature Limited

Keyword: Autism
Link ID: 29939 - Posted: 09.24.2025

By Calli McMurray Studying animal behavior in the wild often gets hairy, with little experimental control and an abundance of extraneous data. And when multiple animals get together, the way they look, act and smell all influence one another, making it difficult to parse complex social interactions, says Andres Bendesky, associate professor of ecology, evolution and environmental biology at Columbia University. Robotic or animated partners, however, can simplify that equation. Studying animal-robot interaction gives researchers complete control over one partner during any tête-à-tête, Bendesky says. It makes it possible to present the same stimulus to an animal repeatedly or compare how different individuals react. And the method complements observation-based research: Scientists can use a robot- or animation-based paradigm to test ideas gleaned from studies that use artificial-intelligence tools to track behavior. Bendesky is part of a growing cohort of neuroscientists turning to robots to help them decode social interactions. The quirks are still being ironed out, but the approach is already helping several groups tackle questions about schooling, fighting and chatting behaviors. The rigor of the results depends on whether a critter believes what it sees, says Tim Landgraf, professor of artificial and collective intelligence at Freie Universität Berlin, who uses robots to study group behavior in guppies. That can be hard to gauge; there’s no handbook that describes what traits make a robot believable, he says. But researchers can compare how animals act toward a real peer versus a counterfeit one, says Steve Chang, associate professor of psychology and neuroscience at Yale University, who doesn’t work with robots but studies the social behavior of macaques and marmosets. © 2025 Simons Foundation

Keyword: Robotics; Sexual Behavior
Link ID: 29936 - Posted: 09.20.2025

By Sujata Gupta Anne-Laure Le Cunff was something of a wild child. As a teenager, she repeatedly disabled the school fire alarm to sneak smoke breaks and helped launch a magazine filled with her teachers’ fictional love lives. Later, as a young adult studying neuroscience, Le Cunff would spend hours researching complex topics but struggled to complete simple administrative tasks. And she often obsessed over random projects before abruptly abandoning them. Then, three years ago, a colleague asked Le Cunff if she might have attention-deficit/hyperactivity disorder, or ADHD, a condition marked by distractibility, hyperactivity and impulsivity. Doctors confirmed her colleague’s suspicions. But fearing professional stigma, Le Cunff — by then by then a postdoctoral fellow in the ADHD Lab at King’s College London — kept her diagnosis secret until this year. Le Cunff knew all too well about the deficits associated with ADHD. But her research — and personal experience — hinted at an underappreciated upside. “I started seeing … breadcrumbs pointing at a potential association between curiosity and ADHD,” she says. People within the ADHD community have long recognized that the condition can be both harmful and helpful. Researchers, though, have largely focused on the harms. And those studying treatments tend to define success as a reduction in ADHD symptoms, with little regard to possible benefits. That’s starting to change. For instance, Norwegian researchers asked 50 individuals with ADHD to describe their positive experiences with the disorder as part of an effort to develop more holistic treatments. People cited their creativity, energy, adaptability, resilience and curiosity, researchers reported in BMJ Open in October 2023. © Society for Science & the Public 2000–2025.

Keyword: ADHD; Attention
Link ID: 29932 - Posted: 09.17.2025

Rachel Fieldhouse Deep in the rainforests of the Democratic Republic of the Congo, Mélissa Berthet found bonobos doing something thought to be uniquely human. During the six months that Berthet observed the primates, they combined calls in several ways to make complex phrases1. In one example, bonobos (Pan paniscus) that were building nests together added a yelp, meaning ‘let’s do this’, to a grunt that says ‘look at me’. “It’s really a way to say: ‘Look at what I’m doing, and let’s do this all together’,” says Berthet, who studies primates and linguistics at the University of Rennes, France. In another case, a peep that means ‘I would like to do this’ was followed by a whistle signalling ‘let’s stay together’. The bonobos combine the two calls in sensitive social contexts, says Berthet. “I think it’s to bring peace.” The study, reported in April, is one of several examples from the past few years that highlight just how sophisticated vocal communication in non-human animals can be. In some species of primate, whale2 and bird, researchers have identified features and patterns of vocalization that have long been considered defining characteristics of human language. These results challenge ideas about what makes human language special — and even how ‘language’ should be defined. Perhaps unsurprisingly, many scientists turn to artificial intelligence (AI) tools to speed up the detection and interpretation of animal sounds, and to probe aspects of communication that human listeners might miss. “It’s doing something that just wasn’t possible through traditional means,” says David Robinson, an AI researcher at the Earth Species Project, a non-profit organization based in Berkeley, California, that is developing AI systems to decode communication across the animal kingdom. As the research advances, there is increasing interest in using AI tools not only to listen in on animal speech, but also to potentially talk back. © 2025 Springer Nature Limited

Keyword: Animal Communication; Language
Link ID: 29931 - Posted: 09.17.2025

By Andrea Thompson A school-aged child in Los Angeles County has died from a rare but always fatal complication from a measles infection they acquired when they were an infant who was too young to be vaccinated. The first dose of the vaccine is typically not administered until one year of age. Experts say the death underscores the need for high levels of vaccination in a population to protect the most vulnerable against the disease, as well as from side effects that can occur long after the initial illness has passed. “This case is a painful reminder of how dangerous measles can be, especially for our most vulnerable community members,” said Los Angeles County Health Officer Muntu Davis in a recent statement. The child who died suffered from subacute sclerosing panencephalitis (SSPE), a progressive brain disorder that usually develops two to 10 years after a measles infection. The measles virus appears to mutate into a form that avoids detection by the immune system, allowing it to hide in the brain and eventually destroy neurons. “It’s just a virus that goes unchecked and destroys brain tissue, and we have no therapy for it,” said Walter Orenstein, an epidemiologist and professor emeritus at Emory University, to Scientific American earlier this year. People with SSPE experience a gradual, worsening loss of neurological function and usually die within one to three years after diagnosis, according to the Los Angeles County Health Department. The disorder affects only about one in every 10,000 people who contract measles. But the risk may be as high as about one in 600 for those who are infected as infants. “There is no treatment for this. Children who suffer from this will always die,” said Paul Offit, director of the Vaccine Education Center and an attending physician in the Division of Infectious Diseases at Children’s Hospital of Philadelphia, in a previous interview with Scientific American. © 2025 SCIENTIFIC AMERICAN,

Keyword: Development of the Brain
Link ID: 29927 - Posted: 09.13.2025

Rachel Fieldhouse An analysis of 56 million people has shown that exposure to air pollution increases the risk of developing a particular form of dementia, the third most common type after Alzheimer’s disease and vascular dementia. The study, published in Science on 4 September1, suggests that there is a clear link between long-term exposure to PM2.5 — airborne particles that are smaller than 2.5 micrometres in diameter — and the development of dementia in people with Lewy body dementia or Parkinson’s disease. The study found that PM2.5 exposure does not necessarily induce Lewy body dementia, but “accelerates the development,” in people who are already genetically predisposed to it, says Hui Chen, a clinician–neuroscientist at the University of Technology Sydney in Australia. PM2.5 exposure Lewy body dementia is an umbrella term for two different types of dementia: Parkinson’s disease with dementia, and dementia with Lewy bodies. In both cases, dementia is caused by the build-up of α-synuclein (αSyn) proteins into clumps, called Lewy bodies, in the brain’s nerve cells, which cause the cells to stop working and eventually die. Studies have suggested that long-term exposure to air pollution from car-exhaust, wildfires and factory fumes, is linked with increased risks of developing neurodegenerative illnesses, including Parkinson's disease with dementia2. Study co-author Xiaobo Mao, who researches neurodegenerative conditions at Johns Hopkins University in Baltimore, Maryland, says he and his colleagues wanted to determine if PM2.5 exposure also influenced the risk of developing Lewy body dementia. They analysed 2000–2014 hospital-admissions data from 56.5 million people with Lewy body dementia and Parkinson’s disease with or without dementia. The data served to identify people with severe neurological diseases. © 2025 Springer Nature Limited

Keyword: Alzheimers; Parkinsons
Link ID: 29920 - Posted: 09.06.2025

Ian Sample Science editor A three-minute brainwave test can detect memory problems linked to Alzheimer’s disease long before people are typically diagnosed, raising hopes that the approach could help identify those most likely to benefit from new drugs for the condition. In a small trial, the test flagged specific memory issues in people with mild cognitive impairment, highlighting who was at greater risk of developing Alzheimer’s. Trials in larger groups are under way. The Fastball test is a form of electroencephalogram (EEG) that uses small sensors on the scalp to record the brain’s electrical activity while people watch a stream of images on a screen. The test detects memory problems by analysing the brain’s automatic responses to images the person sees before the test. “This shows us that our new passive measure of memory, which we’ve built specifically for Alzheimer’s disease diagnosis, can be sensitive to those individuals at very high risk but who are not yet diagnosed,” said Dr George Stothart, a cognitive neuroscientist at the University of Bath, where the test was developed. The trial, run with the University of Bristol, involved 54 healthy adults and 52 patients with mild cognitive impairment (MCI). People with MCI have problems with memory, thinking or language, but these are not usually severe enough to prevent them doing their daily activities. Before the test, volunteers were shown eight images and told to name them, but not specifically to remember them or look out for them in the test. The researchers then recorded the participants’ brain activity as they watched hundreds of images flash up on a screen. Each image appeared for a third of a second and every fifth picture was one of the eight they had seen before. © 2025 Guardian News & Media Limited

Keyword: Alzheimers; Attention
Link ID: 29914 - Posted: 09.03.2025

Jon Hamilton People who inherit two copies of a gene variant called APOE4 have a 60% chance of developing Alzheimer's by age 85. Only about 2% to 3% of people in the U.S. have this genetic profile, and most of them don't know it because they've never sought genetic testing. But three scientists are among those who did get tested, and learned that they are in the high-risk group. Now, each is making an effort to protect not only their own brain, but the brains of others with the genotype known as APOE4-4. "I just felt like the end of the world," says June, who asked to use only her first name out of fear that making her genetic status public could affect her job or health insurance. June was 57 when she found out. As someone with a doctorate in biochemistry, she quickly understood what the results meant. New tests of blood and spinal fluid could help doctors quickly identify patients who would most benefit from treatment. "People with our genotype are almost destined to get the disease," she says. "We tend to get symptoms 7 to 10 years earlier than the general population, which means that I had about seven years left before I may get the disease." At first, June spent sleepless nights online, reading academic papers about Alzheimer's and genetics. She even looked into physician-assisted suicide in an effort to make sure she would not become a burden to her adult son. © 2025 npr

Keyword: Alzheimers; Genes & Behavior
Link ID: 29913 - Posted: 09.03.2025

By Lauren Schenkman Microglia safeguard the proliferation and survival of young GABAergic interneurons by secreting insulin-like growth factor 1 (IGF-1), according to a new study of human brain tissue and organoids. The finding points to the potential origin of the brain signaling imbalance implicated in autism and other conditions. Microglia contribute to brain development, past findings show, but their exact function has been unclear. Some experiments showed that these cells prune neural circuits, but later work called that idea into question. The new research “identifies microglia as really an important source of IGF, and one that sets the supply of GABAergic interneurons in the developing brain,” says Damon Page, principal investigator at Seattle Children’s Research Institute. Page was not involved in this work but led an earlier investigation that showed IGF-1 prevents microcephaly in a mouse model of autism when administered during a critical window soon after birth. This new study “extends back that window into the embryonic period,” he says, with implications for understanding both typical development and conditions such as autism. The study was published 6 August in Nature. The investigators used staining techniques to pinpoint microglia in the medial ganglionic eminence, where interneurons form, in human brain tissue samples at various developmental stages. At early developmental stages, microglia were sprinkled throughout brain matter, but later on these cells arranged themselves around clusters of GABAergic neuroblasts, with their processes extending into the clusters. Microglia also aligned themselves with radial glia, the precursors to many brain cells. Based on existing data, IGF-1 emerged as the chemical most likely to mediate microglia’s effects on developing cell types, and in organoid models of the developing human brain, the cells secreted IGF-1, they found. © 2025 Simons Foundation

Keyword: Glia; Learning & Memory
Link ID: 29911 - Posted: 09.03.2025

By Holly Barker When scientists produced the first map of all synaptic connections in the roundworm Caenorhabditis elegans in 1986, many hailed it as a blueprint for the flow of brain signals. As it turned out, though, models of neuronal activity based on this wiring diagram bore little resemblance to the functional maps of brain activity measured in living worms. This disconnect isn’t limited to worms. Mice, for instance, appear to have widespread silent synapses—wired connections that don’t send signals—and the actual responses of some cells in the fruit fly’s visual system do not match the responses the connectome predicts. A new preprint helps to explain why: Most network features, in C. elegans at least, are not conserved between the anatomical and functional connectomes. Yet the anatomical connectome can still forecast—albeit in a complex way—observed neuronal activity in the worms, according to a second preprint by the same team, because “most signaling is happening along the wires,” says Andrew Leifer, associate professor of physics and neuroscience at Princeton University and principal investigator on both preprints. The findings begin to address the long-standing challenge of reconciling structure and function, and show that “we weren’t entirely wrong” about the importance of synaptic connectivity, says Jihong Bai, professor of basic sciences at the Fred Hutchinson Cancer Center, who was not involved in the work. The debut of a color-coded map of cell types in the worm brain in 2021 split the neuroscience community. It made it possible to identify individual neurons in whole-brain recordings and compare annotated recordings with the connectome—an exercise that revealed no correlation between the two. © 2025 Simons Foundation

Keyword: Brain imaging
Link ID: 29907 - Posted: 08.30.2025

Helen Pearson On 16 April, Robert F. Kennedy Jr held a press conference about rising diagnoses of autism. The US Health and Human Services (HHS) secretary pointed to new data showing that autism prevalence in the United States had risen steeply from one in 150 eight-year-olds in 2000 to one in 31 in 2022. He called it an “epidemic” caused by “an environmental toxin” — and said he would soon be announcing a study to find the responsible agent. The next month, the US National Institutes of Health (NIH), part of the department that Kennedy leads, announced the Autism Data Science Initiative (ADSI). The initiative offered up to US$50 million to fund studies on the causes of autism. The winning applications are expected to be announced in September. Usually, big investments in research are welcomed by scientists — but not this time. Many were dismayed that these developments seemed to ignore decades of work on the well-documented rise in autism diagnoses and on causes of the developmental condition. Although Kennedy said that environmental factors are the main cause of autism, research has shown that genetics plays a bigger part. Population studies1 have linked a handful of environmental factors — mostly encountered during pregnancy — to increased chances of autism, but their precise role has been hard to pin down. More than anything, research has shown that the drivers of autism are fiendishly complicated. “There will never be a sound-bite answer to what causes autism,” says Helen Tager-Flusberg, a psychologist who studies neurodevelopmental conditions at Boston University, Massachusetts. The rise in prevalence, many researchers say, is predominantly caused by an increase in diagnoses rather than a true rise in the underlying symptoms and traits. “We don’t see an epidemic of autism, but we see an ‘epidemic’ of diagnoses,” says Sven Bölte, a specialist in child and adolescent psychiatric science at the Karolinska Institute in Stockholm. Researchers are concerned that Kennedy, an anti-vaccine advocate, will use the ADSI to promote the disproven idea that vaccines are linked to autism. © 2025 Springer Nature Limited

Keyword: Autism
Link ID: 29905 - Posted: 08.27.2025

Welcome to Entanglements. In this episode, hosts Brooke Borel and Anna Rothschild ask: Should we try to prevent autism? It’s a question that has divided the autistic community, and the answer has significant implications on how to focus scientific research and funding. Their guests this week are Jill Escher, a philanthropist, president of the National Council on Severe Autism, and parent of two young adults with severe nonverbal autism, and Eric García, the Washington bureau chief at The Independent and the author of “We’re Not Broken: Changing the Autism Conversation,” who is himself autistic. Robert F. Kennedy Jr: These are kids who will never pay taxes, they’ll never hold a job, they’ll never play baseball, they’ll never write a poem, they’ll never go out on a date. Many of them will never use a toilet unassisted. And we have to recognize we are doing this to our children. Anna Rothschild: That was Health and Human Services Secretary Robert F. Kennedy Jr., talking about autism back in April of 2025. And he promised to find some answers about the cause of the condition, which he called an epidemic. Robert F. Kennedy Jr: This is a preventable disease. We know it’s an environmental exposure. It has to be. Genes do not cause epidemics. Anna Rothschild: On that note, welcome to Entanglements, the show where we wade into the murkiest scientific controversies and search for common ground. I’m science journalist Anna Rothschild. Brooke Borel: And I’m Brooke Borel, articles editor at Undark Magazine. And that was a dramatic cold open. Anna, what’s happening here? Are you about to do an episode on whether vaccines cause autism? Anna Rothschild: No, that is not a murky controversy. That has been rigorously disproven. Brooke Borel: Yeah. Anna Rothschild: No, today we are asking the question: Should we try to prevent autism?

Keyword: Autism
Link ID: 29904 - Posted: 08.27.2025

By Claudia López Lloreda As cats age, they may yowl more than usual at night, have trouble sleeping or sleep too much, and act generally confused or disoriented. Now a new study shows that, just like in humans with Alzheimer’s disease, amyloid-beta plaques build up in the brains of aging felines and may contribute to dementia-like behaviors. In cats, that buildup could be causing a cascade of problems within the brain, such as hyperactivation of immune and other supporting brain cells that attack the synapses that connect nerve cells, researchers report August 11 in European Journal of Neuroscience. Aged cats with and without dementia had similar features and only a small number of cats were studied. But these findings could start helping researchers better understand how cats age and potentially develop treatments for feline dementia, as well as provide new insights into how the disease progresses in humans. Earlier studies had found amyloid beta in the brains of cats, but scientists didn’t know to what extent it was disrupting brain function. Robert McGeachan, a veterinarian at the University of Edinburgh, knew that the number of synapses decreased early in Alzheimer’s disease in humans. And so he and his team decided to focus on these connections in their cat study. They looked at the postmortem brains of seven young cats and 18 older ones, including eight with behavioral signs of dementia. Using fluorescent markers that find and cling to amyloid beta, the team found that the brains of aged cats, with or without dementia, had more of the protein than the younger brain samples. The amyloid beta plaques in the older cats also tended to accumulate right around synapses. © Society for Science & the Public 2000–2025.

Keyword: Alzheimers
Link ID: 29901 - Posted: 08.27.2025

By Angie Voyles Askham The adult cortex can rewire itself after injury, according to a series of classic experiments. When a monkey loses sensory input from a finger, for example, the region of the somatosensory cortex dedicated to that finger becomes overrun by inputs from the animal’s nearby fingers or face; the cortical map for the unused finger fades, and nearby maps of other body parts expand. “This is what I read in my textbook. This is what the lecturers told me in my lectures in university,” says Tamar Makin, professor of cognitive neuroscience at the University of Cambridge. But—contrary to those classic findings—such large-scale cortical reorganization did not happen in three people who lost an arm, according to a new functional imaging study Makin and her colleagues published today in Nature Neuroscience. Instead, the somatosensory map of each person’s hands, feet and lips, generated when they moved or attempted to move that body part, remained stable in the years before and after their hand was removed. “The representation of the hand persists,” says Makin, who led the study. The work is the first longitudinal look at whether amputation changes that cortical mapping. The results confirm what previous cross-sectional studies have hinted at, and they should put an end to the debate about how readily the adult cortex can shift its function, Makin says. But not everyone agrees. The study is an important contribution to the field, and it shows that maps of somatosensation driven by motor input remain stable after amputation, says Ben Godde, professor of neuroscience at Constructor University, who was not involved in the new work or the classic experiments. But that does not mean that other cortical maps are not shifting as a result of changing inputs, he says. “It’s not evidence that there’s no plasticity.” © 2025 Simons Foundation

Keyword: Pain & Touch; Development of the Brain
Link ID: 29900 - Posted: 08.23.2025