Janna Levin Pain and pleasure seem like simple facts of life, however they are anything but that. Neuroscientists still cannot say why physical pain differs from psychological pain, for instance, or why a loved one’s touch soothes while a stranger’s touch repels. To explore the science behind these sensations, Janna Levin talked to Ishmail Abdus-Saboor (opens a new tab), a neuroscientist at Columbia University’s Zuckerman Institute. Their conversation covers how pain serves an evolutionary purpose, how researchers measure pain and pleasure in the lab despite the absence of any objective biomarker, and how touch functions as a social and emotional signal, not just a sensory one. Abdus-Saboor also describes his work with naked mole rats — a species that barely feels pain, shows no signs of aging, and lives in colonies built almost entirely on touch — and the ethical trade-offs when studying sensations in animals that cannot describe what they feel. STROGATZ: It’s really mysterious, especially when you have pain that doesn’t really relate to tissue damage. Like, sometimes I’ll just be washing something at the sink in the kitchen, and then suddenly I have pain, and I think, “Come on, that’s ridiculous. I didn’t do anything to my back.” And, you know, people will tell you pain is mental. You can sort of talk yourself out of certain pain, which raises the point that pain is not as simple as it might seem at first. LEVIN: Yeah, and in particular, he studies this at the level of animals. But it’s one of these things that’s very hard for animals to tell you reliably what they’re experiencing. So, a lot of his work is really trying to interpret the animal’s interiority, the animal’s experience of different sensations. I was very fascinated about biology and biological systems and how animals communicate and cooperated. STROGATZ: Yeah, I wondered as you were describing this work, is it touch as a means to learn about interiority, or is touch the primary object of interest here? LEVIN: I mean, I think that that’s an interesting question. Like, with many scientific ambitions, sure, maybe the big goal is consciousness, right? But no, the big goal is always very far off. That’s not the language in which they’re operating. © 2026 Simons Foundation

Keyword: Pain & Touch
Link ID: 30366 - Posted: 08.08.2026

Stephani Sutherland One night in 2000, Allan Basbaum was at the Pierre Hotel on Central Park, wearing a tuxedo after presenting a neuroscience award to one of his colleagues before a roomful of scientists, Nobel laureates among them. His wife, Carol, a cancer biologist, had accompanied him from San Francisco, where they both ran laboratories at the University of California. Late that night, he was struck by agonising stomach pain. Alarmed, they went to the emergency room at Lenox Hill Hospital, where the waiting area was jammed and hours passed before anyone could see him. ‘So I’m out in the waiting room; I’m periodically screaming,’ Basbaum says. After two hours, Carol went to the bathroom, leaving him alone. Finally, a man came over and began speaking to him, gently prodding him. ‘He checks my pulse, he asks: “Does this hurt?”’ Basbaum says. As the man attended to him, ‘the pain really started to get much better,’ and Basbaum relaxed. When Carol returned, he told her about the long-awaited treatment. ‘She says: “Allan, he’s one of the patients. He’s been doing that to everybody here.” But finally, someone was taking care of me.’ And that brought relief. By then, Basbaum had spent three decades studying the physiology of pain, mapping the neural circuits that carry signals from the body toward the brain. He wanted to understand how those signals become pain. His experience brought to life the questions he’d been marvelling at for years: how do fear, context and expectation shape the body’s most urgent alarm? How do placebos work? And how could someone relieve his pain, just by paying attention? Basbaum understood the Gordian knot at the heart of pain: the brain could influence pain before a person consciously felt it. His work over the past 50 years has been to untangle that loop, following signals through the spinal cord to the brain and back again. © Aeon Media Group Ltd. 2012-2026.

Keyword: Pain & Touch; Attention
Link ID: 30344 - Posted: 07.25.2026

Ushika Kidd Long-term exposure to road traffic noise is associated with a higher risk of Parkinson’s disease, the biggest study of its kind has found. Parkinson’s disease is a progressive disorder in which parts of the brain become damaged over time, affecting movement and balance. Existing research has found potential biological pathways that link noise exposure to Parkinson’s disease, largely due to stress responses and disrupted sleep. The researchers modelled noise exposure at the most and least exposed exterior of the residence of each participant and calculated the difference in noise levels. The magnitude of the effect was modest but consistent; at the most exposed facade, for every 11.5dB rise in noise level, the risk of Parkinson’s disease rose by 3% over the study period. Having a quiet part of the home may mitigate the association between exposure to road traffic noise and higher risk of Parkinson’s disease, according to the findings. The study, published in Jama Neurology, included 3.1 million Danish participants aged 40 and over, and followed them for 18 years. It was established using nationwide health register data, making it the largest study on road traffic noise and Parkinson’s disease. Previous research linked the rise in neurological disorders, including Parkinson’s disease, with exposure to environmental toxins. Environmental risk factors such as air pollution, microplastics and pesticides have become the main focus of prevention strategies. © 2026 Guardian News & Media Limited

Keyword: Parkinsons; Hearing
Link ID: 30339 - Posted: 07.25.2026

By Elie Dolgin Jeff Carroll was in his mid-twenties, fresh out of the U.S. Army, when a genetic test confirmed his worst fear: He was going to develop Huntington’s disease. He had watched his mother’s illness for years; the tremors first, small enough to explain away, then the involuntary movements that looked almost like dancing. The test revealed that the same mutation that caused her disease lived in him: a stretch of three DNA letters in a gene called HTT, repeated over and over again dozens of times. Carroll himself was not sick yet. He would not get sick for many years. But the countdown had begun. In fact, it had likely been running all his life, deep inside vulnerable neurons in his brain. There, the mutant HTT gene was slowly growing longer, its internal repeats piling up toward a threshold that, once crossed, would tip the cell into disarray. The first outward signs of Huntington’s often begin with mood changes and subtle cognitive effects. The hallmark jerky movements come later. Eventually, and relentlessly, patients lose the ability to speak, swallow or move. Most people die within a decade or two of symptom onset. Huntington’s disease is rare, affecting roughly 1 in 20,000 people worldwide. Yet because each child of an affected parent has a 50 percent chance of inheriting the mutation, the disease can haunt families for generations. It had already claimed Carroll’s grandmother and would take his mother at age 54. Without a therapy capable of altering its course, Carroll — along with three of his five siblings who also inherited the mutation — seemed fated to follow his ancestors into an early grave. Carroll decided the only rational response was to become one of the scientists seeking ways to beat the disease. He was midway through his undergraduate studies when he learned, in 2003, that he carried the mutation. He pressed on, earning a Ph.D. and completing postdoctoral training before establishing his own research group devoted to understanding and slowing the disease stalking him from within. © Society for Science & the Public 2000–2026.

Keyword: Huntingtons
Link ID: 30332 - Posted: 07.18.2026

Ian Sample Science editor A man who was paralysed from the chest down in a swimming accident six years ago has been able to feed himself and drink from a cup thanks to a brain implant that bypasses his spinal cord injury. Keith Thomas of Massapequa, New York, could not lift his arms off his wheelchair when he agreed to trial the technology in 2021, but after surgery to implant electrodes in his brain and many months of training, he was able to move the limbs again. Researchers fitted Thomas with a brain-computer interface that not only helped him move his arms and hands, but also sent signals back to his brain to recreate the sensation of touch. He has since been able to feel his sister’s hand and the fur on his pet dog. Remarkably, the technology appears to have partly rewired Thomas’s nervous system, helping to restore some hand functions and sensations that remain even when the system is switched off. “For me this is an incredible moment,” said Prof Chad Bouton, whose team developed the technology at the Feinstein Institutes for Medical Research, the research arm of the New York healthcare provider Northwell Health. “For years, we have been wanting to really tackle the restoration of movement and the sense of touch and bring those together and we’ve also wanted to create lasting effects,” Bouton added. “I think we’re going to continue to see progress and I think it’ll be applicable to the millions of folks around the world who really need this technology.” Thomas was 42 when he broke his neck diving into a swimming pool in July 2020. He blacked out and regained consciousness to see a helicopter on the front lawn. He was immediately taken to hospital. “The next day I couldn’t even move,” he said. The following October, he joined a three-year clinical trial of what the researchers called a “double neural bypass”. It uses electrodes implanted into Thomas’s brain to detect when he wants to move his arms. The signals are then routed to his arms and hands to move them. © 2026 Guardian News & Media Limited

Keyword: Robotics
Link ID: 30331 - Posted: 07.18.2026

Laura Russo A surprisingly large number and diversity of bee species – 74 out of 96 tested – have magnetic properties, according to research my colleagues and I recently published in the journal Science Advances. Some animals are able to use iron-based magnetic compounds such as magnetite to detect and navigate via the Earth’s magnetic field – a sense called magnetoreception. We considered magnetism in the insects we tested to be a proxy for which species might be magnetoreceptive. For decades, biologists have known that social, cavity-nesting honeybees exhibit magnetoreception. Most researchers assumed that this internal compass was tied to living in a colony; honeybees communicate the location of floral resources to other colony members through a dance that indicates direction relative to the position of the Sun and the geomagnetic field. Our study had two goals: to compare magnetism between bee species that live in groups versus on their own, and to track down the evolutionary origin of magnetoreception in bees. To test magnetic responses, we collected bee specimens from across the bee family Apidae, which includes social species such as honeybees along with solitary species such as chimney bees. We ground dried dead bees into a powder, then measured how magnetic this powder was in a magnetometer. To our surprise, we found that the magnetic response was strong in both bees that live in groups and those that live alone. This result forced us to reject our initial hypothesis that magnetism was necessary only for social bee species. - © 2010–2026, The Conversation US, Inc.

Keyword: Animal Migration
Link ID: 30328 - Posted: 07.18.2026

By Aimee Cunningham Reassuring evidence on acetaminophen’s safety during pregnancy keeps growing. A large, two-decade study in Hong Kong is the latest to find no link between use of the drug — known as Tylenol in the United States — and a risk of autism or attention-deficit/hyperactivity disorder in children. The lack of an association persisted no matter the trimester the drug was prescribed, the dose or the recommended frequency, researchers report June 29 in JAMA Internal Medicine. Joining several other analyses, including ones conducted in Sweden and Japan, the research adds to the body of evidence reporting no association between acetaminophen use in pregnancy and long-term neurodevelopmental disorders in children. All the studies compared siblings born to mothers who had taken the drug at some point, such that some siblings were exposed to the drug in utero and others weren’t. This approach accounts for the fact that both ADHD and autism are largely influenced by genetics. If acetaminophen were also a factor, researchers would expect a difference between siblings exposed to the drug and those not. None of the studies have found one. For the new study, the researchers pored over electronic health records from 2001 to 2023 for more than 700,000 pairs of mothers and children. Around 43 percent of the kids encountered acetaminophen in utero. The team focused on pairs of siblings that differed in exposure and used their records to follow the children for at least two years for autism diagnoses and at least five for ADHD. The autism analysis included more than 124,000 children, while the ADHD component had more than 97,000. Going a step further, the analysis also looked at the timing and amount of acetaminophen that was prescribed. © Society for Science & the Public 2000–2026.

Keyword: ADHD; Autism
Link ID: 30303 - Posted: 07.01.2026

By Phie Jacobs When Charles Darwin visited Ascension Island in 1836, he was perplexed by the vast numbers of green sea turtles (Chelonia mydas) nesting on its beaches. Every mating season, these intrepid reptiles leave their feeding grounds along the coast of Brazil and journey more than 2000 kilometers across the sea to lay their eggs on this tiny, remote island. How, Darwin later mused in a letter to Nature, did the animals find their way to a “speck of land in the midst of the great Atlantic Ocean?” Since then, scientists have uncovered convincing evidence that sea turtles can sense components of Earth’s geomagnetic field. Now, data collected using a new kind of tracking device lend further support to the idea that these animals use magnetic maps to navigate during their transoceanic voyages. But the system is far from perfect, researchers report today in Science Advances, which means migrating turtles must periodically reorient themselves after veering off course. The findings fit “very comfortably with what we know about turtle navigation,” says Kenneth Lohmann, a marine biologist at the University of North Carolina at Chapel Hill who wasn’t involved in the research. His team previously conducted laboratory studies demonstrating turtles can sense the strength of geomagnetic fields as well as their angle relative to the surface of Earth—potentially providing migrating turtles with a “bicoordinate” geomagnetic map of their surroundings. Exactly how good they are at using those coordinates in the open ocean, however, has been less clear. Graeme Hays, a marine ecologist at Deakin University, paid his own visit to Ascension Island back in the 1990s. While there, he and Paolo Luschi—now a biologist at the University of Pisa—worked to outfit green sea turtles with satellite tracking devices. Early on, Hays recalls, the pair recognized a significant limitation: Although these tags can accurately track a turtle’s path across the ocean, those data don’t necessarily reflect “where the animal is trying to go.” © 2026 American Association for the Advancement of Science.

Keyword: Animal Migration; Evolution
Link ID: 30299 - Posted: 06.27.2026

By Jackie Rocheleau The cerebellum, the wizened “little brain” nestled in the base of the skull, may help keep us sharp as we age. Regions at the back of the cerebellum that resisted shrinkage with age were tied to better mental functioning, or cognition, even in people in the early stages of Alzheimer’s disease, researchers report June 10 in Nature Neuroscience. Though traditionally thought of as a movement control center, scientists now know the cerebellum is a key player in cognition. Researchers also know that parts of the cerebellum don’t age in unison, but the aging cerebellum is a relatively new area of research. In the new study, the team first analyzed brain scans and cognitive test scores from more than 700 U.S. adults whose data was collected as part of the Human Connectome Project, a brain mapping initiative. The test measured abilities including short-term memory, attention, language and visualizing 3-D objects. A clear trend emerged: The cerebellum tended to be smaller with increasing age, but the bigger the cerebellum, particularly in regions in the rear of the little brain, the higher the score on cognitive tests. The trend held even after adjusting for the different levels of education among participants, Princeton University neuroscientist Frederick d’Oleire Uquillas and colleagues report. The researchers found the same link in more than 35,000 adults in the U.K. Biobank, a biomedical database. The findings point to a larger cerebellum preserving cognition with greater age, says d’Oleire Uquillas. The researchers confirmed that scans of the larger cerebellums showed more brain tissue and connections between nerve cells, a © Society for Science & the Public 2000–2026.

Keyword: Alzheimers
Link ID: 30295 - Posted: 06.24.2026

Miryam Naddaf A brain implant is helping a man with paralysis to communicate with his family and friends and to use his personal computer at home. The brain–computer interface (BCI) has given 48-year-old study participant Casey Harrell, who was diagnosed with a type of motor neuron disease called amyotrophic lateral sclerosis six years ago, the ability to communicate with an average speed of 56 words per minute. It translates neural activity into text that appears on a computer screen and allows him to operate a computer, send text messages and e-mails and continue his job working in climate advocacy. It is “nothing short of revolutionary”, says Harrell, who is based in Oakland, California. “This has allowed me to keep working and earn money and insurance for my family. This is reconnecting me with friends and family who are too shy or too afraid to come over and not be able to understand me.” The study, published in Nature Medicine on 15 June1, analysed Harrell’s home use of the BCI for nearly two years and is “the most extensive data set and the longest-running speech communication of anyone” with such an implant, says co-author Sergey Stavisky, a neuroscientist at the University of California, Davis. Previous studies of participants testing BCIs at home showed that the devices had limited efficiency, and more-advanced devices have been tested only in the laboratory. “This is actually helping the patient in day-to-day life,” says Christian Herff, a computational neuroscientist at Maastricht University in the Netherlands. BCIs are “really becoming a medical device instead of a research tool”, he adds. Remarkable quality In 2023, Harrell had 256 microelectrodes implanted in his brain’s speech motor cortex. The electrodes were connected to electronic recording devices through titanium pedestals attached to his skull. He began to use the BCI device to decode his speech in the lab with the help of Stavisky and his colleagues. The researchers then trained Harrell and his care partners to operate the BCI system at home. After roughly 40 weeks, he began using the device independently; he is still using it today. The device also has a text-to-speech system that can read completed sentences aloud using a synthesized version of Harrell’s voice from before he was diagnosed. © 2026 Springer Nature Limited

Keyword: Robotics; Language
Link ID: 30284 - Posted: 06.17.2026

Hannah Harris Green A range of other medications could serve as alternatives to powerful opioids for pain relief in emergency departments, according to a new study. The review paper examined non-opioid medications available in the emergency department at San Francisco general hospital and examined existing medical literature to figure out which ones might provide pain relief. Opioids have a strong track record of reducing pain effectively, but loose prescriptions with insufficient care towards their addictive properties led to the first wave of the US opioid crisis, which began in the 90s. Akash Shanmugam, a medical student at the University of California, San Francisco (UCSF) and first author on the study, said the goal of the study was to “create a very targeted list for specific pain conditions”, to help add to the “toolboxes” physicians use to treat patients. The study provides recommendations for the most common types of pain that patients experience in emergency departments; abdominal pain, back pain, chest pain, fracture pain and headache. Shanmugam and Dr Kathy LeSaint, an associate professor of emergency medicine at UCSF and another of the paper’s authors, agree that opioids still have a place in medicine. “The desire to reduce opioids shouldn’t come at the expense of under-treating pain,” Shanmugam said. However, alternatives can also have an important role as physicians have become increasingly aware of possible long-term consequences. LeSaint also pointed out that beyond concerns about opioid addiction and overdose, it’s important to have a variety of medications for pain available because what will work best varies from person to person. This variation is often genetic; for example “the enzymes that are responsible for metabolizing opioids can have different strengths in people”, LeSaint explained. © 2026 Guardian News & Media Limited

Keyword: Pain & Touch; Drug Abuse
Link ID: 30283 - Posted: 06.17.2026

By Gina Kolata On my second visit with Nancy Wexler at her Manhattan apartment, she had a gift for me. It was a copy of her newly published memoir, “My Life, My Science: Pursuing a Cure for Huntington’s Disease.” It had been signed with a stamp of her signature — she isn’t able to sign it herself. Nor could she rise from her brown faux-leather recliner to greet me — she can’t get up unassisted. Speaking requires effort. She can manage at most a few badly slurred words or phrases or, with great difficulty, a short sentence. On that bright windy afternoon, Nancy and her sister, Alice Wexler, sat side by side in recliners, their backs to windows that offered a stunning view of the Hudson River far below. Alice lives in California, but she visits Nancy every other month. At age 80, Nancy Wexler has Huntington’s disease, a dreaded brain disease that destroys a person’s ability to control movements. There is no treatment. There is no cure. The disease is inherited: Nancy’s grandfather, three uncles and mother had it. Alice, however, does not: If a parent has Huntington’s, each child has a 50 percent chance of getting it. Their mother attempted suicide, a path that others with the disease have chosen, but ultimately died from Huntington’s. Nancy is not just any Huntington’s disease patient. For decades, she led a research effort in a remote area of Venezuela that found the gene responsible for Huntington’s. That work yielded a blood test that enable at-risk people to find out if they are destined to get the disease. In honor of this work, Nancy has garnered numerous accolades and prizes, including a Lasker award, among the most prestigious in science. She devoted her life to understanding what it’s like to be at risk for Huntington’s disease, what it’s like to have it. © 2026 The New York Times Company

Keyword: Huntingtons
Link ID: 30276 - Posted: 06.13.2026

Jon Hamilton Scientists who've spent decades learning how the brain works say they're now ready to start fixing it when it breaks. That's the premise of the Brain Health accelerator, a collaborative effort launched by the Allen Institute in Seattle, which has become a major player in brain research. The initiative includes plans to develop new genetic therapies — a term that includes gene editing as well as traditional gene therapy — for diseases including Alzheimer's, Parkinson's, ALS, and Huntington's. "The latest genetic treatments allow scientists to control the activity of particular genes," says Ed Lein, who directs the institute's brain health programs. "That opens up the possibility for very specific precision therapies for brain disorders." The accelerator is an outgrowth of the BRAIN Initiative, an ambitious research program unveiled by President Obama in 2013. The goal of this public-private partnership was to create tools that would allow scientists to see the brain's inner workings, and, eventually, to develop treatments. But the effort has progressed far faster than many scientists expected. "I am shocked at how far we've come in the last 10, 12 years," says John Ngai, a senior investigator at the National Institutes of Health who directs the BRAIN Initiative. "It's just been beyond my wildest imagination — and I've been accused of having a pretty good imagination." © 2026 npr

Keyword: Parkinsons; Alzheimers
Link ID: 30267 - Posted: 06.03.2026

By Elizabeth Pennisi Homing pigeons don’t rely on gut instinct to return to the roost. But a nearby organ — the liver — might point the way. White blood cells in the birds’ livers accumulate iron and act as an internal compass when clouds block the sun that normally helps them navigate, researchers report May 28 in Science. While scientists generally agree that some animals use Earth’s magnetic field to guide migrations, they had not pinned down how, and the new work offers a surprising explanation. For decades, researchers have fiercely debated first if and then how birds sense magnetic fields and use them for navigation. One prominent idea involves proteins in their eyes undergoing a reaction in magnetic fields. No one has been able to prove exactly how this so-called “quantum effect” is in play. Other animals that orient using Earth’s magnetism, such as bats and sharks, lack the proteins, so the debate languished unresolved. Ornithologist Martin Wikelski of the Max Planck Institute of Animal Behavior in Radolfzell, Germany, and immunologist Christian Kurts of the University of Bonn in Germany stumbled on another idea more than a decade ago at a conference coffee break. Kurts mentioned how frustrated he was that immune system cells called macrophages in mouse spleens would stick to magnetic columns in instruments used to separate different types of cells, ruining his experiments. The reason the macrophages were sticking, he discovered, was that they accumulated and recycled damaged red blood cells’ iron atoms, which aligned in magnetic fields. © Society for Science & the Public 2000–2026

Keyword: Animal Migration; Neuroimmunology
Link ID: 30264 - Posted: 05.30.2026

By Laura Sanders This is a two-part series on Parkinson’s, detailing the daily struggles with the disease, new treatment programs and how patients’ lives have been impacted by emerging therapies. You can read the first part here. The night before he had brain surgery to treat his Parkinson’s disease symptoms, Robert Goings couldn’t sleep. “He was pacing all night,” says his wife, Diana. That’s because it hurt to stop moving. Normally, Goings’ restless movements, stiffness and muscle cramps were eased by medicine. But doctors wanted his symptoms unmasked for the procedure, which meant he was feeling them full blast. “My legs would cramp up, my arms, you know, everything would cramp up without the medication,” Goings says. The next morning, last November 5, Goings, who at age 68 had been living with increasingly disruptive symptoms for years, slid into an MRI machine at Oregon Health and Science University, or OHSU, in Portland. While Goings was inside the MRI tube, doctors aimed 1,024 ultrasound beams at several spots deep in his brain, burning the problematic tissue there. Afterward, Goings was wheeled to a recovery room. “He held out his hand — dead still,” Diana says. She remembers thinking, “Oh my God, I don’t believe this. It’s gone. Absolutely gone.” In opting for this treatment, called high-intensity focused ultrasound, Goings has joined a small but growing number of people choosing to control their Parkinson’s symptoms with permanent lesions in their brain. Already, an estimated 50 to 60 people have undergone the surgery at OHSU, where the treatment calendar is booked up months in advance. © Society for Science & the Public 2000–2026.

Keyword: Parkinsons
Link ID: 30258 - Posted: 05.27.2026

By Meghan Rosen Neurologist David Standaert can often tell if someone has Parkinson’s disease in a matter of minutes. Maybe their hand trembles and one of their arms doesn’t swing as much as the other when they walk. Maybe their voice sounds softer than usual, and they have a stillness to their body and a masklike look on their face, with little expressivity or blinking. “I always tell patients, ‘It’s not any one thing that tells me you have Parkinson’s. It’s all of these things together,’ ” he says. But Standaert’s is a rare skill. A movement disorder specialist at the University of Alabama at Birmingham, he has been diagnosing people with the disease for decades. He’s one of fewer than 1,000 doctors in the United States trained to spot and treat the sometimes-subtle signs of Parkinson’s. That’s a problem because more than 1 million people in the country have the disease, and the number is climbing as the population ages. “There are nowhere near enough movement disorder specialists to go diagnosing all these people,” Standaert says. A lack of specialists is just one of the problems that plagues Parkinson’s diagnosis, which has proved difficult in part because the disease is so complicated. Over time, and for reasons scientists don’t fully understand, particular nerve cells deep in the brain become damaged and die. For patients, this can manifest as tremors and a constellation of other symptoms that start mild and progressively worsen. Eventually, as muscles stiffen and swallowing becomes difficult, people may become bedridden, in need of round-the-clock care. But Parkinson’s disease varies tremendously, Standaert says. Which symptoms arise, how severe they are and how quickly they progress differ from person to person. “I have seen tens of thousands of patients with Parkinson’s disease, and no two are the same,” he says. © Society for Science & the Public 2000–2026.

Keyword: Parkinsons
Link ID: 30253 - Posted: 05.23.2026

By Natalia Mesa In 1967, Howard Fields was drafted into the U.S. military and stationed at the Walter Reed Army Institute of Research in Silver Spring, Maryland. It was the height of the Vietnam War, and Fields, who had recently graduated from Stanford University with an M.D. and Ph.D., was assigned to treat wounded soldiers. Among his patients was a man with median nerve causalgia, a painful condition caused by nerve damage following physical trauma. Treatment options for pain were limited at the time, and Fields decided to try what he later recalled as “this strange therapy” that electrically stimulated the peripheral nerve. “The results were dramatic,” Fields wrote in an autobiographical narrative. “Immediate, complete relief lasting for several hours.” His experience with the Vietnam War would guide his career in research. “He saw a lot of trauma,” says Jennifer Mitchell, professor of neurology at the University of California, San Francisco (UCSF), who was a graduate student in Fields’ lab. “I think he was compelled to help people that were suffering.” Fields died of complications from prostate cancer on 1 May 2026, at the age of 86. He spent his career mapping the pain-modulating circuits in the central nervous system, and his lab was the first to demonstrate the efficacy of opioids for neuropathic pain and topical lidocaine for postherpetic neuralgia. Later, he pivoted to studying addiction and mapped out the mechanisms by which opioids co-opt reward circuitry. His work around the physiology and anatomy of pain circuits made Fields “a giant in the field,” says Mary Heinricher, professor of neurological surgery and biomedical engineering at Oregon Health & Science University, who did a postdoctoral fellowship with Fields. In fact, Heinricher adds, “It wasn’t really a field of research before his generation.” © 2026 Simons Foundation

Keyword: Pain & Touch
Link ID: 30252 - Posted: 05.23.2026

By Pam Belluck Time was running out for Amanda Sifford, she and her doctors could tell. A.L.S., the paralyzing neurological disorder, was stealing her ability to breathe. On a breathing test, her lung function was only at 48 percent of capacity, a sharp drop from 86 percent five months earlier. “I couldn’t take 10 steps and be able to breathe,” she said. “I could no longer step up on a curb.” Ms. Sifford, 58, a school psychologist in Cape Coral, Fla., has lost 14 family members, including her father and grandfather, to a rare genetic form of A.L.S., also known as amyotrophic lateral sclerosis or Lou Gehrig’s disease. Her symptoms had been developing gradually, but her breathing suddenly nose-dived. “It was very scary,” said Dr. Nathan Carberry, one of her neurologists at the University of Miami Health System. “I worried that we were looking at months of life left.” “Was I thinking about dying?” said Ms. Sifford, pausing to collect herself. “I had my affairs in order.” It was May 2023, and the Food and Drug Administration had just approved the first therapy for a genetic form of A.L.S., even though clinical trial results had not yet proven the drug would be effective. The drug, tofersen, made by Biogen and marketed as Qalsody, targets the form of A.L.S. that Ms. Sifford inherited, so Dr. Carberry and Dr. Michael Benatar, the executive director of University of Miami A.L.S. Center, scrambled to establish a clinic to administer it. She began receiving tofersen monthly, through infusions into her spinal canal. © 2026 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 30245 - Posted: 05.16.2026

Liam Drew Three hearts; blue blood; no skeleton; arms like tongues. These are just some of the alien features of octopuses, squid and cuttlefish — members of the cephalopod family. The outlandish list continues. Cephalopod skin can taste chemicals, sense light and change colour and texture rapidly. In many species, the sucker-covered arms can even regenerate. These invertebrates have evolved independently from the vertebrate lineage for more than 600 million years. Their last common ancestor was probably a worm-like creature with a rudimentary nervous system and eye-like patches of light-sensitive cells. Despite this evolutionary gulf, vertebrates and these highly specialized molluscs share strange similarities. Their eyes, for example. “It’s eerie how similar they ended up,” says Cristopher Niell, a neuroscientist at the University of Oregon in Eugene. “The convergent evolution of the eye still blows my mind.” Now, one similarity is spurring a boom in cephalopod neuroscience. Around 400 million years ago, cuttlefish, squid and octopuses diverged from the only other living cephalopods — the nautiluses. They then lost their protective shells and evolved brains that are uniquely large among invertebrates. These brains bestow the soft-bodied cephalopods with high intelligence. Cuttlefish, squid and octopuses have excellent memories, use tools and are adept problem-solvers; they have a concept of time and are capable of delayed gratification. Cephalopods are the only non-vertebrate animals that have big, smart brains, says Cliff Ragsdale, a comparative neuroscientist at the University of Chicago in Illinois. And that presents a unique opportunity. Neuroscientists have gained a wealth of knowledge about how vertebrate brains work, but are increasingly looking to cephalopods for insights into ways to build large, high-functioning nervous systems. © 2026 Springer Nature Limited

Keyword: Evolution; Intelligence
Link ID: 30231 - Posted: 05.02.2026

Ian Sample Science editor Changes to microbes that live in the gut can identify people at greater risk of Parkinson’s disease long before symptoms develop, according to work that also raises hopes for new therapies. Researchers discovered signature changes in the gut microbiome that are more pronounced in people with a genetic risk for Parkinson’s and even more stark in those diagnosed with the disease. The signature could help doctors spot patients at risk of Parkinson’s years before they display clear symptoms and suggests that healthier diets and treatments that reshape the microbiome might prevent or delay the disease. Prof Anthony Schapira, the head of clinical and movement neurosciences at University College London and lead investigator on the study, said it was the first time a microbial signature in Parkinson’s patients had been seen in people with a genetic susceptibility but had yet to develop symptoms. The signature appears to become stronger as the disease progresses. “These same changes can be found in a small proportion of the general population that may put them at increased risk,” Schapira said. Cases of Parkinson’s have doubled in the past 25 years, with more than 8.5 million people globally now living with the condition. The disease causes progressive brain damage, leading to tremors, slow movement and stiff and inflexible muscles. Patients often experience depression, anxiety, sleep and memory problems, and difficulty with balance. © 2026 Guardian News & Media Limited

Keyword: Parkinsons
Link ID: 30209 - Posted: 04.22.2026