Helen Pearson In some parts of the world, record numbers of people are being diagnosed with attention deficit hyperactivity disorder (ADHD). In the United States, for example, government researchers last year reported that more than 11% of children had received an ADHD diagnosis at some point in their lives1 — a sharp increase from 2003, when around 8% of children had (see ‘ADHD among US boys and girls’). But now, top US health officials argue that diagnoses have spiralled out of control. In May, the Make America Healthy Again Commission — led by US health secretary Robert F. Kennedy Jr — said ADHD was part of a “crisis of overdiagnosis and overtreatment” and suggested that ADHD medications did not help children in the long term. One thing that’s clear is that several factors — including improved detection and greater awareness of ADHD — are causing people with symptoms to receive a diagnosis and treatment, whereas they wouldn’t have years earlier. Clinicians say this is especially true for women and girls, whose pattern of symptoms was often missed in the past. Although some specialists are concerned about the risks of overdiagnosis, many are more worried that too many people go undiagnosed and untreated. At the same time, the rise in awareness and diagnoses of ADHD has fuelled a public debate about how it should be viewed and how best to provide support, including when medication is required. The emergence of the neurodiversity movement is challenging the view of ADHD as a disorder that should be ‘treated’, and instead proposes that it’s a difference that should be better understood and supported — with more focus on adapting schools and workplaces, for instance. “I do have a big problem with ‘disorder’,” says Jeff Karp, a biomedical engineer at Brigham and Women’s Hospital in Boston, Massachusetts, who has ADHD. “It’s the school system that’s disordered. It’s not the kids.” But many clinicians and people with ADHD argue that it is associated with difficulties — ranging from academic struggles to an increased chance of injuries and substance misuse — that justify its label as a medical condition, and say that medication is an important and effective part of therapy for many people. © 2025 Springer Nature Limited

Keyword: ADHD
Link ID: 30034 - Posted: 11.29.2025

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

Keyword: Alzheimers
Link ID: 30033 - Posted: 11.29.2025

By Catherine Offord Researchers have tested a proof-of-concept device that enabled people who had lost their normal sense of smell to detect the presence of certain odors. Rather than exploiting the smell pathway, in which nasal cells send signals along olfactory nerves to the brain, the technology makes use of a less known nerve highway in the nose that transmits other sensations, including the kick of wasabi and the coolness of mint. “It’s an interesting study,” says Zara Patel, a rhinologist at Stanford Medicine who was not involved in the work, published today in Science Advances. “This is not recovering a sense of smell, this is activating a different system.” But she and others caution it remains to be seen how beneficial this kind of technology could be for people with smell loss, or anosmia. Humans have about 400 different olfactory receptors that are thought to enable the nose to detect billions of odors. But people can lose some or all of their sense of smell for a variety of reasons, including head trauma and viral infections such as COVID-19. People with long-term anosmia describe a significantly reduced quality of life and are at higher risk of mental health disorders, notes Halina Stanley, a research scientist at CNRS, the French national research agency, and co-author on the new paper. “The idea that if you lose your sense of smell, this isn’t as bad as losing another sense, I think is actually quite wrong.” Research by another team in 2018 found that electrodes placed in the sinuses near the olfactory bulb, the brain region that processes odor signals, could stimulate perception of smell, with people reporting onion or fruity scents, for example. Scientists are now working to develop implants that could more directly and specifically stimulate the olfactory bulb—akin to cochlear implants, which replace lost hearing by detecting sounds and stimulating the auditory nerve. However, such technology would be complex and invasive, and, at present, is a long way from becoming a therapy. © 2025 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Robotics
Link ID: 30032 - Posted: 11.29.2025

By Trip Gabriel Paul Ekman, a psychologist who linked thousands of facial expressions to the emotions they often subconsciously conveyed, and who used his research to advise F.B.I. interrogators and screeners for the Transportation Security Administration as well as Hollywood animators, died on Nov. 17 at his home in San Francisco. He was 91. His daughter, Eve Ekman, confirmed the death. Dr. Ekman sought to add scientific exactitude to the human impulse to interpret how others feel through their facial expressions. He recorded 18 types of smiles, for example, distinguishing between a forced smile and a spontaneous one; a genuine smile, he discovered, crinkles the orbicularis oculi muscle — that is, it creates crow’s feet around the eyes. Sometimes described as the world’s most famous face reader, Dr. Ekman was ranked No. 15 in 2015 by the American Psychological Association in its list of 200 eminent psychologists of the modern era. He was influential in reshaping the way facial expressions were understood — as the product of evolution rather than environment — and his findings crossed over to popular culture. The Fox TV drama “Lie to Me,” which ran for three seasons starting in 2009, featured a psychologist modeled on Dr. Ekman (played by Tim Roth) who assists criminal investigations by decoding the hidden meanings of facial expressions and body language. The show was developed by the producer Brian Grazer, who was inspired by a lengthy profile of Dr. Ekman by Malcolm Gladwell in The New Yorker in 2002. “The idea that you could tell a liar by some scientific test and know what they’re feeling just by looking at them was staggering to me,” the show’s writer, Samuel Baum, told The New York Times in 2009. As a young research psychologist in the late 1960s, Dr. Ekman changed the scientific consensus on facial expressions. In the postwar era, the conventional wisdom of eminent anthropologists like Margaret Mead was that human facial expressions were learned and that they varied across cultures. © 2025 The New York Times Company

Keyword: Emotions; Evolution
Link ID: 30031 - Posted: 11.29.2025

By Carl Zimmer Last year, Ardem Patapoutian got a tattoo. An artist drew a tangled ribbon on his right arm, the diagram of a protein called Piezo. Dr. Patapoutian, a neuroscientist at Scripps Research in San Diego discovered Piezo in 2010, and in 2021 he won a Nobel Prize for the work. Three years later, he decided to memorialize the protein in ink. Piezo, Dr. Patapoutian had found, allows nerve endings in the skin to sense pressure, helping to create the sense of touch. “It was surreal to feel the needle as it was etching the Piezo protein that I was using to feel it,” he recalled. Dr. Patapoutian is no longer studying how Piezo informs us about the outside world. Instead, he has turned inward, to examine the flow of signals that travel from within the body to the brain. His research is part of a major new effort to map this sixth, internal sense, which is known as interoception. Scientists are discovering that interoception supplies the brain with a remarkably rich picture of what is happening throughout the body — a picture that is mostly hidden from our consciousness. This inner sense shapes our emotions, our behavior, our decisions, and even the way we feel sick with a cold. And a growing amount of research suggests that many psychiatric conditions, ranging from anxiety disorders to depression, might be caused in part by errors in our perception of our internal environment. Someday it may become possible to treat those conditions by retuning a person’s internal sense. But first, Dr. Patapoutian said, scientists need a firm understanding of how interoception works. “We’ve taken our body for granted,” he said. Everyone has a basic awareness of interoception, whether it’s a feeling of your heart racing, your bladder filling or a flock of butterflies fluttering in your stomach. And neuroscientists have long recognized interoception as one function of the nervous system. Dr. Charles Sherrington, a Nobel Prize-winning neuroscientist, first proposed the existence of “intero-ceptors,” in 1906. © 2025 The New York Times Company

Keyword: Obesity; Stress
Link ID: 30030 - Posted: 11.26.2025

By Caroline Hopkins Legaspi In a study published Monday in JAMA Neurology, researchers linked obstructive sleep apnea, a condition that causes temporary pauses in breathing during sleep, with Parkinson’s disease. Parkinson’s disease is a progressive nervous system disorder that causes tremors, stiffness, and difficulty speaking, moving and swallowing. It is the second-most common neurodegenerative disease in the United States, after Alzheimer’s disease, with 90,000 people diagnosed each year. There is no cure for Parkinson’s disease, said Dr. Lee Neilson, a neurologist at Oregon Health & Science University who led the study. But the researchers did find that treating sleep apnea with a continuous positive airway pressure (or CPAP) machine was associated with a reduced likelihood of developing Parkinson’s. So identifying those at highest risk for the neurological condition — and intervening early, Dr. Neilson said, “might make the biggest impact.” The researchers analyzed medical records from more than 11 million U.S. veterans treated through the Department of Veterans Affairs between 1999 and 2022. The group was predominantly male with an average age of 60, representing those at highest risk for sleep apnea, experts said. The researchers found that about 14 percent of the participants had been diagnosed with sleep apnea between 1999 and 2022, according to their medical records. When the researchers looked at their health six years after those diagnoses, they found that the veterans with sleep apnea were nearly twice as likely to have developed Parkinson’s disease compared with those who had not been diagnosed with sleep apnea. This held even after controlling for other factors that could influence the development of sleep apnea or Parkinson’s disease, including high body mass index and conditions like diabetes, high blood pressure, traumatic brain injuries and depression. © 2025 The New York Times Company

Keyword: Sleep; Parkinsons
Link ID: 30029 - Posted: 11.26.2025

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

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

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

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

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

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

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

Keyword: Alzheimers
Link ID: 30025 - Posted: 11.26.2025

Davide Castelvecchi Pigeons can sense Earth’s magnetic field by detecting tiny electrical currents in their inner ears, researchers suggest. Such an inner compass could help to explain how certain animals can achieve astonishing feats of long-distance navigation. The team performed advanced brain mapping as well single-cell RNA sequencing of pigeon inner-ear cells. Both lines of evidence point to the inner ear as the birds’ ‘magnetoreception’ organ. The results appeared in the Science on 20 November 1. “This is probably the clearest demonstration of the neural pathways responsible for magnetic processing in any animal,” says Eric Warrant, a sensory biology researcher at the University of Lund in Sweden. Studies have suggested that various animals, including turtles, trout and robins, can sense the direction and strength of magnetic fields, although the evidence has sometimes been contested — and the mechanisms have remained controversial. Bird-brained navigation Two leading hypotheses have led the research into how birds sense magnetic fields. One is a quantum-physics effect in retina cells where birds ‘see’ magnetic fields. Another is that microscopic iron oxide particles in the beak could act as tiny compass needles. However, it’s largely unknown where magnetic information is sensed in animals’ brains and how sensory neurons confer sensitivity to electromagnetic changes. In 2011, researchers found hints that magnetic fields triggered pigeons’ vestibular system, the organ that enables vertebrates to sense accelerations (including gravity) and helps them to stay balanced2. The structure is made of three fluid-filled loops which are mutually perpendicular, so they can communicate to the brain the direction of an acceleration by breaking it down into three ‘x, y, z’ components. © 2025 Springer Nature Limited

Keyword: Animal Migration; Hearing
Link ID: 30024 - Posted: 11.22.2025

Mark Brown Sophisticated and deadly “brain weapons” that can attack or alter human consciousness, perception, memory or behaviour are no longer the stuff of science fiction, two British academics argue. Michael Crowley and Malcolm Dando, of Bradford University, are about to publish a book that they believe should be a wake-up call to the world. They are this weekend travelling to The Hague for a key meeting of states, arguing that the human mind is a new frontier in warfare and there needs to be urgent global action to prevent the weaponisation of neuroscience. “It does sound like science fiction,” said Crowley. “The danger is that it becomes science fact.” The book, published by the Royal Society of Chemistry, explores how advances in neuroscience, pharmacology and artificial intelligence are coming together to create a new threat. “We are entering an era where the brain itself could become a battlefield,” said Crowley. “The tools to manipulate the central nervous system – to sedate, confuse or even coerce – are becoming more precise, more accessible and more attractive to states.” The book traces the fascinating, if appalling, history of state-sponsored research into central nervous system (CNS)-acting chemicals. During the cold war and after, the US, Soviet Union and China all “actively sought” to develop CNS-acting weapons, said Crowley. Their purpose was to cause prolonged incapacitation to people, including “loss of consciousness or sedation or hallucination or incoherence or paralysis and disorientation”. © 2025 Guardian News & Media Limited

Keyword: Drug Abuse; Aggression
Link ID: 30023 - Posted: 11.22.2025

By Ali Watkins The act has been called many things: Centrifugal motion. Perpetual bliss. The thrill of the moment. Unstoppable. In technical terms, it is “non-agonistic interaction involving directed, intraspecific, oral-oral contact with some movement of the lips/mouthparts and no food transfer.” Or, as her majesty Faith Hill might say, “This kiss.” And, it turns out, it’s also really old. British scientists say they’ve traced the age of the kiss, to anywhere from 16 million to 21 million years ago, and have found that it was far more common among other species than previously understood. Ants? They smooch. Fish? Kissers. Neanderthals? Yep, they puckered up, too — sometimes even with us. But kissing, the researchers said, has always been something of a so-called evolutionary mystery. It doesn’t present much benefit for survival, it has minimal reproductive benefits, and it’s mostly symbolic. “Kissing is a really interesting behavior,” said Matilda Brindle, an evolutionary biologist at Oxford University who led the study. Dozens of societies and cultures use it, it’s common, and it has weighted symbolism. But, she said, “we’ve not really tested it from an evolutionary perspective.” In prehistoric kissing, it seems, could be the primitive origins of our search for intimate connection. The act inherently requires vulnerability, and trust. It’s not always sexual and is often used among and between genders simply to show affection, and often between parents and offspring. Though researchers found evidence of kissing in several species, they narrowed the focus of the study mostly to the behavior of large apes, like gorillas, orangutans and baboons. © 2025 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 30022 - Posted: 11.22.2025

By Laura Sanders SAN DIEGO — A diet low in the amino acid glutamate may ease migraines, a small study suggests. A month of staying away from high-glutamate foods led to fewer migraines in a group of 25 people with Gulf War Illness. The specifics of these veterans’ migraines, part of a collection of symptoms resulting from the Gulf War, may differ from those of other people who suffer from migraines. But if the underlying relationship between glutamate and migraines is similar, the diet could help the estimated 1 billion people worldwide who have migraines. Current drugs for treating migraines, including a new class of compounds that block a chemical messenger called CGRP, can help. But existing drugs don’t work for everyone, says neuroscientist Ian Meng of the University of New England in Biddeford, Maine. A dietary change could be a low-risk and accessible way to bring relief. Glutamate is both a signal that excites nerve signals in the brain and an amino acid found in tomatoes, processed meats, aged cheese, mushrooms and, of course, monosodium glutamate, or MSG. For a month, 25 veterans of the Gulf War ate a low-glutamate diet full of whole fruits and veggies and avoided high-glutamate foods including soy sauce, mushrooms and ultraprocessed foods. Before this diet, 64 percent of these people reported having a migraine in the previous week. After a month of a low-glutamate diet, that number dropped to about 12 percent, neuroscientist Ashley VanMeter said November 16 in a news briefing at the annual meeting of the Society for Neuroscience. After the one-month diet ended, 88 percent of the people in the study chose to remain on the diet. “They feel that [the diet] is definitely benefiting them,” said VanMeter, of Georgetown University in Washington, D.C. © Society for Science & the Public 2000–2025.

Keyword: Pain & Touch
Link ID: 30021 - Posted: 11.22.2025

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

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

Liam Drew Paradromics, a neurotechnology developer, announced today that the US Food and Drug Administration (FDA) has approved a first long-term clinical trial of its brain–computer interface (BCI). Early next year, the company — one of the closet rivals to Elon Musk’s neurotechnology firm Neuralink — will implant its device in two volunteers who were left unable to speak owing to neurological diseases and injuries. It has two goals: to ensure the device is safe; and to restore a person’s ability to communicate with real-time speech. “We’re very excited about bringing this new hardware into a trial,” says Matt Angle, chief executive of Paradromics, which is based in Austin, Texas. Paradromics’ BCI has an active area of roughly 7.5 millimetres in diameter of thin, stiff, platinum-iridium electrodes that penetrate the surface of the cerebral cortex to record from individual neurons around 1.5 mm deep. This is then connected by wire to a power source and wireless transceiver implanted in an individual’s chest. Initially, the two volunteers will each have one electrode array implanted in the area of the motor cortex that controls the lips, tongue and larynx, Angle says. Neural activity will then be recorded from this region as the study participants imagine speaking sentences that are presented to them. Following previous work by researchers who are now collaborating with Paradromics1, the system learns what patterns of neural activity correspond to each intended speech sound. When participants imagine speaking these neural patterns will be converted into text on a screen for participants to approve, or into a real-time voice output based on old recordings of participants’ own voices. This is the first BCI clinical trial to formally target synthetic-voice generation. “Arguably, the greatest quality of life change you can deliver right now with BCI is communication,” Angle says. © 2025 Springer Nature Limited

Keyword: Robotics
Link ID: 30019 - Posted: 11.22.2025

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

Keyword: Robotics
Link ID: 30018 - Posted: 11.19.2025

By Kate Graham-Shaw A long time ago in a galaxy far, far away, R2-D2 beeped and booped—and now birds that copy the Star Wars character are giving scientists fresh insight into how different species imitate complex sounds. A study, published recently in Scientific Reports, analyzed the sounds of nine species of parrots, including Budgies, as well as European Starlings to see how accurately each bird mimicked R2-D2’s robotic whirring. Researchers did acoustic analyses on samples of birds imitating the plucky droid that were already available online to compare how statistically similar each bird’s noises were to a model of R2-D2’s sounds. The starlings, a type of songbird, emerged as star vocalists: their ability to produce “multiphonic” noises—in their case, two different notes or tones expressed simultaneously—allowed them to replicate R2-D2’s complex chirps more accurately. Parrots and budgies, which only produce “monophonic” (or single-tone) noises, imitated the droid’s sounds with less accuracy and musicality. The differing abilities stem from physical variations in the birds’ “syrinx”—a unique vocal organ that sits at the base of the avian windpipe. “Starlings can produce two sounds at once because they control both sides of the syrinx independently,” says study co-author Nick Dam, an evolutionary biologist at Leiden University in the Netherlands. “Parrots are physically incapable of producing two tones simultaneously.” It isn’t exactly known why different species developed differing control over their syrinx. “Likely, some ancestor of songbirds happened to evolve the ability to control the muscles on both sides of the syrinx, and this helped them in some way,” says University of Northern Colorado biologist Lauryn Benedict, who wasn’t involved in the study but sometimes works with its authors. One of the leading explanations involves mating; the better at singing a male songbird is, the more females he attracts. © 2025 SCIENTIFIC AMERICAN,

Keyword: Animal Communication; Language
Link ID: 30017 - Posted: 11.19.2025

Mariana Lenharo The obesity drug tirzepatide, sold as Mounjaro or Zepbound, can suppress patterns of brain activity associated with food cravings, a study suggests. Researchers measured the changing electrical signals in the brain of a person with severe obesity who had experienced persistent ‘food noise’ — intrusive, compulsive thoughts about eating — shortly after the individual began taking the medication. The study is the first to use electrodes to directly measure how blockbuster obesity drugs that mimic the hormone GLP-1 affect brain activity in people, and to hint at how they curb extreme food cravings. “It’s a great strategy to try and find a neural signature of food noise, and then try to understand how drugs can manipulate it,” says Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center in Philadelphia, Pennsylvania. The findings were published today in Nature Medicine1. Casey Halpern, a neurosurgeon-scientist at the University of Pennsylvania in Philadelphia, and his colleagues did not set out to investigate the effects of obesity drugs on the brain. The team’s goal was to test whether a type of deep brain stimulation — a therapy that involves delivering a weak electrical current directly into the brain — can help to reduce compulsive eating in people with obesity for whom treatments such as bariatric surgery haven’t worked. The scientists set up a study in which participants had an electrode implanted into their nucleus accumbens, a region of the brain that is involved in feelings of reward. It also expresses the GLP-1 receptor, notes Christian Hölscher, a neuroscientist at the Henan Academy of Innovations in Medical Science in Zhengzhou, China, “so we know that GLP-1 plays a role in modulating reward here”. This type of electrode, which can both record electrical activity and deliver an electrical current when needed, is already used in people to treat some forms of epilepsy. © 2025 Springer Nature Limited

Keyword: Obesity; Attention
Link ID: 30016 - Posted: 11.19.2025

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

Keyword: Autism
Link ID: 30015 - Posted: 11.19.2025