By Kelly Servick In the past 20 years, mice with glowing cables sprouting from their heads have become a staple of neuroscience. They reflect the rise of optogenetics, in which neurons are engineered to contain light-sensitive proteins called opsins, allowing pulses of light to turn them on or off. The method has powered thousands of basic experiments into the brain circuits that drive behavior and underlie disease. As this research tool matured, hopes arose for using it as a treatment, too. Compared with the electrical or magnetic brain stimulation approaches already in use, optogenetics offers a way to more precisely target and manipulate the exact cell types underlying brain disorders. So far only one optogenetic application—addressing certain kinds of vision loss by introducing opsins into cells in the eye—has made it into human trials. But its promising early results, along with the discovery of more sensitive and sophisticated opsins, are inspiring researchers to look beyond the eye, developing treatments that would act on peripheral nerves or deep in the brain. Initial tests of these strategies in animal models of epilepsy, amyotrophic lateral sclerosis (ALS), and other neurological disorders have been encouraging, researchers reported last month at the annual meeting of the Society for Neuroscience (SfN) in San Diego. One company is hoping to launch a human trial for an optogenetic pain treatment by 2027. “We definitely don’t want to oversell the idea of using optogenetics [on human brains] any time soon, but we also are firmly convinced that this is now the right moment to be thinking about this seriously,” University of Geneva neurologist and neuroscientist Christian Lüscher told an SfN session he chaired, in which participants presented a newly published road map for bringing optogenetics to the clinic. Still, the presenters acknowledged major remaining challenges, including possible risks of inserting genes for opsins—many of which are derived from algae or other microbes—into a person’s nerves or brain cells. © 2025 American Association for the Advancement of Science.

Keyword: Pain & Touch; Epilepsy
Link ID: 30046 - Posted: 12.13.2025

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

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

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

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 Roni Caryn Rabin The most stressful part of the trip for Sunny Brous came when she had to part with her wheelchair so that the flight crew could put it in the luggage hold. You just never know what shape it will be in when you get it back, she said. “I tell them, ‘Take the best care of it you can,’” she said. “Those wheels are my legs! Those wheels are my life.” Ms. Brous, 38, who lives in Hico, Texas, was one of dozens of women who converged on the Sea Crest Beach Resort on Cape Cod toward the end of summer for the gathering of a club no one really wanted to be a member of: women diagnosed in their 20s and early 30s with amyotrophic lateral sclerosis, or A.L.S. The terminal neurodegenerative disorder robs them of the ability to talk, walk, use their hands or even breathe. It has long been seen as a disease of older men, who make up a majority of patients. There is no cure. The women traveled with husbands, mothers, sisters and aides, and they did not travel light. Their packing lists included heavy BiPAP machines to help them breathe, formula for their feeding tubes, commodes, portable bidets, myriad chargers, leg braces and canes, pills and pill crushers and bottles of a medication with gold nanoparticles that was still being tested in clinical trials. Half of Ms. Brous’s suitcase was filled with party gifts for the friends she texts with throughout the year on an endless WhatsApp chat, including bags of popcorn with Texan flavors like Locked and Loaded, a Cheddar, bacon, sour cream and chives combo that you can only get in Hico. Desiree Galvez Kessler’s sister drove her, her mother and an aide up from Long Island in a van with a clunky Hoyer transfer lift in the back. Ms. Kessler — Desi to her friends — was diagnosed at 29, and has not been able to walk or speak for 10 years; the large computer tablet that she communicates with using eye-gaze technology is mounted on her wheelchair. © 2025 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease ; Sexual Behavior
Link ID: 30009 - Posted: 11.12.2025

Jon Hamilton In Alzheimer's, brain cells die too soon. In cancer, dangerous cells don't die soon enough. That's because both diseases alter the way cells decide when to end their lives, a process called programmed cell death. "Cell death sounds morbid, but it's essential for our health," says Douglas Green, who has spent decades studying the process at St. Jude Children's Research Hospital in Memphis, Tennessee. For example, coaxing nerve cells to live longer could help people with Alzheimer's disease, Parkinson's disease or ALS (Lou Gehrig's disease), he says, while getting tumor cells to die sooner could help people with cancer. So researchers have been searching for disease treatments that "modify or modulate the tendency of a cell to die," Green says. One of these researchers is Randal Halfmann at the Stowers Institute for Medical Research in Kansas City, Missouri. He has been studying immune cells that self-destruct when they come into contact with molecules that present a threat to the body. "They have to somehow recognize that [threat] in this vast array of other complex molecules," he says, "and then within minutes, kill themselves." They do this much the way a soldier might dive on a grenade to save others' lives. Halfmann's team has been focusing on special proteins inside cells that can trigger this process. When these proteins recognize molecules associated with a virus or some other pathogen, he says, "they implode." The proteins crumple and begin linking up with other crumpled proteins to form a structure called a "death fold" polymer. That starts a chain reaction of polymerization that ultimately kills the cell. Halfmann's team knew this process takes a burst of energy. But they couldn't locate the source. © 2025 npr

Keyword: Alzheimers; Apoptosis
Link ID: 29973 - Posted: 10.18.2025

By John Branch Photographs by Sophie Park It starts with a tingle, a tremor, a sense that something is off. Dr. Sue Goldie doesn’t recognize the symptoms at first. Maybe she ignores them, wishes them away. It is 2021. She is 59, in the prime of a long teaching career at Harvard. She has just immersed herself in the sport of triathlon. One coach notes something off with her running cadence. Another wonders why her left arm isn’t fully lifting out of the water. A trainer sees a slight tremor. The first time Sue races, she feels a strange vibration, like an internal tremble. Then Sue sees it herself: Twitching fingers on her left hand. Tests reveal it is Parkinson’s, the incurable neurological disease that robs its victims of their motor skills, and sometimes their minds, one extinguished neuron at a time. Parkinson’s doesn’t always alter life spans, but it always upends lives. The diagnosis elicits a storm of emotions, but also raises questions, both pragmatic and deep, that have consumed Sue since. At what point, if ever, do I have to say something? Who needs to know? What do I reveal and what do I conceal? And, most profoundly: Does a diagnosis have to be an identity? For nearly four years, she keeps her diagnosis from most Harvard administrators, colleagues and students, worried about what it will do to her reputation. She grows more comfortable revealing herself away from work, in the world of triathlon. “I feel very strongly that I should be able to disclose this when I want, how I want, and it’s under my control,” she tells me last year. But Parkinson’s does not wait. Maybe others don’t notice the physical signs, not yet. They don’t see her in the early morning, shuffling off-balance to the bathroom before her medications kick in, a daily reminder that Parkinson’s was not something she dreamed last night. Maybe they don’t see the pill boxes in her purse, the exposed feeling she gets when the dopamine medications wear off, the persistent worry behind her cheerful disposition. Her symptoms are worsening. Disguising them is exhausting. Starting today, she is Sue with Parkinson’s. © 2025 The New York Times Company

Keyword: Parkinsons
Link ID: 29969 - Posted: 10.15.2025

By Siddhant Pusdekar Taste and smell are so intimately connected that a whiff of well-loved foods evokes their taste without any conscious effort. Now, brain scans and machine learning have for the first time pinpointed the region responsible for this sensory overlap in humans, a region called the insula, researchers report September 12 in Nature Communications. The findings could explain why people crave certain foods or are turned away from them, says Ivan de Araujo, a neuroscientist at Max Planck Institute for Biological Cybernetics in Tübingen, Germany. Smell and taste become associated from the moment we bite into something, says Putu Agus Khorisantono, a neuroscientist at Karolinska Institutet in Stockholm. Some food chemicals activate sweet, salty, sour, bitter or umami taste receptors on the tongue. Others travel through the roof of the mouth, activating odor receptors in the back of the nose. These “retronasal odors” are what distinguish mangoes from peaches, for example. Both taste mostly sour, Khorisantono says, “but it’s really the aroma that differentiates them.” The brain combines these signals to create our sense of flavor, but scientists have struggled to identify where this happens in the brain. In the new study, Khorisantono and colleagues gave 25 people drops of beverages designed to activate only their taste or retronasal receptors, while scanning brain activity over multiple sessions. Previously, the participants had learned to associate the combination of smells and tastes with particular flavors. © Society for Science & the Public 2000–2025.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29967 - Posted: 10.11.2025

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

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 Bethany Brookshire Even hearing the phrase “Huntington’s disease” will make a room suddenly somber. So the joy that accompanied a recent announcement of results of an experimental gene therapy for the deadly diseases signaled an unfamiliar sense of hope. In a small clinical trial, brain injections of a virus that codes for a tiny segment of RNA may have prevented the formation of the rogue proteins that make Huntington’s so devastating. The early results, announced September 24 in a news release, show that over three years, the treatment slowed Huntington’s progression by up to 75 percent. While not a cure, the treatment could potentially give people living with Huntington’s disease, who might otherwise face early disability and death, the gift of many more years of life. “We’re doing science because it’s interesting and important, but we’re also in this game to save our friends and family from a horrible fate,” says Ed Wild, a neurologist at University College London. “That’s the most meaningful thing, looking my friends in the eye and [saying], ‘We did it.’” Huntington’s disease currently has no effective treatments or cures. It is relatively rare, affecting about 7 out of every 100,000 people, and is the result of mutation in a single gene, appropriately called huntingtin. In the disease, that gene is mutated in only one way, making the front end of the resulting protein grow, says Russell Snell, a geneticist at the University of Auckland in New Zealand who was not involved in the study. This expanded huntingtin is a protein gone toxic. It aggregates in the brain and kills cells largely in brain areas crucial for voluntary movements. Patients end up with increasing involuntary movements, stiffness, difficulties speaking and swallowing and cognitive decline. Huntington’s is genetically dominant — it takes only one copy of the defective gene to cause it — so a patient’s offspring have a 50 percent chance of inheriting the disease. Wild and his colleagues, working with the Dutch pharmaceutical company uniQure, used microRNA — tiny segments of RNA that can trigger machinery to break down huntingtin RNA before it gets made into protein. Some other trials have tried simply injecting some of these RNAs, but have not succeeded, possibly because they were injected into the cerebrospinal fluid and couldn’t infiltrate the right areas of the brain. This time, the scientists injected them directly into the brain, packaged inside a well-studied viral vector. The virus would “infect” neurons in the brain with the RNA, and “it basically reprograms the neuron to become a factory for a molecule that tells it not to make huntingtin protein,” Wild says. © Society for Science & the Public 2000–2025.

Keyword: Huntingtons; Genes & Behavior
Link ID: 29946 - Posted: 09.27.2025

Hannah Devlin Science correspondent Huntington’s disease, a devastating degenerative illness that runs in families, has been treated successfully for the first time in a breakthrough gene therapy trial. The disease, caused by a single gene defect, steadily kills brain cells leading to dementia, paralysis and ultimately death. Those who have a parent with Huntington’s have a 50% chance of developing the disease, which until now has been incurable. The gene therapy slowed the progress of the disease by 75% in patients after three years. Prof Sarah Tabrizi, the director of University College London’s Huntington’s disease centre, who led the trial, said: “We now have a treatment for one of the world’s more terrible diseases. This is absolutely huge. I’m really overjoyed.” The drug, which inactivates the mutant protein that causes Huntington’s, is delivered to the brain in a single shot during a 12- to 20-hour surgical procedure, meaning that it will be expensive. The breakthrough is sending ripples of hope through the Huntington’s community, many of whom have witnessed the brutal impact of the disease on family members. The first symptoms, which typically appear when the affected person is in their 30s or 40s, include mood swings, anger and depression. Later patients develop uncontrolled jerky movements, dementia and ultimately paralysis, with some people dying within a decade of diagnosis. With treatment, people would be able to work and live independently for significantly longer, Tabrizi said, and the dramatic impact of the therapy raises the possibility that it could prevent symptoms occurring if given at an earlier stage. © 2025 Guardian News & Media Limited

Keyword: Huntingtons; Genes & Behavior
Link ID: 29945 - Posted: 09.27.2025

Chris Simms A wearable device could make saying ‘Alexa, what time is it?’ aloud a thing of the past. An artificial intelligence (AI) neural interface called AlterEgo promises to allow users to silently communicate just by internally articulating words. Sitting over the ear, the device facilitates daily life through live communication with the Internet. “It gives you the power of telepathy but only for the thoughts you want to share,” says AlterEgo’s chief executive Arnav Kapur, based in Cambridge, Massachusetts. Kapur unveiled the device on 8 September. The device does not read brain activity, but predicts what a wearer wants to say from signals in muscles used to speak, then sends audio information back into their ear. The researchers say that their non-invasive technology could help people with motor neuron disease (amyotrophic lateral sclerosis; ALS) and multiple sclerosis (MS) who have trouble speaking, but also want to make the devices commercially available for general use. In a promotional video on the AlterEgo website, Kapur says that “it’s a revolutionary breakthrough with the potential to change the way we interact with our technology, with one another and with the world around us”. “The big question about this is ‘how likely is that potential to be realized?,” says Howard Chizeck, an electrical and computer engineer at the University of Washington in Seattle. Chizeck says that the technology seems workable and is less of a privacy risk than listening devices such as Amazon’s Alexa are, but isn’t convinced that the device will catch on for commercial use. © 2025 Springer Nature Limited

Keyword: Robotics; Language
Link ID: 29934 - Posted: 09.20.2025

By Jake Buehler All eight arms of an octopus can be used for whatever their cephalopod owner wishes, but some arms are favored for certain tasks. A new, detailed analysis of how octopuses wield their famously flexible appendages suggests that all eight arms share a skill set, but the front four spend more time on exploration and the back four on movement. The findings, published September 11 in Scientific Reports, provide a comprehensive accounting of how subtle arm movements coordinate the clever invertebrates’ repertoire of behaviors. Octopuses live their lives through their sucker-lined arms, which make up the bulk of their body mass and contain most of their nervous system. Marine biologist Chelsea Bennice wanted to understand how octopuses use the extreme flexibility of their boneless limbs to move, hunt and investigate their environment. Her colleagues had examined some of these behaviors in laboratory settings, but not in the wild. Bennice and her colleagues watched 25 videos, filmed from 2007 to 2015, of multiple species of wild octopuses in Spain and the Caribbean, cataloging their behaviors and arm movements. In all, the researchers logged nearly 4,000 arm actions, which could be broken down into 12 types, including raising, reaching and grasping. The arms could deform in four distinct ways: elongating, shortening, bending and twisting. The team found that the octopuses were exceptionally ambidextrous. “Octopuses are ultimate multitaskers,” says Bennice, of Florida Atlantic University in Boca Raton. “All arms are capable of all arm behaviors and all arm deformations. They can even use multiple arm actions on a single arm and on several arms at the same time.” © Society for Science & the Public 2000–2025.

Keyword: Laterality; Evolution
Link ID: 29926 - 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

Ivana Drobnjak O'Brien An ultrasound “helmet” offers potential new ways for treating neurological conditions without surgery or other invasive procedures, a study has shown. The device can target brain regions 1,000 times smaller than ultrasound can, and could replace existing approaches such as deep brain stimulation (DBS) in treating Parkinson’s disease. It also holds potential for conditions such as depression, Tourette syndrome, chronic pain, Alzheimer’s and addiction. Unlike DBS, which requires a highly invasive procedure in which electrodes are implanted deep in the brain to deliver electrical pulses, using ultrasound sends mechanical pulses into the brain. But no one had managed to create an approach capable of delivering them precisely enough to make a meaningful impact until now. A study published in Nature Communications introduces a breakthrough system that can hit brain regions 30 times smaller than previous deep-brain ultrasound devices could. “It is a head helmet with 256 sources that fits inside an MRI scanner,” said the author and participant Ioana Grigoras, of Oxford University. “It is chunky and claustrophobic putting it on the head at first, but then you get comfortable.” Current DBS methods used on Parkinson’s patients use hard metal frames that are screwed into the head to hold them down. To test the system, the researchers applied it to seven volunteers, directing ultrasound waves to a tiny region the size of a grain of rice in the lateral geniculate nucleus (LGN), the key pathway for visual information that comes from the eyes to the brain. “The waves reached their target with remarkable accuracy,” the senior author Prof Charlotte Stagg of Oxford University said. “That alone was extraordinary, and no one has done it before.” Follow-up experiments showed that modulating the LGN produced lasting effects in the visual cortex, reducing its activity. “The equivalent in patients with Parkinson’s would be targeting a motor control region and seeing tremors disappear,” she added. © 2025 Guardian News & Media Limite

Keyword: Parkinsons; Brain imaging
Link ID: 29919 - Posted: 09.06.2025