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

Rachel Fieldhouse A man with partial paralysis was able to operate a robotic arm when he used a non-invasive brain device partially controlled by artificial intelligence (AI), a study reports1. The AI-enabled device also allowed the man to perform screen-based tasks four times better than when he used the device on its own. Brain–computer interfaces (BCIs) capture electrical signals from the brain, then analyse them to determine what the person wants to do and translate the signals into commands. Some BCIs are surgically implanted and record signals directly from the brain, which typically makes them more accurate than non-invasive devices that are attached to the scalp. Jonathan Kao, who studies AI and BCIs at the University of California, Los Angeles, and his colleagues wanted to improve the performance of non-invasive BCIs. The results of their work are published in Nature Machine Intelligence this week. First, the team tested its BCI by tasking four people — one with paralysis and three without — with moving a computer cursor to a particular spot on a screen. All four were able to complete the task the majority of the time. When the authors added an AI co-pilot to the device, the participants completed the task more quickly and had a higher success rate. The device with the co-pilot doesn’t need to decode as much brain activity because the AI can infer what the user wants to do, says Kao. “These co-pilots are essentially collaborating with the BCI user and trying to infer the goals that the BCI user is wishing to achieve, and then helps to complete those actions,” he adds. The researchers also trained an AI co-pilot to control a robotic arm. The participants were required to use the robotic arm to pick up coloured blocks and move them to marked spots on a table. The person with paralysis could not complete the task using the conventional, non-invasive BCI, but was successful 93% of the time using the BCI with an AI co-pilot. Those without paralysis also completed the task more quickly when using the co-pilot. © 2025 Springer Nature Limited

Keyword: Robotics
Link ID: 29912 - Posted: 09.03.2025

By Carl Zimmer Charles Darwin unveiled his theory of evolution in 1859, in “On the Origin of Species.” But it took him another 12 years to work up the courage to declare that humans evolved, too. In “The Descent of Man,” published in 1871, Darwin argued that humans arose from apes. And one of the most profound changes they underwent was turning into upright walkers. “Man alone has become a biped,” Darwin wrote. Bipedalism, he declared, was one of humanity’s “most conspicuous characters.” Scientists have now discovered some of the crucial molecular steps that led to that conspicuous character millions of years ago. A study published in the journal Nature on Wednesday suggests that our early ancestors became bipeds, as old genes started doing new things. Some genes became active in novel places in the human embryo, while others turned on and off at different times. Scientists have long recognized that a key feature for walking upright is a bone called the ilium. It’s the biggest bone in the pelvis; when you put your hand on your hip, that’s the ilium you feel. The left and right ilium are both fused to the base of the spine. Each ilium sweeps around the waist to the front of the belly, creating a bowllike shape. Many of the leg muscles we use in walking are anchored to the ilium. The bone also supports the pelvic floor, a network of muscles that acts like a basket for our inner organs when we stand up. As vital as the ilium is to everyday life, the bone can also be a source of suffering. The ilium can flare up with arthritis, grow brittle in old age, especially in women, and fracture from a fall. Genetic disorders can deform it, making walking difficult. The ilium also forms much of the birth canal — where babies can sometimes get stuck, endangering the mother’s life. © 2025 The New York Times Company

Keyword: Evolution
Link ID: 29906 - Posted: 08.30.2025

Nicola Davis Science correspondent Big hands might mean big feet, but it seems long thumbs are linked to large brains – at least in primates. Researchers say the results suggest the brain co-evolved with manual dexterity in such mammals. “We imagine an evolutionary scenario in which a primate or human has become more intelligent, and with that comes the ability to think about action planning, think about what you are doing with your hands, and realise that actually you are more efficient at doing it one way or another,” said Dr Joanna Baker, lead author of the research from the University of Reading. “And those that have longer thumbs or more ability to manipulate the objects in the way that the mind can see were likely to be more successful.” Large brains and manual dexterity are both thought to have played an important role in human evolution, with opposable thumbs a key feature that enabled a greater ability to grip and manipulate items – including tools. However, with some other primates having partly opposable thumbs, questions have remained over whether other changes in the hand – such as thumb length – could also be important in the evolution of tool use. “In general terms, you can say that the longer the thumb you have, the more motion you have to pick up and control small objects,” said Baker. To explore the issue Baker and colleagues studied the estimated brain mass and thumb length of 94 primate species, from five of our ancient hominin relatives to lemurs. The results, published in the journal Communications Biology, reveal humans and most other hominins have thumbs that are significantly longer than would be predicted based on the hand proportions of primates as a while. However, further analysis revealed an intriguing pattern. “When you have longer thumbs relative to your overall hand, that tends to come in conjunction with overall increased brain size,” said Baker. © 2025 Guardian News & Media Limited

Keyword: Evolution
Link ID: 29902 - Posted: 08.27.2025

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

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

By Carl Zimmer For decades, neuroengineers have dreamed of helping people who have been cut off from the world of language. A disease like amyotrophic lateral sclerosis, or A.L.S., weakens the muscles in the airway. A stroke can kill neurons that normally relay commands for speaking. Perhaps, by implanting electrodes, scientists could instead record the brain’s electric activity and translate that into spoken words. Now a team of researchers has made an important advance toward that goal. Previously they succeeded in decoding the signals produced when people tried to speak. In the new study, published on Thursday in the journal Cell, their computer often made correct guesses when the subjects simply imagined saying words. Christian Herff, a neuroscientist at Maastricht University in the Netherlands who was not involved in the research, said the result went beyond the merely technological and shed light on the mystery of language. “It’s a fantastic advance,” Dr. Herff said. The new study is the latest result in a long-running clinical trial, called BrainGate2, that has already seen some remarkable successes. One participant, Casey Harrell, now uses his brain-machine interface to hold conversations with his family and friends. In 2023, after A.L.S. had made his voice unintelligible, Mr. Harrell agreed to have electrodes implanted in his brain. Surgeons placed four arrays of tiny needles on the left side, in a patch of tissue called the motor cortex. The region becomes active when the brain creates commands for muscles to produce speech. A computer recorded the electrical activity from the implants as Mr. Harrell attempted to say different words. Over time, with the help of artificial intelligence, the computer accurately predicted almost 6,000 words, with an accuracy of 97.5 percent. It could then synthesize those words using Mr. Harrell’s voice, based on recordings made before he developed A.L.S. © 2025 The New York Times Company

Keyword: Language; Robotics
Link ID: 29892 - Posted: 08.16.2025

Heidi Ledford Scientists are closing in on the ability to apply genome editing to a formidable new target: the human brain. In the past two years, a spate of technological advances and promising results in mice have been laying the groundwork for treating devastating brain disorders using techniques derived from CRISPR–Cas9 gene editing. Researchers hope that human trials are just a few years away. “The data have never looked so good,” says Monica Coenraads, founder and chief executive of the Rett Syndrome Research Trust in Trumbull, Connecticut. “This is less and less science fiction, and closer to reality.” Daunting challenge Researchers have already developed gene-editing therapies to treat diseases of the blood, liver and eyes. In May, researchers reported1 a stunning success using a bespoke gene-editing therapy to treat a baby boy named KJ with a deadly liver disease. But the brain poses special challenges. The molecular components needed to treat KJ were inserted into fatty particles that naturally accumulate in the liver. Researchers are searching for similar particles that can selectively target the brain, which is surrounded by a defensive barrier that can prevent many substances from entering. Although KJ’s story was exciting, it was also frustrating for those whose family members have neurological diseases, says Coenraads, whose organization focuses on Rett syndrome, a rare disorder that affects brain development. “The question that I hear from our families is, ‘It was done so quickly for him. What’s taking us so long?’” she says. That pool of concerned families is growing as physicians and families increasingly turn to genome sequencing to find the causes of once-mysterious brain disorders, says Cathleen Lutz, a geneticist at The Jackson Laboratory in Bar Harbor, Maine. “People are starting to now find out that their child’s seizures, for example, are related to particular genetic mutations,” she says. © 2025 Springer Nature Limited

Keyword: Genes & Behavior
Link ID: 29891 - Posted: 08.16.2025

By Pam Belluck Sometimes the pain felt like lightning bolts. Or snakes biting. Or needles. “Just imagine the worst burn you’ve ever had, all over your body, never going away,” said Ed Mowery, 55, describing his life with chronic pain. “I would wake up in the middle of night, screaming at the top of my lungs.” Beginning with a severe knee injury he got playing soccer at 15, he underwent about 30 major surgeries for various injuries over the decades, including procedures on his knees, spine and ankles. Doctors put in a spinal cord stimulator, which delivers electrical pulses to relieve pain, and prescribed morphine, oxycodone and other medications, 17 a day at one point. Nothing helped. Unable to walk or sit for more than 10 minutes, Mr. Mowery, of Rio Rancho, N.M., had to stop working at his job selling electronics to engineering companies and stop playing guitar with his death metal band. Out of options four years ago, Mr. Mowery signed up for a cutting-edge experiment: a clinical trial involving personalized deep brain stimulation to try to ease chronic pain. The study, published on Wednesday, outlines a new approach for the most devastating cases of chronic pain, and could also provide insights to help drive invention of less invasive therapies, pain experts said. “It’s highly innovative work, using the experience and technology they have developed and applying it to an underserved area of medicine,” said Dr. Andre Machado, chief of the Neurological Institute at Cleveland Clinic, who was not involved in the study. Chronic pain, defined as lasting at least three months, afflicts about 20 percent of adults in the United States, an estimated 50 million people, according to the Centers for Disease Control and Prevention. In about a third of cases, the pain substantially limits daily activities, the C.D.C. reported. © 2025 The New York Times Company

Keyword: Pain & Touch
Link ID: 29889 - Posted: 08.16.2025