By Nazeefa Ahmed Humans prefer fruit at its sweetest, whereas many birds happily snack on the sourest of the bunch, from zesty lemons to unripe honey mangoes. Researchers may now know why. A study published today in Science suggests birds have evolved a specialized taste receptor that’s suppressed by high acidity, which effectively dulls the sharp, sour taste of fruits they eat. The finding reveals the evolutionary history of the pucker-inducing diets of many fruit-eating birds around the world—and may also help explain birds’ knack for survival, by broadening their potential food sources. The study is a “robust” addition to our understanding of how birds taste sour foods, which is still a research area in its infancy, says Leanne Grieves, an ornithologist at Cornell University’s Lab of Ornithology. Scientists identified a sour taste receptor in vertebrates—known as OTOP1—only 7 years ago, and few studies focus on why birds eat what they eat, rather than simply what they eat. Grieves, who studies birds’ sense of smell but who was not involved with the current work, adds that the new study “provides a really nice starting point.” To examine how birds approach sour-tasting foods, scientists exposed OTOP1 receptors from mice, domestic pigeons, and canaries to various acidic solutions. The activity of the mouse version of the receptor increased with greater acidity—meaning more acidic foods register to mice, and other mammals like us, as increasingly sour. However, the pigeon and canary versions of OTOP1 became less active in solutions about as acidic as a lemon. As a result, the birds wouldn’t perceive as much of a sour taste, allowing them to take advantage of the fruits mammals can’t stomach. Determining why bird OTOP1 reacted differently was a challenge, according to study author Hao Zhang, an evolutionary biologist at the Chinese Academy of Sciences (CAS). So, the researchers mutated sections of the gene that encodes the OTOP1 receptor, which let them identify four candidate amino acids within the protein that are responsible for sour tolerance. One of them, known as G378, is found almost exclusively in songbirds such as the canary—a species that showed greater sour tolerance than the pigeon, which lacks this variance. “A single amino acid in the bird OTOP1 can increase sour tolerance,” says study author Lei Luo, a biologist at CAS. © 2025 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 29840 - Posted: 06.21.2025

James Doubek Researchers have some new evidence about what makes birds make so much noise early in the morning, and it's not for some of the reasons they previously thought. For decades, a dominant theory about why birds sing at dawn — called the "dawn chorus" — has been that they can be heard farther and more clearly at that time. Sound travels faster in humid air and it's more humid early in the morning. It's less windy, too, which is thought to lessen any distortion of their vocalizations. But scientists from the Cornell Lab of Ornithology's K. Lisa Yang Center for Conservation Bioacoustics and Project Dhvani in India combed through audio recordings of birds in the rainforest. They say they didn't find evidence to back up this "acoustic transmission hypothesis." It was among the hypotheses involving environmental factors. Another is that birds spend their time singing at dawn because there's low light and it's a bad time to look for food. "We basically didn't find much support for some of these environmental cues which have been purported in literature as hypotheses" for why birds sing more at dawn, says Vijay Ramesh, a postdoctoral research associate at Cornell and the study's lead author. The study, called "Why is the early bird early? An evaluation of hypotheses for avian dawn-biased vocal activity," was published this month in the peer-reviewed journal Philosophical Transactions of the Royal Society B. The researchers didn't definitively point to one reason for why the dawn chorus is happening, but they found support for ideas that the early morning racket relates to birds marking their territory after being inactive at night, and communicating about finding food. © 2025 npr

Keyword: Animal Communication; Evolution
Link ID: 29839 - Posted: 06.21.2025

By Michael A. Yassa For nearly three decades, Alzheimer’s disease has been framed as a story about amyloid: A toxic protein builds up, forms plaques, kills neurons and slowly robs people of their memories and identity. The simplicity of this “amyloid cascade hypothesis” gave us targets, tools and a sense of purpose. It felt like a clean story. Almost too clean. We spent decades chasing it, developing dozens of animal models and pouring billions into anti-amyloid therapies, most of which failed. The few that made it to market offer only modest benefits, often with serious side effects. Whenever I think about this, I can’t help but picture Will Ferrell’s Buddy the Elf, in the movie “Elf,” confronting the mall Santa: “You sit on a throne of lies.” Not because anyone meant to mislead people (though maybe some did). But because we wanted so badly for the story to be true. So what happened? This should have worked … right? I would argue it was never going to work because we have been thinking about Alzheimer’s the wrong way. For decades, we have treated it as a single disease with a single straight line from amyloid to dementia. But what if that’s not how it works? What if Alzheimer’s only looks like one disease because we keep trying to force it into a single narrative? If that’s the case, then the search for a single cause—and a single cure—was always destined to fail. ”What if Alzheimer’s only looks like one disease because we keep trying to force it into a single narrative? If that’s the case, then the search for a single cause—and a single cure—was always destined to fail. Real progress, I believe, requires two major shifts in how we think. First, we have to let go of our obsession with amyloid. © 2025 Simons Foundation

Keyword: Alzheimers
Link ID: 29835 - Posted: 06.18.2025

Associated Press Prairie dogs bark to alert each other to the presence of predators, with different cries depending on whether the threat is airborne or approaching by land. But their warnings also seem to help a vulnerable grassland bird. Curlews have figured out that if they eavesdrop on alarms from US prairie dog colonies they may get a jump on predators coming for them, too, according to research published on Thursday in the journal Animal Behavior. “Prairie dogs are on the menu for just about every predator you can think of – golden eagles, red-tailed hawks, foxes, badgers, even large snakes,” said Andy Boyce, a research ecologist in Montana at the Smithsonian’s National Zoo and Conservation Biology Institute. Such animals also gladly snack on grassland nesting birds such as the long-billed curlew, so the birds have adapted. Previous research has shown birds frequently eavesdrop on other bird species to glean information about food sources or danger, said Georgetown University ornithologist Emily Williams, who was not involved in the study. But, so far, scientists have documented only a few instances of birds eavesdropping on mammals. “That doesn’t necessarily mean it’s rare in the wild,” she said, “it just means we haven’t studied it yet.” Prairie dogs, a type of ground squirrel, live in large colonies with a series of burrows that may stretch for miles underground, especially on the vast US plains. When they hear each other’s barks, they either stand alert watching or dive into their burrows. “Those little barks are very loud; they can carry quite a long way,” said research co-author Andrew Dreelin, who also works for the Smithsonian. © 2025 Guardian News & Media Limited

Keyword: Animal Communication; Language
Link ID: 29832 - Posted: 06.18.2025

By Sofia Quaglia When octopuses extend their eight arms into hidden nooks and crannies in search of a meal, they are not just feeling around in the dark for their food. They are tasting their prey, and with even more sensory sophistication than scientists had already imagined. Researchers reported on Tuesday in the journal Cell that octopus arms are fine-tuned to “eavesdrop into the microbial world,” detecting microbiomes on the surfaces around them and deriving information from them, said Rebecka Sepela, a molecular biologist at Harvard and an author of the new study. Where octopus eyes cannot see, their arms can go to identify prey and make sense of their surroundings. Scientists knew that those eight arms (not tentacles) sense whether their eggs are healthy or need to be pruned. And the hundreds of suckers on each arm have over 10,000 chemotactile sensory receptors each, working with 500 million neurons to pick up that information and relay it throughout the nervous system. Yet, what exactly the octopus is tasting by probing and prodding — and how its arms can distinguish, say, a rock from an egg, a healthy egg in its clutch from a sick one or a crab that’s safe to eat from a rotting, toxic one — has long baffled scientists. What about the surfaces are they perceiving? For Dr. Sepela, this question was heightened when her team discovered 26 receptors along the octopuses’ arms that didn’t have a known function. She supposed those receptors were tuned only to molecules found on surfaces, rather than those diffused in water. So she and her colleagues collected swaths of molecules coating healthy and unhealthy crabs and octopus eggs. They grew and cultured the microbes from those surfaces in the lab, then tested 300 microbial strains, one by one, on two of those 26 receptors. During the screening, only particular microbes could switch open the receptors, and these microbes were more abundant on the decaying crabs and dying eggs than on their healthy counterparts. © 2025 The New York Times Company

Keyword: Chemical Senses (Smell & Taste); Neuroimmunology
Link ID: 29831 - Posted: 06.18.2025

By Tina Hesman Saey People trying to lose weight often count calories, carbs, steps and reps and watch the scales. Soon, they may have another number to consider: a genetic score indicating how many calories a person needs to feel full during a meal. This score may help predict whether someone will lose more weight on the drugs liraglutide or phentermine-topiramate, researchers report June 6 in Cell Metabolism. A separate study, posted to medRXiv.org in November, suggests that individuals with a higher genetic propensity for obesity benefit less from semaglutide compared to those with a lower genetic predisposition. Such genetic tests may one day help doctors and patients select personalized weight-loss treatments, some researchers say. But the genetic scores “are not perfect predictors of drug response,” says Paul Franks, a genetic epidemiologist at Queen Mary University of London who was not involved in either study. “They show a tendency.” For the Cell Metabolism study, Mayo Clinic researchers measured how many calories it took for about 700 adults with obesity to feel full when given an all-you-can-eat meal of lasagna, pudding and milk. The calorie intake varied widely, ranging from about 140 to 2,200 calories, with men generally needing more than women. The team used machine learning to compile a genetic score based on variants of 10 genes associated with obesity. That score is designed to reflect the calories people required to feel full. Then, the Mayo team and colleagues from Phenomix Sciences Inc, headquartered in Menlo Park, Calif., conducted two clinical trials. In one 16-week trial, people with obesity received either a placebo or liraglutide­ — a GLP-1 drug branded as Saxenda. GLP-1s are a class of diabetes drugs that have shown promise with weight loss. People with a lower genetic score lost more weight on liraglutide than those with higher genetic scores. © Society for Science & the Public 2000–2025.

Keyword: Obesity; Genes & Behavior
Link ID: 29830 - Posted: 06.14.2025

Elie Dolgin Sheree had maintained a healthy weight for 15 years, thanks to a surgery that wrapped a silicone ring around the top of her stomach. But when the gastric band repeatedly slipped and had to be removed, the weight came back — fast. She gained nearly 20 kilograms in just 2 months. Frustrated, she turned to the latest generation of anti-obesity medications, hoping to slow the rapid weight gain. She cycled through various formulations of the blockbuster therapies semaglutide (sold under the brand names Ozempic and Wegovy) and tirzepatide (sold as Zepbound for weight loss), finding some success with higher doses of these drugs, which mimic the effects of the appetite-suppressing hormone GLP-1. But each time, drug shortages disrupted her treatment, forcing her to start again with a new formulation or to go without the drugs for weeks. Tired of the uncertainty around the therapies, she decided to try something different. Sheree, who asked that her middle name be used to protect her privacy, underwent two minimally invasive procedures designed to reduce the size of her stomach and to blunt hunger cues. Developed over the past two decades, these ‘endoscopic’ procedures — performed using flexible tubes inserted through the mouth, and no scalpels — are just one part of a growing toolkit to help people who want to move away from GLP-1 therapy. More-conventional bariatric surgeries, used routinely since the 1980s to reroute the flow of food through the gut or to restrict the stomach’s size, might also gain wider appeal. And the search is picking up for other drugs that could offer lasting alternatives for a post-GLP-1 population. That momentum is driven by a convergence of factors: chronic shortages of GLP-1 therapies, high costs, insurance barriers and debilitating side effects. As a result, many people who start the drugs ultimately stop — with discontinuation rates in clinical trials ranging from 37% to 81% in the first year1. And once treatment ends, the weight lost often piles back on. © 2025 Springer Nature Limited

Keyword: Obesity
Link ID: 29829 - Posted: 06.14.2025

By Marta Hill Every year, black-capped chickadees perform an impressive game of hide-and-seek. These highly visual birds cache tens of thousands of surplus food morsels and then recover them during leaner times. Place cells in the hippocampus may help the birds keep track of their hidden bounty, according to a study published 11 June in Nature. The cells activate not only when a bird visits a food stash but also when it looks at the stash from far away, the study shows. “What is really profound about the work is it’s trying to unpack how it is that we’re able to combine visual information, which is based on where we currently are in the world, with our understanding of the space around us and how we can navigate it,” says Nick Turk-Browne, professor of psychology and director of the Wu Tsai Institute at Yale University, who was not involved in the study. With each gaze shift, the hippocampus first predicts what the bird is about to see and then reacts to what it actually sees, the study shows. “It really fits beautifully into this picture of this dual role for the system in representing actual and representing possible,” says Loren Frank, professor of physiology and psychiatry at the University of California, San Francisco, who was not involved in the work. The findings help explain how the various functions of the hippocampus—navigation, perception, learning and memory—work together, Turk-Browne adds. “If we can have a smart, abstract representation of place that doesn’t depend on actually physically being there, then you can imagine how this can be used to construct memories.” © 2025 Simons Foundation

Keyword: Learning & Memory
Link ID: 29827 - Posted: 06.14.2025

By Ellen Barry Thirty-six hours after dropping his date off at her apartment, Bradley Goldman was on a video call with his dating coach, breaking down the events of the evening. Listen to this article with reporter commentary For one thing, he told the coach, he had chosen the wrong venue for someone on the autism spectrum — a bar of the Sunset Strip hipster variety, so loud and overstimulating that he could almost feel himself beginning to dissociate. Mr. Goldman, a tall, rangy 42-year-old who works as an office manager, hadn’t decided in advance of the date whether to mention that he had been diagnosed with autism, or that he was working with a coach. So he deflected, and they found themselves, briefly, in a conversational blind alley. “I struggle with how to disclose,” he said. “Do I say I am ‘neuro-spicy’? Or ‘neurodiverse’? Or do I disclose at all?” His coach, Disa Jean-Pierre, was sympathetic. “You could just wait for it to come up naturally after a few dates,” she suggested. Mr. Goldman thought this over. “I’m still figuring this out,” he said. Nevertheless, it was a solidly enjoyable date, something he credited to the coaching he had received from a team of psychologists at the Semel Institute for Neuroscience and Human Behavior at the University of California, Los Angeles. He had avoided “info dumping” or making too many Jeffrey Dahmer jokes, and he had carefully observed his date’s body language to detect whether she was signaling openness to a good night kiss. (She was.) “She was like, ‘I really want you to let me know you got home,’” he said. “So, that © 2025 The New York Times Company

Keyword: Autism
Link ID: 29826 - Posted: 06.14.2025

By Andrew Jacobs and Jacey Fortin News reports detailing Elon Musk’s drug use have prompted renewed attention to ketamine, a powerful anesthetic that has become increasingly popular as a therapy for treatment-resistant depression and other mental health issues. Although Mr. Musk has acknowledged using ketamine in the past to treat depression, he has denied suggestions that he is currently using ketamine — or any other drug. “I am NOT taking drugs!” he wrote last week in a social media post following the publication of an article in The New York Times that described reports of his use of drugs on the campaign trail last year. Those drugs included ketamine and other psychedelic compounds, among them MDMA and psilocybin mushrooms. Mr. Musk left the White House last week. Since then, he and President Trump have traded barbs on social media over the president’s domestic policy bill and have mentioned government contracts with Mr. Musk’s companies and Mr. Musk’s relationship to the White House. Mr. Trump, who was briefed on the article in The Times, has been telling associates in the last day or so that Musk’s “crazy” behavior is linked to his drug use, according to a Times report citing two people with knowledge of Mr. Trump’s private conversations. But later on Friday, Mr. Trump told reporters he did not want to comment on Mr. Musk’s drug use. The very public feud between the two men has once again drawn unflattering attention to ketamine, a drug that has become increasingly available at legal clinics across the country. It is also used recreationally and can be dangerous when misused. What is ketamine, and is it legal? Ketamine is an injectable, short-acting dissociative anesthetic that can have hallucinogenic effects at certain doses. It distorts perceptions of sight and sound and makes users feel detached from pain and their surroundings. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29824 - Posted: 06.07.2025

By Calli McMurray The hunt for a soulmate can be hard work—particularly for naive neurons. During development, the cells’ axons snake through burgeoning brain areas in search of the perfect dendrite to form a synapse with. Cell surface proteins serve as molecular identification tags to help axons distinguish “Mr. Wrong” dendrite from “Mr. Right,” according to the chemoaffinity hypothesis. But there are too many cells and too few cell surface proteins for this to be the only strategy, says Claude Desplan, professor of biology and neural science at New York University. “There is no way you can find your partner in a big mess of many different thousands of types of neurons. So you do need to reduce the issue.” In this brain region, 50 types of olfactory receptor neurons link up with 50 types of neurons that project to a sensory integration hub called the mushroom body; each synapse type bunches together inside the lobe to form its own distinct glomerulus. The axons of olfactory receptor neurons do not search the entire structure for their postsynaptic partner. Instead, the projection neurons inside the lobe send their dendrites to meet axons traveling along the surface. Once the two join up, they descend to their proper place in the lobe, imaging experiments show. “Axons don’t need to delve deep. They only need to survey the surface in order to find their target,” says the study’s principal investigator, Liqun Luo, professor of biology at Stanford University. To make matters even simpler, the axons stick to a narrow, genetically determined trajectory, Luo says. Cortical regions may achieve a similar simplification through columns and layers: Axons travel to a certain brain region and then plunge to a particular depth, Luo suggests. Genetically altering these trajectories precludes the olfactory receptor neurons from finding their proper mate, additional experiments show. Dendrites from the postsynaptic cell still wait for their partner at the surface, but “they will be sitting there waiting forever,” Luo says. Some cells “are still sticking their dendrites out” in adulthood, and in at least one case the team observed, a cell eventually matched with another partner. © 2025 Simons Foundation

Keyword: Development of the Brain
Link ID: 29823 - Posted: 06.07.2025

David Farrier Charles Darwin suggested that humans learned to speak by mimicking birdsong: our ancestors’ first words may have been a kind of interspecies exchange. Perhaps it won’t be long before we join the conversation once again. The race to translate what animals are saying is heating up, with riches as well as a place in history at stake. The Jeremy Coller Foundation has promised $10m to whichever researchers can crack the code. This is a race fuelled by generative AI; large language models can sort through millions of recorded animal vocalisations to find their hidden grammars. Most projects focus on cetaceans because, like us, they learn through vocal imitation and, also like us, they communicate via complex arrangements of sound that appear to have structure and hierarchy. Sperm whales communicate in codas – rapid sequences of clicks, each as brief as 1,000th of a second. Project Ceti (the Cetacean Translation Initiative) is using AI to analyse codas in order to reveal the mysteries of sperm whale speech. There is evidence the animals take turns, use specific clicks to refer to one another, and even have distinct dialects. Ceti has already isolated a click that may be a form of punctuation, and they hope to speak whaleish as soon as 2026. The linguistic barrier between species is already looking porous. Last month, Google released DolphinGemma, an AI program to translate dolphins, trained on 40 years of data. In 2013, scientists using an AI algorithm to sort dolphin communication identified a new click in the animals’ interactions with one another, which they recognised as a sound they had previously trained the pod to associate with sargassum seaweed – the first recorded instance of a word passing from one species into another’s native vocabulary. The prospect of speaking dolphin or whale is irresistible. And it seems that they are just as enthusiastic. In November last year, scientists in Alaska recorded an acoustic “conversation” with a humpback whale called Twain, in which they exchanged a call-and-response form known as “whup/throp” with the animal over a 20-minute period. In Florida, a dolphin named Zeus was found to have learned to mimic the vowel sounds, A, E, O, and U. © 2025 Guardian News & Media Limited

Keyword: Language; Evolution
Link ID: 29821 - Posted: 06.04.2025

By Lina Zeldovich When Catherine Lord was a psychology student a half century ago, she took part in a pioneering effort to move kids with autism from psychiatric institutions into the community. Lord was inspired by positive changes in the kids and devoted her life to developing therapies for people with autism and understanding the biology of the condition. Today, Lord is a professor of psychiatry at the University of California, Los Angeles, and renowned worldwide for developing tools to diagnose autism, which have become clinical standards, and for her efforts to improve the lives of people with autism and their families. Along with her research, Lord maintains a clinical practice where she works with people with autism, from toddlers to adults. So I couldn’t think of a better scientist to address the views of autism espoused by Robert F. Kennedy, Jr. Since being appointed as the United States Secretary of Health and Human Services, Kennedy has continued to spread misinformation about the condition, a pattern that began two decades ago when he claimed childhood vaccines cause autism, a charge long ago proven to be false. Earlier this year, Kennedy announced the National Institutes of Health would launch a new study to investigate the causes of autism. To conduct its study, he said, the NIH would gather medical records of Americans with autism from federal and commercial databases. In conversation, Lord spoke with authority and concern as she pointed out the mendacity and danger of Kennedy’s comments, and clarified the state of autism research and science. He has made a variety of statements about autism that suggests he doesn’t really know what he’s talking about. © 2025 NautilusNext Inc.,

Keyword: Autism
Link ID: 29818 - Posted: 06.04.2025

By Lauren Schenkman Addiction may be known as a disease of “more,” but drug-taking also taps a powerful drive for less that can suppress reward in the brain, even at low doses, according to a new study of nicotine responses in mice. The results suggest that the systems of reward and aversion that regulate addiction are more intertwined than previously thought. “That’s absolutely fascinating, because the field has been dominated by this notion of the go, the drive to get drug, but the drive is moderated by the stop,” says Paul Kenny, professor of neuroscience at the Icahn School of Medicine at Mount Sinai, who was not involved in the work. A faulty “stop” signal could be one of the culprits in addiction, he adds. Recent studies have begun to explore this stop signal. Intravenous nicotine activates nicotinic acetylcholine receptors on dopamine neurons in the midbrain’s ventral tegmental area (VTA), generating a rewarding effect that promotes more drug consumption. And high doses activate a tiny adjacent area, the interpeduncular nucleus (IPN), which drives aversion, previous studies have suggested. But doses too low to excite the VTA also activate the IPN in mice, the new work shows. In another experiment, the team used fluorescent proteins to find where axons from the IPN terminate and to identify the intermediate player connecting the IPN and the VTA: the laterodorsal tegmental nucleus (LDTg). The findings were published in Neuron in April. “This was very thrilling,” says the study’s principal investigator, Alexandre Mourot, research director in brain plasticity at the Institut National de la Santé et de la Recherche Médicale (INSERM). It suggests that at very low doses, the VTA does not respond because the IPN “erases the rewarding properties of the drug,” he says. © 2025 Simons Foundation

Keyword: Drug Abuse
Link ID: 29817 - Posted: 06.04.2025

By Abby Ellin Sally Odenheimer starved herself because she was an athlete and thought she’d run faster on an empty stomach. Karla Wagner starved herself because she wanted to be in charge of at least one aspect of her life. Janice Bremis simply felt too fat. They all sought perfection and control. Not eating helped. They are women in their 60s and 70s who have struggled with anorexia nervosa since childhood or adolescence. Years later, their lives are still governed by calories consumed, miles run, laps swum, pounds lost. “It’s an addiction I can’t get rid of,” said Ms. Odenheimer, 73, a retired teacher who lives outside Denver. For decades, few people connected eating disorders with older people; they were seen as an affliction of teenage girls and young women. But research suggests that an increasing number of older women have been seeking treatment for eating disorders, including bulimia, binge eating disorder (known as BED) and anorexia, which has the highest mortality rate of any psychiatric disorder, and brings with it an elevated risk of suicide. In a 2017 paper in the journal BMC Medicine, researchers reported that more than 15 percent of 5,658 women surveyed met the criteria for a lifetime eating disorder while in their 30s and 40s. A 2023 review of recent research reported that the prevalence rates among women 40 and older with full diagnoses of eating disorders were between 2.1 and 7.7 percent. (For men, they were less than 1 percent.) © 2025 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 29816 - Posted: 06.04.2025

Jon Hamilton Joe Walsh, 79, is waiting to inhale. He's perched on a tan recliner at the Center for Alzheimer Research and Treatment at Brigham and Women's Hospital in Boston. His wife, Karen Walsh, hovers over him, ready to depress the plunger on a nasal spray applicator. "One, two, three," a nurse counts. The plunger plunges, Walsh sniffs, and it's done. The nasal spray contains an experimental monoclonal antibody meant to reduce the Alzheimer's-related inflammation in Walsh's brain. He is the first person living with Alzheimer's to get the treatment, which is also being tested in people with diseases including multiple sclerosis, ALS and COVID-19. Sponsor Message Health A man genetically destined to develop Alzheimer's isn't showing any symptoms And the drug appears to be reducing the inflammation in Walsh's brain, researchers report in the journal Clinical Nuclear Medicine. "I think this is something special," says Dr. Howard Weiner, a neurologist at Mass General Brigham who helped develop the nasal spray, along with its maker, Tiziana Life Sciences. Whether a decrease in inflammation will bring improvements in Walsh's thinking and memory, however, remains unclear. The experimental treatment is part of a larger effort to find new ways to interrupt the cascade of events in the brain that lead to Alzheimer's dementia. Two drugs now on the market clear the brain of sticky amyloid plaques, clumps of toxic protein that accumulate between neurons. Other experimental drugs have targeted the tau tangles, a different protein that builds up inside nerve cells. © 2025 npr

Keyword: Alzheimers
Link ID: 29813 - Posted: 05.31.2025

By Sydney Wyatt Donald Hebb famously proposed in 1949 that when neurons fire together, the synaptic connections between them strengthen, forming the basis for long-term memories. That theory—which held up in experiments in rat hippocampal slice cultures—has shaped how researchers understand synaptic plasticity ever since. But a new computational modeling study adds to mounting evidence that Hebbian plasticity does not always explain how changing neuronal connections enable learning. Rather, behavioral timescale synaptic plasticity (BTSP), which can strengthen synapses even when neurons fire out of sync, better captures the changes seen in CA1 hippocampal cells as mice learn to navigate a new environment, the study suggests. Hebbian spike-timing-dependent plasticity occurs when a neuron fires just ahead of one it synapses onto, leading to a stronger connection between the two cells. BTSP, on the other hand, relies on a complex spike, or a burst of action potentials, in the postsynaptic cell, which triggers a calcium signal that travels across the dendritic arbor. The signal strengthens synaptic connections with the presynaptic cell that were active within seconds of that spike, causing larger changes in synaptic strength. BTSP helps hippocampal cells establish their place fields, the positions at which they fire, previous work suggests. But it was unclear whether it also contributes to learning, says Mark Sheffield, associate professor of neurobiology at the University of Chicago, who led the new study. The new findings suggest that it does—challenging how researchers traditionally think about plasticity mechanisms in the hippocampus, says Jason Shepherd, associate professor of neurobiology at the University of Utah, who was not involved in the research. “The classic rules of plasticity that we have been sort of thinking about for decades may not be actually how the brain works, and that’s a big deal.” © 2025 Simons Foundation

Keyword: Learning & Memory
Link ID: 29810 - Posted: 05.28.2025

By Paula Span & KFF Health News Kristin Kramer woke up early on a Tuesday morning 10 years ago because one of her dogs needed to go out. Then, a couple of odd things happened. When she tried to call her other dog, “I couldn’t speak,” she said. As she walked downstairs to let them into the yard, “I noticed that my right hand wasn’t working.” But she went back to bed, “which was totally stupid,” said Kramer, now 54, an office manager in Muncie, Indiana. “It didn’t register that something major was happening,” especially because, reawakening an hour later, “I was perfectly fine.” So she “just kind of blew it off” and went to work. It’s a common response to the neurological symptoms that signal a TIA, a transient ischemic attack or ministroke. At least 240,000 Americans experience one each year, with the incidence increasing sharply with age. Because the symptoms disappear quickly, usually within minutes, people don’t seek immediate treatment, putting them at high risk for a bigger stroke. Kramer felt some arm tingling over the next couple of days and saw her doctor, who found nothing alarming on a CT scan. But then she started “jumbling” her words and finally had a relative drive her to an emergency room. By then, she could not sign her name. After an MRI, she recalled, “my doctor came in and said, ‘You’ve had a small stroke.’” Did those early-morning aberrations constitute a TIA? Might a 911 call and an earlier start on anticlotting drugs have prevented her stroke? “We don’t know,” Kramer said. She’s doing well now, but faced with such symptoms again, “I would seek medical attention.” © 2025 SCIENTIFIC AMERICAN,

Keyword: Stroke
Link ID: 29808 - Posted: 05.28.2025

Sofia Marie Haley I approach a flock of mountain chickadees feasting on pine nuts. A cacophony of sounds, coming from the many different bird species that rely on the Sierra Nevada’s diverse pine cone crop, fill the crisp mountain air. The strong “chick-a-dee” call sticks out among the bird vocalizations. The chickadees are communicating to each other about food sources – and my approach. Mountain chickadees are a member of the family Paridae, which is known for its complex vocal communication systems and cognitive abilities. Along with my advisers, behavioral ecologists Vladimir Pravosudov and Carrie Branch, I’m studying mountain chickadees at our study site in Sagehen Experimental Forest, outside of Truckee, California, for my doctoral research. I am focusing on how these birds convey a variety of information with their calls. The chilly autumn air on top of the mountain reminds me that it will soon be winter. It is time for the mountain chickadees to leave the socially monogamous partnerships they had while raising their chicks to form larger flocks. Forming social groups is not always simple; young chickadees are joining new flocks, and social dynamics need to be established before the winter storms arrive. I can hear them working this out vocally. There’s an unusual variety of complex calls, with melodic “gargle calls” at the forefront, coming from individuals announcing their dominance over other flock members. Examining and decoding bird calls is becoming an increasingly popular field of study, as scientists like me are discovering that many birds – including mountain chickadees – follow systematic rules to share important information, stringing together syllables like words in a sentence. © 2010–2025, The Conversation US, Inc.

Keyword: Language; Evolution
Link ID: 29807 - Posted: 05.28.2025

Konstantina Kilteni Gargalesis, or tickle, is one of the most trivial yet enigmatic human behaviors. We do not know how a touch becomes ticklish or why we respond to other people’s tickles but not our own. No theory satisfactorily explains why touch on some body areas feels more ticklish than on others or why some people are highly sensitive while others remain unresponsive. Gargalesis is likely the earliest trigger for laughter in life, but it is unclear whether we laugh because we enjoy it. Socrates, Aristotle, Bacon, Galileo, Descartes, and Darwin theorized about tickling, but after two millennia of intense philosophical interest, experimentation remains scarce. This review argues that gargalesis is an exhilarating scientific puzzle with far-reaching implications for developmental, sensorimotor, social, affective, clinical, and evolutionary neuroscience. We reflect on the challenges in defining and eliciting ticklish sensations in the lab and unraveling their neural mechanism, discuss five classic yet unanswered questions about tickle, and suggest directions for future research. Gargalesis, commonly known as tickle, is a very familiar sensation that most of us have experienced at least once in life. Whether actively tickling our babies, family, friends, partners, or pets, or being on the receiving end of a tickle attack, humans undoubtedly engage in tickling behaviors. However, despite its triviality, the scientific understanding of gargalesis is extremely poor. Today, we do not know why certain areas of the body are more ticklish than others and why some people enjoy being tickled, while others dislike it but still burst into laughter. We have also not fully understood why we cannot tickle ourselves and why some people are very ticklish, while others are not responsive at all. Furthermore, the primary function of tickling in humans, as well as in other species, remains a big enigma. Are these questions new, and is that why we do not have any scientific answers yet? Definitely not! Inquiries about the epistemological role of gargalesis have persisted throughout human history, from Ancient Greece to the Renaissance and beyond (1). Socrates (in Plato’s “Philebus”), Aristotle (in “Parts of Animals”), Desiderius Erasmus (in “Adagia”), Francis Bacon (in “Sylva Sylvarum”), Galileo Galilei (in “Il Saggiatore”), René Descartes (in “Treatise on Man” and “The Passions of the Soul”), and Charles Darwin (in “The Expression of the Emotions in Man and Animals”) all theorized about different aspects of gargalesis including its nature and underlying mechanism.

Keyword: Emotions; Evolution
Link ID: 29805 - Posted: 05.24.2025