By Siddhant Pusdekar Deer mice, common across North America, come in two varieties: One lives in prairies, whereas the other inhabits forests. The life of the forest mouse requires greater dexterity—a skill it possesses thanks to its higher number of corticospinal tract axons, according to a January preprint. The existence of “genetically tractable subspecies of deer mice with different behavioral niches” made the discovery possible, says Eiman Azim, associate professor of molecular neurobiology at the Salk Institute for Biological Studies, who wasn’t involved in the study. It enabled the researchers to link genetically driven changes in corticospinal abundance and morphology to dexterity. The new work reveals one way dexterous skill may emerge, while also suggesting neuroscience should investigate “behaviors that evolved for the natural niches” to discover fresh insights, says Ariel Levine, a senior investigator at the U.S. National Institute of Neurological Disorders and Stroke, who wasn’t involved in the study. Dexterity in primates coevolved with direct connections between layer 5 cortical neurons and motor neurons in the spinal cord, Levine says. In rodents, cats and less dexterous monkeys, however, corticospinal neurons connect to motor neurons via interneurons. Direct cortical-motor neuron connections exist in juvenile mice, but they are pruned during development, a 2017 paper showed. Artificially stopping the pruning process created adult lab mice with greater skill at gathering food pellets.

Keyword: Evolution; Development of the Brain
Link ID: 30196 - Posted: 04.11.2026

Lynne Peeples In 2021, dermatologist David Ozog was on holiday with his family in the Bahamas, when his 18-year-old son had a massive stroke. The teenager was airlifted to Florida, and then to Chicago for surgery. As his son was lying partially paralysed in a hospital bed, Ozog got a call from a colleague who had an unconventional suggestion. The colleague, a dermatologist at Harvard Medical School in Boston, Massachusetts, told Ozog about research he was conducting with the US Department of Defense. Early results hinted that red and near-infrared light applied to the head might protect neural tissue after brain injury. He urged Ozog to consider trying it on his son. Ozog stayed up until 4 a.m. that night reading scientific papers and, ultimately, ordering several panels made of red and near-infrared light-emitting diodes (LEDs). “I started sneaking them into the hospital,” says Ozog, who works at Henry Ford Health in Grand Rapids, Michigan. Today, his son is walking and back in university. Ozog cannot prove that light therapy made a difference, but he thinks that it helped. He has since become a convert to an idea that, at the time, was considered fringe. “I thought the same thing,” he says, “How could shining this thing on you possibly have any biologic effect?” But what was at the margins of medicine just a few years ago is now edging towards the mainstream. Red-light devices are increasingly appearing in dermatology offices, wellness centres, locker rooms and homes. According to some projections, the global market will surpass US$1 billion by 2030, propelled by a surge of companies promising benefits for everything from ageing skin to attention deficit hyperactivity disorder (ADHD) — claims echoed widely across social media. Experts warn that there is considerable hype about red-light therapy. But a growing body of legitimate science has been exploring the benefits for several conditions. Clinical studies have reported improvements in peripheral neuropathy1, retinal degeneration2 and certain neurological disorders3. For some indications, expert groups now recommend red-light regimens1. Researchers are also uncovering how red and near-infrared light might exert these effects. Mitochondria — the power plants of the cell — are emerging as a central piece of the puzzle. © 2026 Springer Nature Limited

Keyword: Stroke; Parkinsons
Link ID: 30182 - Posted: 03.28.2026

by Pam Belluck Tango is the national dance of Argentina, known for its passion, precision and heart. In a hospital in Buenos Aires, it has another purpose: as a therapy for patients with Parkinson’s disease. Once a week, about a dozen patients come to Ramos Mejía Hospital to dance — a session that uses the movements of tango to help address issues of balance, stiffness and coordination. The goal is to give them approaches to movement that they can use in their daily lives, as well as a social and emotional boost from moving to music. The program began about 15 years ago, inspired by a patient who had danced tango since childhood and found it offered strategies that improved her mobility and gait problems, said Dr. Nélida Garretto, a neurologist who helped spearhead the sessions. Dr. Tomoko Arakaki, another neurologist leading the program, said Parkinson’s patients can struggle with the stop-and-start motions of walking and can benefit from practicing the “slow, short steps” and pauses of tango. Dr. Garretto said that because tango involves “multitasking with motor stimuli, visual stimuli and auditory stimuli,” it can help patients execute the series of small movements in everyday activities. First, warm-up exercises, usually in a circle, “try to tune everyone in, to prepare the body, to awaken the body,” said Manuel Firmani, a professional tango dancer leading the workshops. Some are done standing, some seated, depending on “the state people are in,” he said. After exercises focusing on posture, balance and other skills, dancing begins. Each patient is paired with a partner who doesn’t have Parkinson’s, often friends, relatives or volunteers. © 2026 The New York Times Company

Keyword: Parkinsons
Link ID: 30173 - Posted: 03.25.2026

Mariana Lenharo Exercise pumps up your muscles — but it might also be pumping up your neurons. According to a study published today in Neuron1, repeated exercise sessions on a treadmill strengthen the wiring in a mouse’s brain, making certain neurons quicker to activate. This ‘rewiring’ was essential for mice in the study to gradually improve their running endurance. The work reveals that the brain — in mice and, presumably, in humans — is actively involved in the development of endurance, the ability to get better at a physical activity with repeated practice, says Nicholas Betley, a neuroscientist at the University of Pennsylvania in Philadelphia, and a co-author of the paper. “You go for a run, and your lungs expand, your heart gets pumping better, your muscles break down and rebuild. All this great stuff happens, and the next time, it gets easier,” Betley says. “I didn’t expect that the brain was coordinating all of that.” Betley and his colleagues were curious about what happens in the brain as people get stronger through exercise. They decided to focus on the ventromedial hypothalamus, a brain region that regulates appetite and blood sugar. The team then zeroed in on a group of neurons in that region that produce a protein called steroidogenic factor 1 (SF1), which is known to play a part in regulating metabolism2. A previous study3 found that the deletion of the gene that codes for SF1 impairs endurance in mice. © 2026 Springer Nature Limited

Keyword: Obesity; Learning & Memory
Link ID: 30120 - Posted: 02.14.2026

Jon Hamilton Parkinson's disease does more than cause tremor and trouble walking. It can also affect sleep, smell, digestion and even thinking. That may be because the disease disrupts communication in a brain network that links the body and mind, a team reports in the journal Nature. "It almost feels like a tunnel is jammed, so no traffic can go normally," says Hesheng Liu, a brain scientist at Changping Laboratory and Peking University in Beijing and an author of the study. The finding fits nicely with growing evidence that Parkinson's is a network disorder, rather than one limited to brain areas that control specific movements, says Peter Strick, a professor and chair of neurobiology at the University of Pittsburgh who was not involved in the study. Other degenerative brain diseases affect other brain networks in different ways. Alzheimer's, for example, tends to reduce connectivity in the default mode network, which supports memory and sense of self. ALS (amyotrophic lateral sclerosis) primarily damages the motor system network, which controls movement. Understanding the network affected by Parkinson's, which affects about 1 million people in the United States, could change the way doctors treat the disease. A mystery solved? People with Parkinson's often have symptoms that vary in ways that are hard to explain. For example, someone who usually is unable to stand may suddenly leap when faced with an emergency. And Parkinson's patients who can still walk may freeze if they try to carry on a conversation. © 2026 npr

Keyword: Parkinsons
Link ID: 30116 - Posted: 02.11.2026

By Corinna da Fonseca-Wollheim The placid chords of a Debussy prelude splashed through a darkened auditorium during a recital by the pianist Nicolas Namoradze at the University of California, San Francisco, on a November evening. A translucent image of Namoradze’s brain appeared above him on a screen: Electrical currents of different wavelengths, associated with varying levels of alertness, registered as colorful activity coursing through the model like storm fronts on a weather map. With each chord, clouds of green and blue bloomed, then faded as the sound receded. As the recital progressed with works by Bach, Beethoven and Scriabin, the image of the gently rotating brain showed a complex choreography of signals that sometimes ping-ponged between different areas or flickered simultaneously across the organ’s hemispheres. As a visual spectacle accompanying Namoradze’s pellucid playing, it was mesmerizing: an X-ray, seemingly, of virtuosity at work. But to the scientists in the audience, attendees at a conference on the neuroscience of music and dance, it was more than entertainment. It was evidence of a breakthrough in experiment design — one that opens up possibilities in an area that has long eluded scientific study: how music activates the brain, not in listeners, but in performers. It was also a reminder of the value artists can bring to scientific inquiry as active participants shaping studies of their craft. The neuroscientist Theodore Zanto, a member of the Neuroscape lab at U.C.S.F. that created the “Glass Brain” animations, said in an interview the next day that he was surprised — and moved — by the result. “It’s probably the cleanest real-time representation of what’s happening inside the brain during a piano performance,” he said. © 2026 The New York Times Company

Keyword: Hearing; Brain imaging
Link ID: 30115 - Posted: 02.11.2026

By Natalia Mesa A region of the cerebellum shows language specificity akin to that of cortical language regions, indicating that it might be part of the broader language network, according to a new brain-imaging study. “This is the first time we see an area outside of the core left-hemisphere language areas that behaves so similarly to those core areas,” says study investigator Ev Fedorenko, associate professor of brain and cognitive sciences at the Massachusetts Institute of Technology. Initially thought to coordinate only movement, the cerebellum also contributes to cognitive processes, such as social reward, abstract reasoning and working memory, according to studies from the past decade. But despite the fact that people with cerebellar lesions have subtle language struggles, the region’s contributions to that skill have been ignored until recently, Fedorenko says. With this new work, “I think it becomes harder to dismiss language responses as somehow artifactual.” Fedorenko and her team analyzed nearly 1,700 whole-brain functional MRI experiments conducted over the course of 15 years. They originally collected and analyzed those scans to identify language-selective regions of the neocortex, but they reanalyzed many of them to determine the cerebellum’s role in linguistic processing. Four cerebellar regions activated robustly when participants performed language-related tasks, such as reading passages of text or listening to someone else reading the passages aloud, in line with previous work. But only one region responded exclusively to these language-related tasks; it did not activate during a variety of nonlinguistic tasks—including movement, arithmetic tasks and a spatial working memory task—or when participants listened to music or watched videos of faces and bodies. The findings were published last month in Neuron. © 2026 Simons Foundation

Keyword: Language
Link ID: 30110 - Posted: 02.07.2026

By Laura Sanders The brain’s “little brain” may hold big promise for people with language trouble. Tucked into the base of the brain, the fist-sized cerebellum is most known for its role in movement, posture and coordination. A new study maps the language system in this out-of-the-way place. These results, published January 22 in Neuron, uncover a spot in the cerebellum that shows strong and selective activity for language. The new study is “excellent,” says neurologist and cerebellum researcher Jeremy Schmahmann of Massachusetts General Hospital and Harvard Medical School in Boston. His work and that of others have shown that the cerebellum contributes to language and thinking more generally. The new research scrutinized the cerebellum in detail, “confirming and extending previous observations and contributing to our understanding” of the cerebellum’s activity, he says. Neuroscientist Colton Casto combed through about 15 years of brain scanning data collected by study coauthor Evelina Fedorenko, a cognitive neuroscientist at MIT, and her colleagues. Putting the data all together, the scans of 846 people showed brain activity in four spots in the right side of the cerebellum as people read or listened to a story. Three of these spots were also active when people did other things, such as working out a math problem, or listening to music or watching a movie without words. But one spot was more discerning, says Casto, of MIT and Harvard University. This region didn’t respond to nonverbal movies or math. It also ignored orchestral or jazz music, which, like language, relies on syntax and patterns and sound. Instead, this spot is attuned specifically to words. “You have to be reading or listening to language to fully recruit this region,” Casto says. © Society for Science & the Public 2000–2026.

Keyword: Language
Link ID: 30091 - Posted: 01.24.2026

Allison Aubrey If you feel a lift after exercise, you're in good company. Movement can boost mood, and according to the results of a new study, it can also help relieve symptoms of depression. As part of a review of evidence by the Cochrane collaboration — an independent network of researchers — scientists evaluated 73 randomized controlled trials that included about 5,000 people with depression, many of whom also tried antidepressant medication. "We found that exercise was as effective as pharmacological treatments or psychological therapies as well," says Andrew Clegg, a professor at the University of Lancashire in the U.K. The findings are not a surprise to psychiatrist Dr. Stephen Mateka, medical director of psychiatry at Inspira Health. "This new Cochrane review reinforces the evidence that exercise is one of the most evidence-based tools for improving mood," says Mateka. He explains how it mirrors some of the effects of medication. "Exercise can help improve neurotransmitter function, like serotonin as well as dopamine and endorphins. So there is certainly overlap between exercise and how antidepressants offer relief," Mateka says. And there's another powerful effect too. Exercise can trigger the release of brain growth factors, explains Dr. Nicholas Fabiano of the University of Ottawa. He says depression can decrease neuroplasticity, making it harder for the brain to adapt and change. "The brain in depression is thought to be less plastic. So there's less what we call neurotrophic factors, or BDNF," Fabiano explains. He calls it the Miracle-Gro for the brain. "And we know that exercise can also boost it. So I think exercise is a fundamental pillar we really need to counsel patients on," he says. © 2026 npr

Keyword: Depression
Link ID: 30077 - Posted: 01.14.2026

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

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 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