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

Dyani Lewis Human brain cells engineered to evade detection by the immune system have successfully restored muscle control in a rat model of Parkinson’s disease1. The study is a step towards the development of a ‘universal’ cell line that can be transplanted into anyone, to cure a raft of diseases without the need for anti-rejection drugs. “It’s a one-cell-fits-all proposal,” says Clare Parish, a stem-cell biologist at the Florey Institute of Neuroscience and Mental Health in Melbourne, Australia, and a co-author of the study. The work, published today in Cell Stem Cell, builds on earlier efforts to ‘cloak’ cells from the immune system. Cloaking is a key goal for cell-replacement therapies being tested for conditions ranging from type 2 diabetes and Parkinson’s disease to heart failure and blindness. It would eliminate the need for immunosuppressant drugs, which increase the risk of infection and cancer, and cause tissue damage that ultimately shortens the life of a recipient. To help cells to evade the immune system, the researchers created a cell line with eight genes altered to increase their activity so they acted as an immune invisibility cloak. All of the genes have been shown to assist the placenta and cancer cells in naturally evading immune surveillance. For example, mouse embryonic stem cells engineered with the same set of genes were able to evade detection when transplanted into mice2. Instead of mouse embryonic cells, Parish and her team used human pluripotent stem cells, which can develop into most types of cell found in the body. After being engineered with the cloaking genes, the cells differentiated into nerve cells suitable for treating Parkinson’s disease. The researchers injected the neurons into mice whose immune systems had been replaced with human immune cells, and the neurons were not rejected, suggesting that they were able to evade detection. © 2025 Springer Nature Limited

Keyword: Parkinsons
Link ID: 29742 - Posted: 04.12.2025

Jon Hamilton Researchers created an assembloid by integrating four organoids that represent the four components of the human sensory pathway, along which pain stimuli signals are conveyed to the brain. Stimulation of the sensory organoid (top) by pain-inducing substances, such as capsaicin, triggers neuronal activity in that organoid which is then transmitted to the adjacent spinal-cord organoid, the thalamic organoid and, finally, to the cortical organoid (bottom) Researchers integrated four organoids that represent the four components of the human sensory pathway, along which pain signals are conveyed to the brain. Stimulation of the sensory organoid (top) by substances, such as capsaicin, triggers neuronal activity that is then transmitted throughout the rest of the organoids. Pasca lab/Stanford Medicine Scientists have re-created a pain pathway in the brain by growing four key clusters of human nerve cells in a dish. This laboratory model could be used to help explain certain pain syndromes, and offer a new way to test potential analgesic drugs, a Stanford team reports in the journal Nature. "It's exciting," says Dr. Stephen Waxman, a professor at Yale School of Medicine who was not involved in the research. © 2025 npr

Keyword: Pain & Touch; Development of the Brain
Link ID: 29739 - Posted: 04.12.2025

By Mitch Leslie Unlike the combative immune cells that protect us from pathogens, regulatory T cells (Tregs) are nurturers. They salve inflammation, promote healing of injured tissue, and rein in immune attacks to curb self-inflicted damage. Now, a study of mice reported today in Science suggests some Tregs also act on nerve cells to quell a specific type of pain—but only in females. Why only female rodents seem to benefit remains unclear, but researchers hope they might someday enlist these Tregs to address pain conditions, many of which disproportionately affect women. “It’s a very impressive paper,” says neuroscientist Gila Moalem-Taylor of the University of New South Wales Sydney, who wasn’t connected to the research. The study “uses elegant, sophisticated methods to conclusively demonstrate the mechanisms” by which the cells reduce one kind of sensitivity to pain, she says. Tregs, a type of white blood cell, are best known for their role in keeping the immune system in balance and preventing autoimmunity. But researchers have recently found that they also help control pain. For example, a 2021 study by neuroscientist Allan Basbaum of the University of California San Francisco (UCSF) and colleagues showed that Tregs reduce mice’s sensitivity to pain triggered by other immune cells that reside in the brain and spinal cord. That research and additional work suggested Tregs influence pain by targeting various immune cells and tamping down inflammation. But these studies left open the possibility that Tregs might also directly affect pain-sensing nerve cells. Basbaum, his postdoc Élora Midavaine, UCSF dermatologist Sakeen Kashem, and their colleagues launched the new study to nail down how the regulatory cells curb pain. They focused on Tregs that dwell in the meninges—the membranes that sheathe the brain and spinal cord—and in similar nearby membranes. The cells are much more abundant in these structures than elsewhere in the nervous system. To find out whether the cells affect pain perception, the scientists used genetically engineered mice whose Tregs are vulnerable to a toxin produced by the bacteria that cause diphtheria. Injecting this toxin into the meninges in the lower back killed about 90% of the Tregs in the membranes without harming Tregs in the rest of the body.

Keyword: Pain & Touch; Glia
Link ID: 29729 - Posted: 04.05.2025

Vicki Hird Does a worm feel pain if it gets trodden on? Does a fly ache when its wings are pulled off? Is an ant happy when it finds a food source? If so, they may be sentient beings, which means they can “feel”, a bit or a lot, like we do. Invertebrate sentience is becoming an ever livelier topic of debate and with new science we are getting new insights. But Dr Andrew Crump at the Royal Veterinary College, who helped ensure that new UK laws recognising animal sentience were amended to include large cephalopod molluscs and decapod crustaceans – octopuses, lobsters, crabs to you and me – says this is not at all straightforward. Nervous systems are hugely complex, and identifying consciousness and sentience – and not just automatic pain reflexes – is hard. Are responses or reactions you see from an animal – be it a wolf or a wolf ant – feelings or just automatic reflexes? Crump and his colleagues found that bees, for example, were not simple stimulus-response robots, but reacted to stimuli in sophisticated, context-dependent ways. They were found to learn colour cues for their decisions on feeding – choosing painful overheated sugars they previously avoided when non-heated options had a low sugar concentration. So they made trade-offs by processing in the brain then modifying their behaviour. In fact, new research has shown that many responses in the larger invertebrates were complex, long-lasting, and pretty consistent with criteria for pain that had been produced initially for vertebrates such as rats. Octopuses, for example, can perform amazing feats of learning to avoid painful environments and choose painkilling environments. All this establishes and quantifies “feelings” in beings that are very different from us. The work of Crump and other scientists meant that the Animal Welfare (Sentience) Act 2022 recognised for the first time in UK law (vertebrate sentience was previously covered by EU regulation) that certain invertebrates can “feel”, requiring modifications to their treatment in areas such as farming and research. © 2025 Guardian News & Media Limited

Keyword: Pain & Touch; Evolution
Link ID: 29684 - Posted: 02.26.2025

By Fred Schwaller Andrea West remembers the first time she heard about a new class of migraine medication that could end her decades of pain. It was 2021 and she heard a scientist on the radio discussing the promise of gepants, a class of drug that for the first time seemed to prevent migraine attacks. West followed news about these drugs closely, and when she heard last year that atogepant was approved for use in the United Kingdom, she went straight to her physician. West had endured migraines for 70 years. Since she started taking the drug, she hasn’t had one. “It’s marvellous stuff. It’s genuinely changed my life,” she says. For ages, the perception of migraine has been one of suffering with little to no relief. In ancient Egypt, physicians strapped clay crocodiles to people’s heads and prayed for the best. And as late as the seventeenth century, surgeons bored holes into people’s skulls — some have suggested — to let the migraine out. The twentieth century brought much more effective treatments, but they did not work for a significant fraction of the roughly one billion people who experience migraine worldwide. Now there is a new sense of progress running through the field, brought about by developments on several fronts. Medical advances in the past few decades — including the approval of gepants and related treatments — have redefined migraine as “a treatable and manageable condition”, says Diana Krause, a neuropharmacologist at the University of California, Irvine. At the same time, research is leading to a better understanding about the condition — and pointing to directions for future work. Studies have shown, for example, that migraine is a broad phenomenon that originates in the brain and can manifest in many debilitating symptoms, including light sensitivities and aura, brain fog and fatigue. “I used to think that disability travels with pain, and it’s only when the pain gets severe that people are impaired. That’s not only false, but we have treatments to do something about it,” says Richard Lipton, a neurologist at the Albert Einstein College of Medicine in New York City. © 2025 Springer Nature Limited

Keyword: Pain & Touch
Link ID: 29681 - Posted: 02.22.2025

By Gina Kolata The Food and Drug Administration approved a new medication Thursday to treat pain from an injury or surgery. It is expensive, with a list price of $15.50 per pill. But unlike opioid pain medicines, it cannot become addictive. That is because the drug, suzetrigine, made by Vertex Pharmaceuticals and to be sold as Journavx, works only on nerves outside the brain, blocking pain signals. It cannot get into the brain. Researchers say they expect it to be the first of a new generation of more powerful nonaddictive drugs to relieve pain. To test the drug, Vertex, which is based in Boston, conducted two large clinical trials, each with approximately 1,000 patients who had pain from surgery. They were randomly assigned to get a placebo; to get the opioid sold as Vicodin, a widely used combination pain medicine of acetaminophen (Tylenol) and hydrocodone; or to get suzetrigine. In one trial, patients had an abdominoplasty, or tummy tuck. In the other, they had a bunionectomy. Side effects of suzetrigine reported by patients were similar to the ones reported by those taking the placebo. The company also submitted data from a 250-person study that assessed the drug’s safety and tolerability in patients with pain from surgery, trauma or accidents. Suzetrigine eased pain as much as the combination opioid. Both were better than the placebo at relieving pain. Suzetrigine’s price, though, is much higher than that of acetaminophen plus hydrocodone. Patients are expected to take two pills a day, for a total cost of $31 a day. The older drug, said Dr. John D. Loeser, an emeritus pain expert at the University of Washington, is “dirt cheap” at pennies per pill. But suzetrigine does not have opioids’ unpleasant side effects like nausea and drowsiness, and it is nonaddictive. © 2025 The New York Times Company

Keyword: Pain & Touch; Drug Abuse
Link ID: 29653 - Posted: 02.01.2025

By Laura Sanders Scratching an itch can bring a contradictory wave of pleasure and misery. A mouse study on scratching, reported in the Jan. 31 Science, fleshes out this head-scratching paradox and could point out ways to better curb pernicious itch in people. First, the bad news: Scratching itchy ears led to a round of inflammation. Itch-provoking substances, such as the oil in poison ivy, activate mast cells, immune sentries that release itch signals and kick off inflammation. But so does scratching, the new study suggests. “The act of scratching is actually triggering the inflammation by synergizing with mast cells to make them more effective,” says study coauthor Daniel Kaplan, a dermatologist and immunologist at the University of Pittsburgh. Mice that couldn’t scratch their itchy ears, thanks to tiny cones of shame, had less inflammation than mice that scratched. The same was true for mice that didn’t sense the itch, the researchers report. Kaplan relates the results to a mosquito bite. “Most of the time, it’ll go away in five, 10 minutes,” he says. “But if you start scratching it, now, you get a really big, inflamed, itchy lesion on your skin that can stick around for several days. It’s a lot worse. And I think this could be a mechanism that explains why.” Now onto the good news: Scratching lessened the amount of potentially harmful bacteria (Staphylococcus aureus) on mice’s skin, perhaps through the heightened immune reaction it prompts. “That was a clear demonstration that scratching can have a benefit in the context of an acute infection,” Kaplan says. But too much scratching can rip the skin and usher in more bacteria, he cautions. “In that sense, scratching, through a different mechanism, also makes things even worse.” © Society for Science & the Public 2000–2025.

Keyword: Pain & Touch
Link ID: 29648 - Posted: 02.01.2025

By Katherine Ellison “American Ninja Warrior” contestant Jimmy Choi was 27 when he was diagnosed with young-onset Parkinson’s disease after a routine medical exam. Today, Choi, 50, is an adviser to the Michael J. Fox Foundation for Parkinson’s Research who champions physical fitness and works to inspire others via public speaking and social media posts. More than 1 million Americans have Parkinson’s disease, a neurological illness that can cause tremors, loss of balance, confusion and depression. Choi spent the eight years after his diagnosis in denial as his symptoms grew worse. After a mortifying fall, however, his perspective changed, and he embraced exercise — in a big way. Since 2011, the Chicago-based former tech executive (he retired from full-time work in 2018, though he still works as a consultant) has run 16 marathons and earned three Guinness World records, the most recent in 2023 for consecutive double high five push-ups. He has also competed seven times on “American Ninja Warrior,” the reality-TV show in which contestants make their way past daunting obstacles, crossing unstable bridges, running up walls and leaping through the air, all while trying to avoid falling into a large pool of water. Last year Choi finished his seventh, and, he insists, last “Ninja” appearance. It’s set to air this spring. Q: What led to your diagnosis? A: It was a routine exam for health insurance, in 2003. A nurse noticed the way I was walking and said I should talk to my doctor. I had to see four neurologists before I got diagnosed, and for several years afterward, I lost my motivation. I started isolating from friends, gained a lot of weight and couldn’t walk without a cane.

Keyword: Parkinsons
Link ID: 29645 - Posted: 01.29.2025

By Angie Voyles Askham More than 150 years after the first known description of Huntington’s disease and 32 years after the causative gene, HTT, was identified, new evidence has emerged to explain how variants linked to the disease devastate the brain: The toxicity comes not from the initial variant itself but rather from its dynamic expansion past a set threshold in specific cells, according to a study published today in Cell. The results help explain why most people with Huntington’s disease don’t start to show symptoms—including muscle rigidity, irregular movements and severe psychological issues—until age 30 to 50, with the gradual loss of striatal projection neurons, also called medium spiny neurons, says co-lead researcher Steven McCarroll, professor of biomedical science and genetics at Harvard Medical School. “We hadn’t been thinking about mutations as dynamic things” that become toxic only later in life, he says. The HTT variants associated with Huntington’s disease all have extra repeats of the DNA triplet CAG. Typical people carry about 15 to 30 of these repeats, and those with the disease tend to have 40 or more. The disease-linked expansions, which are known to grow even larger over time, result in a gangly version of the Huntington’s protein that is thought to cause neurons to malfunction and degenerate. But the expansion does not appear to affect a cell’s biology until it exceeds 150 CAG copies, according to the new study. And the repeats accumulate quietly over the course of years, and at different rates for different cells. Striatal projection neurons with more than 150 repeats have severely dysregulated transcriptomes, McCarroll and his colleagues found by analyzing gene expression in postmortem tissue from people with Huntington’s disease. But other cell types in the striatum, including oligodendrocytes and interneurons, do not end up with as many repeats, nor do they undergo similar transcriptomic changes, the work shows. © 2025 Simons Foundation

Keyword: Huntingtons; Genes & Behavior
Link ID: 29636 - Posted: 01.22.2025