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 Ellen Barry The Food and Drug Administration has taken a crucial step toward expanding access to the antipsychotic medication clozapine, the only drug approved for treatment-resistant schizophrenia, among the most devastating of mental illnesses. The agency announced on Monday that it was eliminating a requirement that patients submit blood tests before their prescriptions can be filled. Clozapine, which was approved in 1989, is regarded by many physicians as the most effective available treatment for schizophrenia, and research shows that the drug significantly reduces suicidal behavior. Clozapine is also associated with a rare side effect called neutropenia, a drop in white blood cell counts that, in its most severe form, can be life-threatening. In 2015, federal regulators imposed a regimen known as risk evaluation and mitigation strategies, or REMS, that required patients to submit to weekly, biweekly and monthly blood tests that had to be uploaded onto a database and verified by pharmacists. Physicians have long complained that, as a result, clozapine is grossly underutilized. Dr. Frederick C. Nucifora, director of the Adult Schizophrenia Clinic at the Johns Hopkins School of Medicine, said he believed that around 30 percent of patients with schizophrenia would benefit from clozapine — far more than the 4 percent who currently take it. “I have had many patients who were doing terribly, who struggled to function outside the hospital, and cycled through many medications,” he said. “If they go on clozapine, they really tend to not be hospitalized again. I’ve had people go on to finish college and work. It’s quite remarkable.” © 2025 The New York Times Company

Keyword: Schizophrenia
Link ID: 29683 - Posted: 02.26.2025

By Lydia Denworth When Mala Murthy and Sebastian Seung of Princeton University saw high-resolution 2D electron microscope images in a 2018 Cell paper, they decided to try to build a fruit fly connectome with that dataset. Funded by the U.S. National Institutes of Health BRAIN Initiative, Murthy and Seung used the electron microscopy data to launch the work that resulted in FlyWire, a nine-paper package published in Nature in October 2024. The work made international headlines for its novelty and ambition. Not long ago, the length of the author list on the flagship FlyWire paper also would have been newsworthy: 46 researchers, including Murthy, Seung and first author Sven Dorkenwald. Neuroscience research has long been driven by individual labs and individual investigators, but today it is increasingly becoming a team sport similar to the FlyWire work—a 2024 preprint describing a study of hundreds of thousands of neuroscience papers published worldwide between 2001 and 2022 found a consistent rise in the number of authors per paper in nearly every country examined. There were 66 Nature Neuroscience papers in 2023 that had double-digit author counts, with the longest author list for that year comprising 209 names. The causes of this shift are related to technology breakthroughs that have allowed for the generation of massive datasets, as well as the general maturation of neuroscience, which is catching up with the large-scale, collaborative efforts put forth in other fields. The dual landmark papers in 2001 revealing the first draft of the Human Genome Project boasted 249 authors (in Nature) and 274 authors (in Science), and a fruit fly genome paper published in 2015 had more than 1,000. In physics, a 2015 paper providing an estimate of the mass of the Higgs boson listed more than 5,000 authors, thought to be a record. But researchers say long author lists are also raising questions about what kind of work is most productive for neuroscience and how to best parcel out credit. A stack of author names can diffuse “responsibility for what’s in the paper,” says neuroscientist J. Anthony Movshon of New York University. “We’re going to a place where it’s very hard to establish whose work you’re actually reading.” © 2025 Simons Foundation

Keyword: Miscellaneous
Link ID: 29682 - 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

Aaron Priester Traumatic brain injury is a leading cause of death and disability in the world. Blunt force trauma to the brain, often from a bad fall or traffic accident, accounts for the deaths of over 61,000 Americans each year. Over 80,000 will develop some long-term disability. While much of the physical brain damage occurs instantly – called the primary stage of injury – additional brain damage can result from the destructive chemical processes that arise in the body minutes to days to weeks following initial impact. Unlike the primary stage of injury, this secondary stage could potentially be prevented by targeting the molecules driving damage. I am a materials science engineer, and my colleagues and I are working to design treatments to neutralize the harm of secondary traumatic brain injury and reduce neurodegeneration. We designed a new material that could target and neutralize brain-damaging molecules in mice, improving their cognitive recovery and offering a potential new treatment for people. The primary stage of traumatic brain injury can severely damage and even destroy the blood-brain barrier – an interface protecting the brain by limiting what can enter it. Disruption of this barrier triggers damaged neurons or the immune system to release certain chemicals that result in destructive biochemical processes. One process called excitotoxicity occurs when too many calcium ions are allowed into neurons, activating enzymes that fragment DNA and damage cells, causing death. Another process, neuroinflammation, results from the activation of cells called microglia that can trigger inflammation in damaged areas of the brain. © 2010–2025, The Conversation US, Inc.

Keyword: Brain Injury/Concussion
Link ID: 29680 - Posted: 02.22.2025

By Bill Newsome What paper changed your life?: Activity of superior colliculus in behaving monkey. II. Effect of attention on neuronal responses. M.E. Goldberg and R.H. Wurtz Journal of Neurophysiology (1972) In 1972, Mickey Goldberg and Bob Wurtz published a quadrilogy of papers in the Journal of Neurophysiology—yes, you could do that in those days—on the physiological activity of single superior colliculus neurons in alert monkeys trained to perform simple eye fixation and eye movement tasks. The experiments revealed a rich variety of sensory and motor signals: Some neurons fired at the onset of a visual stimulus; others showed bursts of activity immediately prior to the eye movement. The researchers found that visually evoked activity differed depending on whether the monkey ultimately used the stimulus as a target for a saccadic eye movement. The neural response to the visual stimulus was stronger and continued until the time of the eye movement, forming a sort of temporal bridge between stimulus and evoked behavioral response. This bridge was alluring because it hinted at intermediate processes—perhaps the stuff of cognition—between sensory input and behavioral output. But it was also mysterious, in that no models existed for how such activity might be initiated and maintained until the behavioral response. These papers were revelatory to me because they pointed toward a mechanistic physiological understanding of such complex cognitive functions as attention. I was particularly fascinated by the second paper in the series of four, which dug into that mystery. Goldberg and Wurtz explicitly made a suggestive leap from physiology to psychology: “[Because] we can infer that the monkey attended to the stimulus when he made a saccade to it, the enhancement can be viewed as a neurophysiological event related to the psychological phenomenon of attention.” They also issued appropriate caveats, noting that “the unitary behavioral concept” of attention “may not have a single physiological mechanism.” h. © 2025 Simons Foundation

Keyword: Vision; Attention
Link ID: 29679 - Posted: 02.22.2025

Nell Greenfieldboyce Putting the uniquely human version of a certain gene into mice changed the way that those animals vocalized to each other, suggesting that this gene may play a role in speech and language. Mice make a lot of calls in the ultrasonic range that humans can't hear, and the high-frequency vocalizations made by the genetically altered mice were more complex and showed more variation than those made by normal mice, according to a new study in the journal Nature Communications. The fact that the genetic change produced differences in vocal behavior was "really exciting," says Erich Jarvis, a scientist at Rockefeller University in New York who worked on this research. Still, he cautioned, "I don't think that one gene is going to be responsible — poof! — and you've got spoken language." For years, scientists have been trying to find the different genes that may have been involved in the evolution of speech, as language is one of the key features that sets humans apart from the rest of the animal kingdom. "There are other genes implicated in language that have not been human-specific," says Robert Darnell, a neuroscientist and physician at Rockefeller University, noting that one gene called FOXP2 has been linked to speech disorders. He was interested in a different gene called NOVA1, which he has studied for over two decades. NOVA1 is active in the brain, where it produces a protein that can affect the activity of other genes. NOVA1 is found in living creatures from mammals to birds, but humans have a unique variant. Yoko Tajima, a postdoctoral associate in Darnell's lab, led an effort to put this variant into mice, to see what effect it would have. © 2025 npr

Keyword: Language; Genes & Behavior
Link ID: 29678 - Posted: 02.19.2025

By Moises Velasquez-Manoff When President Trump announced plans to impose tariffs on Mexico and Canada, one of his stated rationales was to force those countries to curb the flow of fentanyl into the United States. In fiscal year 2024, United States Customs and Border Protection seized nearly 22,000 pounds of pills, powders and other products containing fentanyl, down from 27,000 pounds in the previous fiscal year. More than 105,000 people died from overdoses, three-quarters of them from fentanyl and other opioids, in 2023. It doesn’t take much illicit fentanyl — said to be about 50 times as powerful as heroin and 100 times as powerful as morphine — to cause a fatal overdose. In my article for the magazine, I note that one of the many tragedies of the opioid epidemic is that a proven treatment for opioid addiction, a drug called buprenorphine, has been available in the United States for more than two decades yet has been drastically underprescribed. Tens of thousands of lives might have been saved if it had been more widely used earlier. In his actions and rhetoric, Trump seems to emphasize the reduction of supply as the answer to the fentanyl crisis. But Mexico’s president, Claudia Sheinbaum, has pointed to American demand as a driver of the problem. Indeed, if enough opioid users in the United States ended up receiving buprenorphine and other effective medication-based treatments, perhaps that demand for illicit opioids like fentanyl could be reduced. Devastating losses. Drug overdose deaths, largely caused by the synthetic opioid drug fentanyl, reached record highs in the United States in 2021. Here’s what you should know to keep your loved ones safe: Understand fentanyl’s effects. Fentanyl is a potent and fast-acting drug, two qualities that also make it highly addictive. A small quantity goes a long way, so it’s easy to suffer an overdose. With fentanyl, there is only a short window of time to intervene and save a person’s life during an overdose. Stick to licensed pharmacies. Prescription drugs sold online or by unlicensed dealers marketed as OxyContin, Vicodin and Xanax are often laced with fentanyl. Only take pills that were prescribed by your doctor and came from a licensed pharmacy. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29677 - Posted: 02.19.2025

By Laura Sanders Depression can affect not just the mind, but the body, too. Inner experiences of mental struggles are private. But in this episode, Jon Nelson and another volunteer, Amanda, let listeners in. Woven into their stories is a brief history of deep brain stimulation, the experimental treatment that involves permanent brain implants. You’ll hear how that research — with its ups and downs — carried the experiments to where they are today. Laura Sanders: This episode deals with mental illness, depression, and suicide. Please listen with care. Previously on The Deep End: Support Science Today. Barbara: He would be up in bed with the lights out or watching like endless hours of television and it was very unpredictable and then there’s a whole life going on downstairs. Jon: That isolation, there’s a little bit of lying involved because you just wanna get out of things, right? Mayberg: I think part of why this kind of treatment resistant depression is so painful and so associated with high rates of suicide, is that you’re suffering. You know exactly what you’re trying to get away from and you can’t move. And if you do move, it follows you. There’s no relief. Jon: I’d be the one standing up in front of everybody leading the champagne toast, and then I’d be driving home and wanting to slam my car into a tree. Sanders: Today we’re going to get into some heavy stuff, but there’s light at the end, I promise. We’re going to pull back the curtain on what depression can do to the body and to the brain. Maybe you know that feeling firsthand. If you don’t, you probably know somebody who does. You’ll also hear the backstory of some people who volunteered for the experiment and the backstory of the science itself. I’m Laura Sanders. Welcome to The Deep End. © Society for Science & the Public 2000–2025.

Keyword: Depression
Link ID: 29676 - Posted: 02.19.2025

Jon Hamilton People who inherit one very rare gene mutation are virtually guaranteed to develop Alzheimer's before they turn 50. Except for Doug Whitney. "I'm 75 years old, and I think I'm functioning fairly well," says Whitney, who lives near Seattle. "I'm still not showing any of the symptoms of Alzheimer's." Now a team of scientists is trying to understand how Whitney's brain has defied his genetic destiny. "If we are able to learn what is causing the protection here, then we could translate that to therapeutic approaches and apply that to the more common forms of the disease," says Dr. Jorge Llibre-Guerra, an assistant professor of neurology at Washington University School of Medicine in St. Louis. One possibility is high levels of heat shock proteins found in Whitney's brain, the team reports in the journal Nature Medicine. There are hints that these proteins can prevent the spread of a toxic protein that is one of the hallmarks of Alzheimer's, Llibre-Guerra says. A genetic surprise Early-onset Alzheimer's is everywhere in Whitney's family. His mother and 11 of her 13 siblings all had the disease by about age 50. "None of them lasted past 60," Whitney says. Whitney's wife, Ione, saw this up close. "We went home for Thanksgiving, and his mom couldn't remember the pumpkin pie recipe," she says. "A year later when we went back, she was already wandering off and not finding her way back home." © 2025 npr

Keyword: Alzheimers; Genes & Behavior
Link ID: 29675 - Posted: 02.19.2025

By Elie Dolgin For Kristian Cook, every pizza box he opened was another door closed on the path to overcoming obesity. “I had massive cravings for pizza,” he says. “That was my biggest downfall.” At 114 kilograms and juggling a daily regimen of medications for high cholesterol, hypertension and gout, the New Zealander resolved to take action. In late 2022, at the age of 46, Cook joined a clinical trial that set out to test a combination of the weight-loss drug semaglutide — better known by its brand names, Ozempic or Wegovy — and an experimental drug designed to preserve muscle while shedding fat. Muscle loss is a big concern for people on anti-obesity medications such as semaglutide. These ‘GLP-1 agonists’ mimic a natural gut hormone — glucagon-like peptide 1 — to suppress appetite and regulate metabolism. But reducing calories leads to an energy deficit, which the body often makes up for by burning muscle. The experimental drug that Cook received, called bimagrumab, seems to counteract this muscle loss. It’s one of more than 100 anti-obesity drug candidates that are in various stages of development. The next wave of medications, which are likely to hit pharmacy shelves in the next few years, resemble drugs that are already on the market. But close behind are numerous therapies being developed specifically for their muscle-sparing weight-loss potential. Dozens more are aimed at different biological pathways and could redefine obesity treatment in decades to come. “We’re working to create the next generation of healthy weight-loss solutions,” says Philip Larsen, who played a key part in the early development of GLP-1 drugs and is now chief executive of SixPeaks Bio, an obesity-focused start-up company in Basel, Switzerland. The surge in anti-obesity drug development has been made possible by the blockbuster success of semaglutide and its rival drug tirzepatide — sold as Zepbound or Mounjaro. These drugs have unlocked the potential for a global market that is projected to surpass US$100 billion by the end of the decade. © 2025 Springer Nature Limited

Keyword: Obesity
Link ID: 29674 - Posted: 02.15.2025

By Michael S. Rosenwald In early February, Vishvaa Rajakumar, a 20-year-old Indian college student, won the Memory League World Championship, an online competition pitting people against one another with challenges like memorizing the order of 80 random numbers faster than most people can tie a shoelace. The renowned neuroscientist Eleanor Maguire, who died in January, studied mental athletes like Mr. Rajakumar and found that many of them used the ancient Roman “method of loci,” a memorization trick also known as the “memory palace.” The technique takes several forms, but it generally involves visualizing a large house and assigning memories to rooms. Mentally walking through the house fires up the hippocampus, the seahorse-shaped engine of memory deep in the brain that consumed Dr. Maguire’s career. We asked Mr. Rajakumar about his strategies of memorization. His answers, lightly edited and condensed for clarity, are below. Q. How do you prepare for the Memory League World Championship? Hydration is very important because it helps your brain. When you memorize things, you usually sub-vocalize, and it helps to have a clear throat. Let’s say you’re reading a book. You’re not reading it out loud, but you are vocalizing within yourself. If you don’t drink a lot of water, your speed will be a bit low. If you drink a lot of water, it will be more and more clear and you can read it faster. Q. What does your memory palace look like? Let’s say my first location is my room where I sleep. My second location is the kitchen. And the third location is my hall. The fourth location is my veranda. Another location is my bathroom. Let’s say I am memorizing a list of words. Let’s say 10 words. What I do is, I take a pair of words, make a story out of them and place them in a location. And I take the next two words. I make a story out of them. I place them in the second location. The memory palace will help you to remember the sequence. © 2025 The New York Times Company

Keyword: Learning & Memory; Attention
Link ID: 29673 - Posted: 02.15.2025

By Angie Voyles Askham Identifying what a particular neuromodulator does in the brain—let alone how such molecules interact—has vexed researchers for decades. Dopamine agonists increase reward-seeking, whereas serotonin agonists decrease it, for example, suggesting that the two neuromodulators act in opposition. And yet, neurons in the brain’s limbic regions release both chemicals in response to a reward (and also to a punishment), albeit on different timescales, electrophysiological recordings have revealed, pointing to a complementary relationship. This dual response suggests that the interplay between dopamine and serotonin may be important for learning. But no tools existed to simultaneously manipulate the neuromodulators and test their respective roles in a particular area of the brain—at least, not until now—says Robert Malenka, professor of psychiatry and behavioral sciences at Stanford University. As it turns out, serotonin and dopamine join forces in the nucleus accumbens during reinforcement learning, according to a new study Malenka led, yet they act in opposition: dopamine as a gas pedal and serotonin as a brake on signaling that a stimulus is rewarding. The mice he and his colleagues studied learned faster and performed more reliably when the team optogenetically pressed on the animals’ dopamine “gas” as they simultaneously eased off the serotonin “brake.” “It adds a very rich and beguiling picture of the interaction between dopamine and serotonin,” says Peter Dayan, director of computational neuroscience at the Max Planck Institute for Biological Cybernetics. In 2002, Dayan proposed a different framework for how dopamine and serotonin might work in opposition, but he was not involved in the new study. The new work “partially recapitulates” that 2002 proposal, Dayan adds, “but also poses many more questions.” © 2025 Simons Foundation

Keyword: Learning & Memory
Link ID: 29672 - Posted: 02.15.2025

By Michael S. Rosenwald Eleanor Maguire, a cognitive neuroscientist whose research on the human hippocampus — especially those belonging to London taxi drivers — transformed the understanding of memory, revealing that a key structure in the brain can be strengthened like a muscle, died on Jan. 4 in London. She was 54. Her death, at a hospice facility, was confirmed by Cathy Price, her colleague at the U.C.L. Queen Square Institute of Neurology. Dr. Maguire was diagnosed with spinal cancer in 2022 and had recently developed pneumonia. Working for 30 years in a small, tight-knit lab, Dr. Maguire obsessed over the hippocampus — a seahorse-shaped engine of memory deep in the brain — like a meticulous, relentless detective trying to solve a cold case. An early pioneer of using functional magnetic resonance imaging (f.M.R.I.) on living subjects, Dr. Maguire was able to look inside human brains as they processed information. Her studies revealed that the hippocampus can grow, and that memory is not a replay of the past but rather an active reconstructive process that shapes how people imagine the future. “She was absolutely one of the leading researchers of her generation in the world on memory,” Chris Frith, an emeritus professor of neuropsychology at University College London, said in an interview. “She changed our understanding of memory, and I think she also gave us important new ways of studying it.” In 1995, while she was a postdoctoral fellow in Dr. Frith’s lab, she was watching television one evening when she stumbled on “The Knowledge,” a quirky film about prospective London taxi drivers memorizing the city’s 25,000 streets to prepare for a three-year-long series of licensing tests. Dr. Maguire, who said she rarely drove because she feared never arriving at her destination, was mesmerized. “I am absolutely appalling at finding my way around,” she once told The Daily Telegraph. “I wondered, ‘How are some people so bloody good and I am so terrible?’” In the first of a series of studies, Dr. Maguire and her colleagues scanned the brains of taxi drivers while quizzing them about the shortest routes between various destinations in London. © 2025 The New York Times Company

Keyword: Learning & Memory
Link ID: 29671 - Posted: 02.15.2025

By Georgia E. Hodes Psychiatric conditions have long been regarded as issues of “mental health,” a term that inherently ties our understanding of these disorders to the brain. But the brain does not exist in a vacuum. Growing evidence over the past 10 years highlights a link between the body and what we think of as mental health. Many studies, for example, report that the peripheral immune system is altered in people who experience neurological and psychiatric conditions, including mood disorders, anxiety and schizophrenia. Researchers traditionally assumed that peripheral inflammation was a downstream effect of these conditions, but basic research is now revealing that the immune system, the gut microbiome and peripheral inflammation are not just bystanders or results of psychiatric conditions—they are active participants and may hold the key to new treatments. Scientists are beginning to uncover the mechanisms by which the body influences the brain, challenging the notion that mental health is solely a matter of brain chemistry and reshaping ideas on the etiology of psychiatric disorders. Like other neuroscience groups, we started our work in this area with the “brain-first” perspective: the idea that immune changes in the brain trigger stress-induced changes in behavior and peripheral inflammation. Our earliest studies supported this idea, demonstrating that directly infusing an inflammatory molecule, the cytokine interleukin 6 (IL6), into an area of the brain associated with reward behavior made male mice more likely to avoid others. Our later work, however, found that the source of IL6 in the brain is actually peripheral immune cells. Either stopping the immune cells from producing this molecule or just blocking it from entering the brain made the animals resilient to social stress. These studies offered some of the first evidence that treating the body with a compound that does not cross the blood brain-barrier could prevent a brain-mediated behavior. Before this, blood markers were considered only indirect indicators of brain changes—and not direct mediators or potential targets for treatment. © 2025 Simons Foundation

Keyword: Depression; Stress
Link ID: 29670 - Posted: 02.12.2025

By Max Kozlov A sliver of human brain in a small vial starts to melt as lye is added to it. Over the next few days, the caustic chemical will break down the neurons and blood vessels within, leaving behind a grisly slurry containing thousands of tiny plastic particles. Toxicologist Matthew Campen has been using this method to isolate and track the microplastics — and their smaller counterparts, nanoplastics — found in human kidneys, livers and especially brains. Campen, who is at the University of New Mexico in Albuquerque, estimates that he can isolate about 10 grams of plastics from a donated human brain; that’s about the weight of an unused crayon. Microplastics have been found just about everywhere that scientists have looked: on remote islands, in fresh snow in Antarctica, at the bottom of the Mariana Trench in the western Pacific, in food, in water and in the air that we breathe. And scientists such as Campen are finding them spread throughout the human body. Detection is only the first step, however. Determining precisely what these plastics are doing inside people and whether they’re harmful has been much harder. That’s because there’s no one ‘microplastic’. They come in a wide variety of sizes, shapes and chemical compositions, each of which could affect cells and tissues differently. This is where Campen’s beige sludge comes into play. Despite microplastics’ ubiquity, it’s difficult to determine which microplastics people are exposed to, how they’re exposed and which particles make their way into the nooks and crannies of the body. The samples that Campen collects from cadavers can, in turn, be used to test how living tissues respond to the kinds of plastic that people carry around with them. “Morbidly speaking, the best source I can think of to get good, relevant microplastics is to take an entire human brain and digest it,” says Campen. © 2025 Springer Nature Limited

Keyword: Neurotoxins; Robotics
Link ID: 29669 - Posted: 02.12.2025

By Laura Sanders Meet Jon Nelson. He’s a dad, a husband, a coach and a professional who works in marketing. But underneath it all, he suffered – for years – from severe depression. His suffering was so great that he volunteered for an experimental treatment called deep brain stimulation, in which electrodes are permanently implanted in his brain. In this episode, you’ll hear from Jon about his life before the surgery, and you’ll be introduced to the neuroscience designed to save him. Laura Sanders: This podcast touches on mental illness, depression, and suicide. There are moments of darkness. There are moments of lightness, too. Please keep that in mind before you listen. Jon Nelson is a guy who’s probably a lot like a guy you know. He lives in Newtown, a picturesque small town northeast of Philadelphia. He has three kids, a loving wife, a dog, a cat, and a bearded dragon named Lizzie. He works in marketing. He coaches his kids in softball and hockey, and he’s a ride-or-die Steelers fan. The Nelsons are, in fact, so perfect that they’re almost a caricature, like a sitcom family with a zany dad who’s fond of the phrase, “I’m going to give you some life advice.” Jon Nelson: You know, we try to do the standard sit down and cook together and have meals together. We’re the messy house in the neighborhood with basketballs outside and, you know, we’re constantly playing and doing stuff like that. But, you know, truly we like to spend time together. Sanders: But the view from the outside was a lot different than what Jon felt on the inside. On the outside, Jon lived a charmed life, but inside, he had been fighting with everything he had to stay alive for years. Jon: I would literally read a newspaper article about a plane wreck and I would have instantaneous, like, “Oh, like why couldn’t I have been on that?” Right? Or, you know, you, somebody died in a car wreck, like, “Why couldn’t that have been me?” © Society for Science & the Public 2000–2025

Keyword: Depression
Link ID: 29668 - Posted: 02.12.2025

By Sara Reardon A man who seemed genetically destined to develop Alzheimer’s disease while still young has reached his mid-70s without any cognitive decline — in only the third recorded case of such resistance to the disease. The findings, published today in Nature Medicine1, raise questions about the role of the proteins that ravage the brain during the disease and the drugs that target them. Since 2011, a study called the Dominantly Inherited Alzheimer Network (DIAN) has been following a family in which many members have a mutation in a gene called PSEN2. The mutation causes the brain to produce versions of the amyloid protein that are prone to clumping into the sticky plaques thought to drive neurodegeneration. Family members with the mutation invariably develop Alzheimer’s at around age 50. Then, a 61-year-old man from this family showed up at the DIAN study’s clinic with full cognitive function, and the researchers were shocked to discover that he had the fateful PSEN2 mutation. The man’s mother had had the same mutation, as had 11 of her 13 siblings; all had developed dementia around age 50. The researchers were even more shocked when scans revealed that his brain looked like that of someone with Alzheimer’s. “His brain was full of amyloid,” says behavioural neurologist and study co-author Jorge Llibre-Guerra at Washington University in St. Louis, Missouri. What the man’s brain didn’t contain, however, were clusters of tau — another protein that forms tangled threads inside neurons. Positron emission tomography (PET) scans revealed that he had a small amount of abnormal tau and that it was only in the occipital lobe, a brain region involved in visual perception that is not usually affected in Alzheimer’s disease. © 2025 Springer Nature Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 29667 - Posted: 02.12.2025

By Jason Bittel Elaborate poses, tufts of feathers, flamboyant shuffles along an immaculate forest floor — male birds-of-paradise have many ways to woo a potential mate. But now, by examining prepared specimens at the American Museum of Natural History in New York, scientists have discovered what could be yet another tool in the kit of the tropical birds — a visual effect known as photoluminescence. Sometimes called biofluorescence in living things, this phenomenon occurs when an object absorbs high-energy wavelengths of light and re-emits them as lower energy wavelengths. Biofluorescence has already been found in various species of fishes, amphibians and even mammals, from bats to wombats. Interestingly, birds remain woefully understudied when it comes to the optical extras. Until now, no one had looked for the glowing property in birds-of-paradise, which are native to Australia, Indonesia and New Guinea and are famous for their elaborate mating displays. In a study published on Tuesday in the journal Royal Society Open Science, researchers examined prepared specimens housed at the American Museum of Natural History and found evidence of biofluorescence in 37 of 45 birds-of-paradise species. “What they’re doing is taking this UV color, which they can’t see, and re-emitting it at a wavelength that is actually visible to their eyes,” said Rene Martin, the lead author of the study and a biologist at the University of Nebraska-Lincoln. “In their case, it’s kind of a bright green and green-yellow color.” In short, biofluorescence supercharges a bright color to make it even brighter. © 2025 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 29666 - Posted: 02.12.2025

By Laura Sanders Ancient ear-wiggling muscles kick on when people strain to hear. That auricular activity, described January 30 in Frontiers in Neuroscience, probably doesn’t do much, if anything. But these small muscles are at least present, and more active than anyone knew. You’ve probably seen a cat or dog swing their ears toward a sound, like satellite dishes orienting to a signal. We can’t move our relatively rigid human ears this dramatically. And yet, humans still possess ear-moving muscles, as those of us who can wiggle our ears on demand know. Neuroscientist Andreas Schröer and colleagues asked 20 people with normal hearing to listen to a recorded voice while distracting podcasts played in the background. All the while, electrodes around the ears recorded muscle activity. An ear muscle called the superior auricular muscle, which sits just above the ear and lifts it up, fired up when the listening conditions were difficult, the researchers found. Millions of years ago, these muscles may have helped human ancestors collect sounds. Today, it’s doubtful that this tiny wisp of muscle activity helps a person hear better, though scientists haven’t tested that. “It does its best, but it probably doesn’t work,” says Schröer, of Saarland University in Saarbrücken, Germany. These vestigial muscles may not help us hear, but their activity could provide a measurement of a person’s hearing efforts. That information may be useful to hearing aid technology, telling the device to change its behavior when a person is struggling, for instance. © Society for Science & the Public 2000–2025.

Keyword: Hearing; Evolution
Link ID: 29665 - Posted: 02.12.2025