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

By Roni Caryn Rabin The Food and Drug Administration on Wednesday approved a medical device that offers new hope to patients incapacitated by rheumatoid arthritis, a chronic condition that afflicts 1.5 million Americans and is often resistant to treatment. The condition is usually managed with medications. The device represents a radical departure from standard care, tapping the power of the brain and nervous system to tamp down the uncontrolled inflammation that leads to the debilitating autoimmune disease. The SetPoint System is an inch-long device that is surgically implanted into the neck, where it sits in a pod wrapped around the vagus nerve, which some scientists believe is the longest nerve in the body. The device electrically stimulates the nerve for one minute each day. The stimulation can turn off crippling inflammation and “reset” the immune system, research has shown. Most drugs used to treat rheumatoid arthritis suppress the immune system, leaving patients vulnerable to serious infections. On a recent episode of the American College of Rheumatology podcast, the SetPoint implant was described as representing a “true paradigm shift” in treatment of the disease, which until now has relied almost entirely on an evolving set of pharmaceutical interventions, from gold salts to powerful agents called biologics. The F.D.A. designated the implant as a breakthrough last year in order to expedite its development and approval. It represents an early test of the promise of so-called bioelectronic medicine to modulate inflammation, which plays a key role in diseases including diabetes, heart disease and cancer. Clinical trials are already underway testing vagus nerve stimulation to manage inflammatory bowel disease in children, lupus and other conditions. Trials for patients with multiple sclerosis and Crohn’s disease are also planned. In a yearlong randomized controlled trial of 242 patients that included a sham-treatment arm, over half of the participants using the SetPoint implant alone achieved remission or saw their disease recede. Measures of joint pain and swelling fell by 60 percent and 63 percent, respectively. © 2025 The New York Times Company

Keyword: Pain & Touch; Neuroimmunology
Link ID: 29873 - Posted: 08.02.2025

By Tom Zeller Jr. During the week between two experimental infusions at the Danish Headache Center, where I had agreed to be a test subject, I rented a small flat in central Copenhagen, near Assistens Cemetery. This is where many notable Danes have been laid to rest, and I took some time that September to visit the monuments, which were shrouded in manicured stands of mature poplars and willows. The accompanying article is adapted from “The Headache: The Science of a Most Confounding Affliction — and a Search for Relief,” by Tom Zeller Jr. (Mariner Books, 310 pages). Copyright © 2025. Reprinted by permission. The grave of Niels Bohr, one of the 20th century’s leading figures in theoretical physics, is marked by a gray stone pillar with an owl perched on top. Hans Christian Andersen, the author who gave us “The Little Mermaid” and “The Ugly Duckling,” among other treasured stories, resides here too. But it felt most appropriate to my mission that Danish philosopher Søren Kierkegaard, who thought suffering was where life’s meaning is forged, occupied his own leafy corner of the park. In the Kierkegaardian tradition, suffering is redemptive — the feedstock of enlightenment — and rather than wallow in its insults and pains, the sufferer should embrace its power to transform. “Even the heaviest suffering cannot be heavier than a mountain,” he once wrote. “And thus, if the sufferer believes that his suffering is beneficial to him — yes, then he moves mountains. In order to move a mountain, you must get under it.” I was thinking of Kierkegaard when I first presented my arm to Lanfranco Pellesi, then a researcher at the Danish Headache Center, for my initial infusion. Pellesi had an early interest in studying near-death experiences, before turning his attention to pain, and then from pain to headaches. It struck me as such an obvious trajectory — one that followed an almost inevitable path — and I asked him how he made sense of that progression. “I think probably it links to the problem of conscience — where it is, where it’s not.”

Keyword: Pain & Touch
Link ID: 29861 - Posted: 07.19.2025

Sally Adee Keith Krehbiel lived with Parkinson’s disease for nearly 25 years before agreeing to try a brain implant that might alleviate his symptoms. He had long been reluctant to submit to the surgery. “It was a big move,” he says. But by 2020, his symptoms had become so severe that he grudgingly agreed to go ahead. Deep-brain stimulation involves inserting thin wires through two small holes in the skull into a region of the brain associated with movement. The hope is that by delivering electrical pulses to the region, the implant can normalize aberrant brain activity and reduce symptoms. Since the devices were first approved almost three decades ago, some 200,000 people have had them fitted to help calm the tremors and rigidity caused by Parkinson’s disease. But about 40,000 of those who received devices made after 2020 got them with a special feature that has largely not yet been turned on. The devices can read brain waves and then adapt and tailor the rhythm of their output, in much the same way as a pacemaker monitors and corrects the heart’s electrical rhythms, says Helen Bronte-Stewart, a neurologist at Stanford University in California. Bronte-Stewart received approval to start a clinical trial of this new technology, known as adaptive deep-brain stimulation (aDBS), the same week that Krehbiel was preparing for surgery. He recalls the phone call in which she asked him if he wanted to be her first participant: “I said, ‘Boy, do I!’” Five years on, the results of this 68-person trial, called ADAPT-PD, are under review for publication. Although the exact details are still under wraps, they were convincing enough to earn approval for the technology earlier this year from both US and European regulators. © 2025 Springer Nature Limited

Keyword: Parkinsons
Link ID: 29858 - Posted: 07.16.2025

By Celina Ribeiro Some say it was John Sattler’s own fault. The lead-up to the 1970 rugby league grand final had been tense; the team he led, the South Sydney Rabbitohs, had lost the 1969 final. Here was an opportunity for redemption. The Rabbitohs were not about to let glory slip through their fingers again. Soon after the starting whistle, Sattler went in for a tackle. As he untangled – in a move not uncommon in the sport at the time – he gave the Manly Sea Eagles’ John Bucknall a clip on the ear. Seconds later – just three minutes into the game – the towering second rower returned favour with force: Bucknall’s mighty right arm bore down on Sattler, breaking his jaw in three places and tearing his skin; he would later need eight stitches. When his teammate Bob McCarthy turned to check on him, he saw his captain spurting blood, his jaw hanging low. Forty years later Sattler would recall that moment. One thought raged in his shattered head: “I have never felt pain like this in my life.” But he played on. Tackling heaving muscular players as they advanced. Being tackled in turn, around the head, as he pushed forward. All the while he could feel his jaw in pieces. At half-time the Rabbitohs were leading. In the locker room, Sattler warned his teammates, “Don’t play me out of this grand final.” McCarthy told him, “Mate, you’ve got to go off.” He refused. “I’m staying.” Sattler played the whole game. The remaining 77 minutes. At the end, he gave a speech and ran a lap of honour. The Rabbitohs had won. The back page of the next day’s Sunday Mirror screamed “BROKEN JAW HERO”. © 2025 Guardian News & Media Limited

Keyword: Pain & Touch
Link ID: 29857 - Posted: 07.16.2025

Smriti Mallapaty A gene variant known to increase the risk of Alzheimer’s disease also makes people vulnerable to a host of other age-related brain disorders, from Parkinson’s disease to motor neuron disease. The gene variant, a version of apolipoprotein E called APOE ε4, produces a distinct set of proteins that contribute to chronic inflammation, finds an analysis1 using the largest proteomics database for neurodegenerative disease. Neurodegenerative diseases affect more than 57 million people worldwide. Researchers know that people who carry the APOE ε4 variant have an increased risk of developing late-onset Alzheimer’s disease, but studies are beginning to implicate this version, or allele, of APOE in other neurodegenerative diseases. Caitlin Finney and Artur Shvetcov, who study neurodegenerative diseases at the Westmead Institute for Medical Research in Sydney, Australia, and their colleagues wanted to better understand how this genetic risk factor contributes to disease. They took advantage of a newly established proteomics database that allowed them to look beyond individual diseases, says Finney. The Global Neurodegeneration Proteomics Consortium (GNPC) data set2 includes samples from more than 18,600 individuals, mainly of European ancestry, including many with Alzheimer’s, Parkinson’s, a form of motor neuron disease called amyotrophic lateral sclerosis (ALS) and types of dementia, as well as individuals without neurological disorders. The consortia collected around 250 million measurements of proteins found in the blood and cerebrospinal fluid, which surrounds the brain and spinal cord, taken at some two dozen clinics across the United States and Europe. “It’s one of the most powerful databases that we have available for proteomics right now,” says Maryam Shoai, a bioinformatician at University College London. Predicting risk © 2025 Springer Nature Limited

Keyword: Alzheimers; Parkinsons
Link ID: 29855 - Posted: 07.16.2025

Sydney Lupkin Jerry Abrams, a 64-year-old marketing strategist in Minneapolis, used to run marathons. But two decades of degenerative spine disease have left him unable to run — and he's grieving. For Abrams, losing running felt like "the loss of a loved one – that friend who's been with you every day you needed him. "You know, having that taken away from you because of pain is the hardest thing of all," he says. The constant pain in his lower back makes running impossible. Sometimes, when the pain isn't under control, he can't get out of bed. Abrams has tried taking opioids. They help, but he feels he has to be careful because they're potentially addictive. He's also worried about building up a tolerance to them "I don't ever want to be in a situation where I need surgery and need to recover and opioid medication no longer does what it needs to do," he explains. The Food and Drug Administration approved a new non-opioid drug earlier this year called Journavx. It's a pill for severe acute pain that works by blocking plain signals from where someone hurts. It's offered hope for the 1 in 5 Americans who suffer from chronic pain, but it's also just out of reach. Journavx is the first new kind of painkiller in more than 20 years, and the medical community is cautiously optimistic that Journavx doesn't have the same addictive potential as opioids do. But the new pills are expensive, and not everyone has been able to access them, thanks to a narrowly-focused FDA approval and limited insurance coverage Abrams' doctor wanted him to be able to try Journavx. But the FDA only approved the medication for short-term use for acute pain, which is usually defined as lasting less than three months, such as right after surgery. Because Abrahm's pain is chronic, his insurance wouldn't cover it. A single Journavx pill costs around $15 without insurance, according to Vertex Pharmaceuticals, the drug's manufacturer. © 2025 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 29849 - Posted: 07.12.2025

By Laura Sanders GLP-1 drugs may possess a new power: Easing migraines. In a small, preliminary study, a GLP-1 drug nearly halved the number of days people spent with a migraine in a given month. The results, presented June 21 at the European Academy of Neurology Congress in Helsinki, Finland, expand the possible benefits of the powerful new class of obesity and diabetes drugs. These pernicious, debilitating headaches are estimated to affect one billion people worldwide. Earlier studies have shown that GLP-1 agonists can reduce the pressure inside the skull, a squeeze that’s been implicated in migraines. Neurologist Simone Braca of the University of Naples Federico II in Italy and his colleagues explored whether liraglutide, an older relative of Ozempic and Wegovy, might help migraine sufferers. Thirty-one adults, 26 of them women, got daily injections of liraglutide for 12 weeks. These adults all had obesity and continued to take their current migraine medicines too. At the start of the experiment, participants had headaches on about 20 days out of a month. After 12 weeks of liraglutide, the average number dropped to about 11 days. “Basically, we observed that patients saw their days with headache halved, which is huge,” Braca says. Participants’ weight stayed about the same during the trial, suggesting that headache reductions weren’t tied to weight loss. If the results hold up in larger studies, they may point to treatments for migraine sufferers who aren’t helped by existing drugs. The results may also lead to a deeper understanding of the role of pressure inside the head in migraines, Braca says. © Society for Science & the Public 2000–2025.

Keyword: Obesity; Pain & Touch
Link ID: 29846 - Posted: 07.02.2025

By Amber Dance Back in 2008, neurovirologist Renée Douville observed something weird in the brains of people who’d died of the movement disorder ALS: virus proteins. But these people hadn’t caught any known virus. Instead, ancient genes originally from viruses, and still lurking within these patients’ chromosomes, had awakened and started churning out viral proteins. Our genomes are littered with scraps of long-lost viruses, the descendants of viral infections often from millions of years ago. Most of these once-foreign DNA bits are a type called retrotransposons; they make up more than 40 percent of the human genome. Pie chart shows that retrotransposons make up nearly half the human genome. Our genomes are riddled with DNA from ancient viral infections known as jumping genes. The majority of these are retrotransposons, which copy themselves via RNA intermediates; a smaller portion are cut-and-paste DNA transposons. Many retrotransposons seem to be harmless, most of the time. But Douville and others are pursuing the possibility that some reawakened retrotransposons may do serious damage: They can degrade nerve cells and fire up inflammation and may underlie some instances of Alzheimer’s disease and ALS (amyotrophic lateral sclerosis, or Lou Gehrig’s disease). The theory linking retrotransposons to neurodegenerative diseases — conditions in which nerve cells decline or die — is still developing; even its proponents, while optimistic, are cautious. “It’s not yet the consensus view,” says Josh Dubnau, a neurobiologist at the Renaissance School of Medicine at Stony Brook University in New York. And retrotransposons can’t explain all cases of neurodegeneration. Yet evidence is building that they may underlie some cases. Now, after more than a decade of studying this possibility in human brain tissue, fruit flies and mice, researchers are putting their ideas to the ultimate test: clinical trials in people with ALS, Alzheimer’s and related conditions. These trials, which borrow antiretroviral medications from the HIV pharmacopeia, have yielded preliminary but promising results. © 2025 Annual Reviews

Keyword: ALS-Lou Gehrig's Disease ; Alzheimers
Link ID: 29834 - Posted: 06.18.2025

By Sydney Wyatt The red nucleus—a pale pink brainstem structure that coordinates limb movements in quadruped animals—also projects to brain areas that shape reward-motivated and action-based movements in people, according to a new functional imaging study. The finding suggests the region, like the cerebral cortex, took on a more complex role over the course of evolution. Many researchers had assumed that brainstem structures remained stuck in evolutionarily ancient roles, says Joan Baizer, professor of physiology and biophysics at the University at Buffalo. Activity in the red nucleus, a structure that emerged once animals began to use limbs for walking, coordinates the speed and accuracy of those movements in rats and helps to control posture in monkeys, previous electrophysiological recordings have shown. And in nonhuman primates, neurons in the red nucleus project to the motor cortex and spinal cord, anatomical studies have demonstrated, seemingly confirming the area’s role in motor function. By contrast, the human red nucleus primarily connects to cortical and subcortical regions involved in action control, reward and motivated behavior, the new work reveals. “If this is such a motor structure, why isn’t it projecting to the spinal cord? That doesn’t really fit with our notion of what this structure is supposed to be doing,” says study investigator Samuel Krimmel, a postdoctoral fellow in Nico Dosenbach’s lab. The new imaging suggests that, at least in people, the neural underpinnings of motivated movement—previously considered to be the role of higher-order brain areas—reach “all the way down into the brainstem,” says Dosenbach, professor of neurology at Washington University School of Medicine, who led the work. The findings were published last month in Nature Communications. © 2025 Simons Foundation

Keyword: Learning & Memory; Evolution
Link ID: 29790 - Posted: 05.17.2025

Bobbi-Jean MacKinnon A new scientific study has found no evidence of a mystery brain disease in New Brunswick, says a report published Wednesday in the Journal of the American Medical Association, known as JAMA. Instead, an independent reassessment of 25 of 222 patients diagnosed by Moncton neurologist Alier Marrero as having a "neurological syndrome of unknown cause" concluded that all of the cases were attributable to well-known conditions. These include common neurodegenerative diseases, such as Alzheimer's and Parkinson's, functional neurological disorder, traumatic brain injury, and metastatic cancer, says the report. Despite the small sample size, "when we did the statistics … the chances of any of those other individuals having a mystery disease was less than one in a million," said Dr. Anthony Lang, a senior neurologist and neuroscientist in Toronto, and one of the 13 co-authors. The researchers, affiliated with the University of Toronto, New Brunswick's Horizon Health Network and other Canadian institutions, do not believe exposure to something in the environment, such as the herbicide glyphosate or heavy metals, made the patients ill either, said Lang, director of the Edmund J Safra Program in Parkinson's Disease at the University Health Network. "The neurological problems varied a great deal. Some had neurodegenerative diseases, but others had other neurological problems and therefore a single environmental toxin … could never have explained this broad variety of neurological abnormalities." Lang, who got involved in the study because he started hearing about a mystery disease but wasn't seeing any publications in medical literature, is not surprised by the results. ©2025 CBC/Radio-Canada.

Keyword: Movement Disorders; Alzheimers
Link ID: 29779 - Posted: 05.10.2025

Sammie Seamon Peter was working late, watching two roulette tables in play at a London casino, when he felt something stir behind his right eye. It was just a shadow of sensation, a horribly familiar tickle. But on that summer night in 2018, as chips hit the tables and gamblers’ conversation swelled, panic set in. He knew he only had a few minutes. Peter found his boss, muttered that he had to leave, now, and ran outside. By then, the tickle had escalated; it felt like a red-hot poker was being shoved through his right pupil. Tears flowed from that eye, which was nearly swollen shut, and mucus from his right nostril. Half-blinded, gripping at his face, he stumbled along the street, eventually escaping into a company car that whisked him home, where he blacked out. Every day that followed, Peter, then in his early 40s, would experience the same attack at 10am, 2pm and 6pm, like perfect clockwork. “Oh God, here it comes,” he’d think to himself, before fireworks exploded in his temple and the poker stabbed into the very roots of his teeth, making him scream and sometimes vomit. “It just grows, and it thumps, and it thumps, and it thumps with my heartbeat,” said Peter, recalling the pain. Peter had experienced these inexplicable episodes since he was a kid, always in the summer. An attack left him shaking and exhausted, and waiting on the next bout was a kind of psychological torture – within the short respites, he dreaded the next. Once, when Peter felt one starting, he threw on his shoes and sprinted through the streets of south London. He didn’t care which turns he took. Maybe if he ran fast enough, his lungs full of air, he could outrun the thing. His heart pumped in his chest, more from fear than the exercise itself. When the pain escalated to an unbearable pitch, he slowed to a stop, dry heaving, and sat down to press on his eye. He was three miles away from home. © 2025 Guardian News & Media Limited

Keyword: Pain & Touch
Link ID: 29761 - Posted: 04.26.2025

Humberto Basilio What Rina Green calls her “living hell” began with an innocuous backache. By late 2022, two years later, pain flooded her entire body daily and could be so intense that she couldn’t get out of bed. Painkillers and physical therapy offered little relief. She began using a wheelchair. Green has fibromyalgia, a mysterious condition with symptoms of widespread and chronic muscle pain and fatigue. No one knows why people get fibromyalgia, and it is difficult to treat. But eight months ago, Green received an experimental therapy: pills containing living microorganisms of the kind that populate the healthy human gut. Her pain decreased substantially, and Green, who lives in Haifa, Israel, and is now 38, can go on walks — something she hadn’t done since her fibromyalgia diagnosis. Green was one of 14 participants in a trial of microbial supplements for the condition. All but two reported an improvement in their symptoms. The trial is so small that “we should take the results with a grain of salt”, says co-organizer Amir Minerbi, a pain scientist at the Technion — Israel Institute of Technology in Haifa. “But it is encouraging [enough] to move forward.” The trial results and data from other experiments linking fibromyalgia to gut microbes are published today in Neuron1. Fibromyalgia affects up to 4% of the global population and occurs in the absence of tissue damage. In 2019, Minerbi and his colleagues discovered that the gut microbiomes — the collection of microbes living in the intestines — of women with fibromyalgia differed significantly from those of healthy women2. This led the scientists to wonder whether a dose of microbes from healthy people would ease the pain and fatigue caused by the condition. After all, previous research3 had shown that gut microbes might indirectly influence an array of chemical signals tied to pain perception. The team transplanted minuscule samples of microbe-laden faeces from both women with fibromyalgia and healthy women into mice without any microbes in their bodies. The researchers found that mice that received microbes from women with fibromyalgia showed signs of greater sensitivity to pain in response to pressure, heat and cold than did mice that got microbes from healthy women. The first group also showed more evidence of spontaneous pain. © 2025 Springer Nature Limited

Keyword: Pain & Touch; Obesity
Link ID: 29760 - Posted: 04.26.2025

Smriti Mallapaty Two hotly anticipated clinical trials using stem cells to treat people with Parkinson’s disease have published encouraging results. The early-stage trials demonstrate that injecting stem-cell-derived neurons into the brain is safe1,2. They also show hints of benefit: the transplanted cells can replace the dopamine-producing cells that die off in people with the disease, and survive long enough to produce the crucial hormone. Some participants experienced visible reductions in tremors. The studies, published by two groups in Nature today, are “a big leap in the field”, says Malin Parmar, a stem-cell biologist at Lund University, Sweden. “These cell products are safe and show signs of cell survival.” Japan’s big bet on stem-cell therapies might soon pay off with breakthrough therapies The trials were mainly designed to test safety and were small, involving 19 individuals in total, which is not enough to indicate whether the intervention is effective, says Parmar. “Some people got slightly better and others didn’t get worse,” says Jeanne Loring, a stem-cell researcher at Scripps Research in La Jolla, California. This could be due to the relatively small number of cells transplanted in these first early-stage trials. Parkinson’s is a progressive neurological condition driven by the loss of dopamine-producing neurons, which causes tremors, stiffness and slowness in movement. There is currently no cure for the condition, which is projected to affect 25 million people globally by 2050. Cell therapies are designed to replace damaged neurons, but previous trials using fetal tissue transplants have had mixed results. The latest findings are the first among a handful of global trials testing more-advanced cell therapies. © 2025 Springer Nature Limited

Keyword: Parkinsons; Stem Cells
Link ID: 29751 - Posted: 04.19.2025