Chapter 13. Memory and Learning

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Rachel Fieldhouse During ageing, men experience a greater reduction in volume across more regions of the brain than women do, according to a longitudinal study published today in the Proceedings of the National Academy of Sciences1. The authors suggest this means that age-related brain changes do not explain why women are more frequently diagnosed with Alzheimer’s disease than men are. “It’s really important that we understand what happens in the healthy brain so that we can better understand what happens when people get these neurodegenerative conditions,” says Fiona Kumfor, a clinical neuropsychologist at the University of Sydney, Australia. This study adds to scientists’ understanding of typical brain ageing, she adds. Nearly twice as many women are diagnosed with Alzheimer’s disease as men, and ageing is the biggest risk factor for the disease. This has prompted research into age-related sex differences in the brain. “If women’s brains declined more, that could have helped explain their higher Alzheimer’s prevalence,” says co-author Anne Ravndal, a PhD student at the University of Oslo. Previous research investigating sex differences in brain ageing has shown mixed results, Ravndal adds. Several studies have found that men experience greater loss of total grey matter and hippocampus size compared with women, whereas other work has reported a sharper decline of grey matter in women. Brain scans The latest study included more than 12,500 magnetic resonance imaging (MRI) brain scans from 4,726 people — at least two scans per person, taken an average of three years apart — who did not have Alzheimer’s disease or any cognitive impairments and were control participants in 14 larger data sets. The researchers compared how the individuals’ brain structures changed over time, looking at factors including the thickness of grey matter and the size of areas that are associated with Alzheimer’s disease, such as the hippocampus, which is essential to memory. © 2025 Springer Nature Limited

Keyword: Alzheimers; Sexual Behavior
Link ID: 29968 - Posted: 10.15.2025

By Jennie Erin Smith The marine whiff of ambergris. The citrusy tang of grapefruit. The must of “corked” wine. The human nose can detect a virtually infinite palette of odors, some at vanishingly low concentrations. But puzzlingly, our bodies only use about 400 receptor proteins to interpret them. Now, fragrance researchers in Switzerland have landed on a new way to study the proteins in the laboratory—and their results, they say, challenge a foundational theory of how smell works. For decades, scientists have struggled to get cells commonly used in laboratory settings to express the genes that encode olfactory receptors (ORs), proteins primarily found on neurons in our nasal cavities. Using a process they describe today in Current Biology, researchers at the Swiss fragrance and flavorings company Givaudan say they have tweaked lab-friendly cells into readily expressing ORs. The result was an in vitro system for identifying specific ORs, including those that strongly respond to molecules in ambergris, grapefruit, and corked wine. The Swiss group’s discovery, other olfaction researchers say, stands to make ORs much easier to study. But more controversially, the group also claims to have observed patterns of receptor activity that call into question combinatorial coding, a long-standing hypothesis of olfaction that helped Linda Buck and Richard Axel win a Nobel Prize in 2004. Combinatorial coding holds that multiple ORs act in concert to pick up different parts of an odorant molecule, creating patterns or codes that are recognized by the brain. Beyond that, says neuroscientist Joel Mainland of the Monell Chemical Senses Center, the model is “pretty vague on the details.” It has been hard to test, because olfactory neurons can’t be cultured in the lab. Determining which OR detects which odorant required extensive tests in rodents, and it’s not ideal “to have to sacrifice an animal each time you want to do an experiment,” says Claire de March, a chemist at CNRS, the French national research agency. As a result, investigators were left with many so-called orphan receptors whose ligands, or binding molecules, are unknown. © 2025 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Development of the Brain
Link ID: 29966 - Posted: 10.11.2025

By David Adam In February of this year, George Mentis and his colleagues published data from a small clinical trial they said showed that degraded motor neurons aren’t irreparable. In the study, electrical stimulation to the spine in three people with spinal muscular atrophy (SMA) appeared to resuscitate lost motor neurons, the authors said, as well as restore some of the cellular processes needed to activate muscle. “It was incredible,” says Mentis, professor of pathology and cell biology (in neurology) at Columbia University. “We’re unleashing or tapping on the potential of dysfunctional neurons to show plasticity.” The authors wrote that the results showed it was possible to “effectively rescue motor neuron function” and that the electrical stimulation had rebuilt neuronal circuitry and reversed—at least for a while—some degeneration. Mentis and his team think their results are coalescing into a theory, even if they don’t fully understand it yet. The researchers are essentially altering the electrical properties of the motor neurons so they start to behave better and closer to normal, says Genís Prat-Ortega, a postdoctoral associate in the Rehab Neural Engineering Labs at the University of Pittsburgh and an investigator on the study. “The motor neurons change and repair,” he says. “Somehow, we are reversing a neurodegenerative process.” Not everyone is so sure. Tim Hagenacker, professor of neurology at the University of Duisburg-Essen, says rebuilding the neural circuit is “not entirely convincing” as an explanation for the study’s results. He thinks that “other cell types play a crucial co-role” in restoring neuronal plasticity or that dysfunctional motor neurons could exist in some form of hibernation. © 2025 Simons Foundation

Keyword: ALS-Lou Gehrig's Disease ; Regeneration
Link ID: 29965 - Posted: 10.11.2025

Violeta Ruiz On 25 November 1915, the American newspaper The Review published the extraordinary case of an 11-year-old boy with prodigious mathematical abilities. Perched on a hill close to a set of railroad tracks, he could memorise all the numbers of the train carriages that sped by at 30 mph, add them up, and provide the correct total sum. What was remarkable about the case was not just his ability to calculate large numbers (and read them on a moving vehicle), but the fact that he could barely eat unassisted or recognise the faces of people he met. The juxtaposition between his supposed arrested development and his numerical facility made his mathematical feats even more impressive. ‘How can you account for it?’ asked the article’s author. The answer took the form of a medical label: the boy was what 19th-century medicine termed an ‘idiot savant’. He possessed an exceptional talent, despite a profound impairment of the mental faculties that affected both his motor and social skills. A century after The Review relayed the prodigious child’s mathematical abilities, trying to understand ‘how they do it’ still drives psychological research into savantism or ‘savant syndrome’ to this day. The SSM Health Treffert Centre in Wisconsin – named after Darold Treffert (1933-2020), one of the leading experts in the field – defines the savant phenomenon as ‘a rare condition in which persons with various developmental disorders, including autistic disorder, have an amazing ability and talent’. Today, savantism is largely comprehended through the lens of neurodivergence, since the association between savantism and autism is strong: roughly one in 10 people with autism exhibit some savant skills, while savantism in the absence of autism is much rarer. Psychological studies by Simon Baron-Cohen and Michael Lombardo, for example, have focused on the neurological basis of ‘systemising’, where exceptional mathematical or musical skills exist among people diagnosed with autism: such people are ‘hypersystemisers’, that is, they are especially good at identifying ‘laws, rules, and/or regularities’. It is believed that their brain’s systemising mechanisms are ‘tuned to very high levels’, making them acutely sensitive to sensory input and also capable of intense attentional focus and rule-learning. © Aeon Media Group Ltd. 2012-2025.

Keyword: Intelligence; Learning & Memory
Link ID: 29964 - Posted: 10.11.2025

By Pam Belluck Before dawn on a March morning, Doug Whitney walked into a medical center 2,000 miles from home, about to transform from a mild-mannered, bespectacled retiree into a superhuman research subject. First, a doctor inserted a needle into his back to extract cerebral spinal fluid — “liquid gold,” a research nurse called it for the valuable biological information it contains. Then, the nurse took a sample of his skin cells. After that came an injection of a radioactive tracer followed by a brain scan requiring him to lie still for 30 minutes with a thermoplastic mask over his face. Then, another tracer injection and another brain scan. During his three-day visit to the center, at Washington University School of Medicine in St. Louis, he also had cognitive assessments, neurological evaluations and blood draws that extracted multiple tubes for analysis. For 14 years now, Mr. Whitney has been the one-person focus of exceptionally detailed scientific investigation, for which he travels periodically to St. Louis from his home in Port Orchard, Wash. It is not because he is ill. It is because he was supposed to be ill. Mr. Whitney, 76, is a scientific unicorn with potential to provide answers about one of the world’s most devastating diseases. He has a rare genetic mutation that essentially guaranteed he would develop Alzheimer’s disease in his late 40s or early 50s and would likely die within a decade. His mother and nine of her 13 siblings developed Alzheimer’s and died in the prime of their lives. So did his oldest brother, and other relatives going back generations. It is the largest family in the United States known to have an Alzheimer’s-causing mutation. “Nobody in history had ever dodged that bullet,” Mr. Whitney said. © 2025 The New York Times Company

Keyword: Alzheimers; Genes & Behavior
Link ID: 29962 - Posted: 10.08.2025

By Zunnash Khan You can inherit a talent for athletics from your parents, but physical fitness—which is determined in large part by exercise and other lifestyle choices—doesn’t seem like it can be inherited. But now, a paper suggests male mice that exercise can pass their newly gained fitness on to male offspring. If the same holds true in humans, the researchers say, fathers could help improve the health of any future children by staying in shape themselves. The study is the latest example of how traits can be passed to the next generation not through the DNA in genes, but via snippets of DNA’s chemical cousin, RNA, packed as cargo into sperm cells and delivered to the embryo. “You’re having the animals exercise and then you’re getting the transmission of the phenotype to the next generation,” says Colin Conine, an epigeneticist at the University of Pennsylvania who was not involved in the work. “I think that’s interesting.” Most heritable traits are passed from parents to their offspring through the DNA in genes. (Inheriting genes for a large lung volume might increase your chances of becoming a runner, for example.) But things you experience or learn—such as the ability to make a soufflé or read Sanskrit—aren’t encoded into genes and can’t be passed on this way. Still, recent advances in biology have shown there’s more to heritability than genes. Some acquired traits can alter the chemical packaging of the DNA and affect the properties of the offspring, a phenomenon known as epigenetics. Recent research has identified so-called microRNAs (miRNAs) in sperm cells as one way epigenetic information can be passed on. For example, scientists have shown that diet, stress, and toxins can have an impact on the embryo through miRNAs. A 2021 paper suggested male mice can confer a susceptibility to depression to their offspring this way. © 2025 American Association for the Advancement of Science.

Keyword: Epigenetics
Link ID: 29960 - Posted: 10.08.2025

By Meghie Rodrigues Babies start processing language before they are born, a new study suggests. A research team in Montreal has found that newborns who had heard short stories in foreign languages while in the womb process those languages similarly to their native tongue. The study, published in August in Nature Communications Biology, is the first to use brain imaging to show what neuroscientists and psychologists had long suspected. Previous research had shown that fetuses and newborns can recognize familiar voices and rhythms and even that they prefer their native language soon after birth. But these findings come mostly from behavioral cues—sucking patterns, head turns or heart rate changes—rather than direct evidence from the brain. “We cannot say babies ‘learn’ a language prenatally,” says Anne Gallagher, a neuropsychologist at the University of Montreal and senior author of the study. What we can say, she adds, is that neonates develop familiarity with one or more languages during gestation, which shapes their brain networks at birth. The research team recruited 60 people for the experiment, all of them about 35 weeks into their pregnancy. Of those, 39 exposed their fetuses to 10 minutes of prerecorded stories in French (their native language) and another 10 minutes of the same stories in either Hebrew or German at least once every other day until birth. These languages were chosen because their acoustic and phonological properties are very distinctfrom French and from each other, explains co-lead author Andréanne René, a Ph.D. candidate in clinical neuropsychology at the University of Montreal. The other 21 participants were part of the control group; their fetuses were exposed to French in their natural environments, with no special input. © 2025 SCIENTIFIC AMERICAN

Keyword: Language; Development of the Brain
Link ID: 29959 - Posted: 10.08.2025

By Ellen Barry Around the time of the pandemic, I began to notice something happening in my social circle. A close friend, then in her early 50s, got a diagnosis of attention deficit hyperactivity disorder. She described it as a profound relief, releasing her from years of self-blame — about missed deadlines and lost receipts, but also things that were deeper and more complicated, like her sensitivity to injustice. Listen to this article with reporter commentary Something similar happened to a co-worker, and a cousin in his 30s, and an increasing number of people I met covering mental health. It wasn’t always A.D.H.D. For some of them, the revelation was a diagnosis of autism spectrum disorder: After years of inarticulate unease in social situations, they felt freed by the framework of neurodivergence, and embraced by the community that came along with it. Since then I’ve heard accounts from people who received midlife diagnoses of binge eating disorder, post-traumatic stress disorder, anxiety. Nearly all of them said the diagnosis provided relief. Sometimes it led to an effective treatment. But sometimes, simply identifying the problem — putting a name to it — seemed to help. Lately, it seems as if we never stop talking about the rising rates of chronic diseases, among them autism, A.D.H.D., depression, anxiety and PTSD. Health Secretary Robert F. Kennedy Jr. has pointed to these trends as evidence that Americans are “the sickest people in the world,” and has set about upending whole swaths of our public health system in search of causes, like vaccines or environmental toxins. But much of what we’re seeing is a change in diagnostic practices, as we apply medical labels to ever milder versions of disease. There are many reasons for this: The shame that once accompanied many disorders has lifted. Screening for mental health problems is now common in schools. Social media gives us the tools to diagnose ourselves. And clinicians, in a time of mental health crisis, see an opportunity to treat illnesses early. © 2025 The New York Times Company

Keyword: ADHD; Autism
Link ID: 29955 - Posted: 10.04.2025

Gemma Conroy Whether it’s dancing the tango or playing the guitar, engaging in a creative pastime can slow brain ageing, according to a study of dancers, musicians, artists and video game players from multiple countries. The analysis used brain clocks — models that measure the difference between a person’s chronological age and the age their brain appears to be — to assess whether creative activities help to maintain neurological youth. In brain regions that are most susceptible to ageing, engaging in creative activities increased connections with different areas of the brain. Although experts had ‘younger’ brains than their less-experienced counterparts did, even learning a creative skill from scratch had an anti-ageing effect on the brain. The findings were published on 3 October in Nature Communications1. Song and dance Previous studies suggest that engaging in creative activities can help to keep the brain young and foster emotional well-being. But few have investigated the biological basis of these brain benefits or what drives them, says study co-author Agustín Ibáñez, a neuroscientist at Adolfo Ibáñez University in Santiago, Chile. “There is really poor mechanistic evidence,” he says. How fast are you ageing? Ordinary brain scans reveal the pace To address this gap, Ibáñez and his colleagues created brain clocks using neuroimaging data of brain activity taken from 1,240 participants across 10 countries. These machine-learning models used functional connectivity, a measure of how brain regions work together, to estimate brain age. The researchers then applied their brain clocks to 232 tango dancers, musicians, visual artists and video game players of different ages and experience levels to calculate their ‘brain age gap’ — the difference between their predicted brain age and their actual age. © 2025 Springer Nature Limited

Keyword: Alzheimers; Learning & Memory
Link ID: 29954 - Posted: 10.04.2025

By Yasemin Saplakoglu From Santiago Ramón y Cajal’s hand came branches and whorls, spines and webs. Now-famous drawings by the neuroanatomist in the late 19th and early 20th centuries showed, for the first time, the distinctiveness and diversity of the fundamental building blocks of the mammalian brain that we call neurons. In the century or so since, his successors have painstakingly worked to count, track, identify, label and categorize these cells. There is now a dizzying number of ways to put neurons in buckets, often presented in colorful, complex brain cell atlases. With such catalogs, you might organize neurons based on function by separating motor neurons that help you move from sensory neurons that help you see or number neurons that help you estimate quantities. You might distinguish them based on whether they have long axons or short ones, or whether they’re located in the hippocampus or the olfactory bulb. But the vast majority of neurons, regardless of function, form or location, fall into one of two fundamental categories: excitatory neurons that trigger other neurons to fire and inhibitory neurons that stop others from firing. Maintaining the correct proportion of excitation to inhibition is critical for keeping the brain healthy and harmonious. “Imbalances in either direction can be really catastrophic,” said Mark Cembrowski (opens a new tab), a neuroscientist at the University of British Columbia, or lead to neurological conditions. Too much excitation and the brain can produce epileptic seizures. Too little excitation can be associated with conditions such as autism. Neuroscientists are working to uncover how these two classes of cells work — and specifically, how they interact with a rarer third category of cells that influence their behavior. These insights could eventually help reveal how to restabilize networks that get out of balance, which can even occur as a result of normal aging. © 2025 Simons Foundation

Keyword: Epilepsy; Attention
Link ID: 29952 - Posted: 10.01.2025

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