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 Nala Rogers Coffer illusion What do you see when you stare at this grid of line segments: a series of rectangles, or a series of circles? The way you perceive this optical illusion, known as the Coffer illusion, may tie back to the visual environment that surrounds you, a recent preprint suggests.Anthony Norcia/Smith-Kettlewell Eye Research Institute Himba people from rural Namibia can see right through optical illusions that trick people from the United States and United Kingdom. Even when there’s no “right” or “wrong” way to interpret an image, what Himba people see is often vastly different from what people see in industrialized societies, a new preprint suggests. That could mean people’s vision is fundamentally shaped by the environments they’re raised in—an old but controversial idea that runs counter to the way human perception is often studied. For example, when presented with a grid of line segments that can be seen as either rectangles or circles—an optical illusion known as the Coffer illusion—people from the U.S. and U.K. almost always see rectangles first, and they often struggle to see circles. The researchers suspect this is because they are surrounded by rectangular architecture, an idea known as the carpentered world hypothesis. In contrast, the traditional villages of Himba people are composed of round huts surrounding a circular livestock corral. People from these villages almost always see circles first, and about half don’t see rectangles even when prompted. “I’m surprised that you can’t see the round ones,” says Uapwanawa Muhenije, a Himba woman from a village in northern Namibia, speaking through an interpreter over a Zoom interview. “I wonder how you can’t see them.” Muhenije didn’t participate in the research because her village is less remote than those in the study, and it includes rectangular as well as circular buildings. She sees both shapes in the Coffer illusion easily. Although the study found dramatic differences in how people see four illusions, “the one experiment that’s going to overwhelm people is this Coffer,” says Jules Davidoff, a psychologist at the University of London who was not involved in the study. “There are other striking cultural differences in perception, but the one that they’ve produced here is a real humdinger.” The findings were published as a preprint on the PsyArXiv in February and updated this week. © 2025 American Association for the Advancement of Science.

Keyword: Vision; Development of the Brain
Link ID: 29838 - Posted: 06.21.2025

Katie Kavanagh Scientists have identified a group of neurons that might explain the mechanism behind how stress gives rise to problems with sleep and memory. The study — published last week in The Journal of Neuroscience1 — shows that neurons in a brain area called the hypothalamus mediate the effects of stress on sleep and memory, potentially providing a new target for the treatment of stress-related sleep disorders. Previous work has shown that in the hypothalamus, neurons in a structure called the paraventricular nucleus communicate with other areas important for sleep and memory. The neurons of the paraventricular nucleus release a hormone called corticotropin and have a role in regulating stress. But the neural mechanisms underlying the effect of stress on sleep and memory have remained elusive. For co-author Shinjae Chung, a neuroscientist at the University of Pennsylvania in Philadelphia, the question of exactly how stress affects these processes is personal, because, she says, “I experience a lot of sleep problems when I’m stressed”. She adds that “when I have an exam deadline, I have a tendency to have bad sleep that really affects my score the next day”. To study how neurons in the paraventricular nucleus translate stress into sleep and memory problems, the researchers put laboratory mice through a stressful experience by physically restraining the animals in a plastic tube. The team then tested the creatures’ spatial memory and monitored their brain activity as they slept. © 2025 Springer Nature Limited

Keyword: Sleep; Stress
Link ID: 29837 - Posted: 06.21.2025

Diana Kwon There might be a paradox in the biology of ageing. As humans grow older, their metabolisms tend to slow, they lose muscle mass and they burn many fewer calories. But certain cells in older people appear to do the exact opposite — they consume more energy than when they were young. These potential energy hogs are senescent cells, older cells that have stopped dividing and no longer perform the essential functions that they used to. Because they seem idle, biologists had assumed that zombie-like senescent cells use less energy than their younger, actively replicating counterparts, says Martin Picard, a psychobiologist at Columbia University in New York City. But in 2022, Gabriel Sturm, a former graduate student of Picard’s, painstakingly observed the life course of human skin cells cultured in a dish1 and, in findings that have not yet been published in full, found that cells that had stopped dividing had a metabolic rate about double that of younger cells. For Picard and his colleagues, the energetic mismatch wasn’t a paradox at all: ageing cells accumulate energetically costly forms of damage, such as alterations in DNA, and they initiate pro-inflammatory signalling. How that corresponds with the relatively low energy expenditure for ageing organisms is still unclear, but the researchers hypothesize that this tension might be an important driver of many of the negative effects of growing old, and that the brain might be playing a key part as mediator2. As some cells get older and require more energy, the brain reacts by stripping resources from other biological processes, which ultimately results in outward signs of ageing, such as greying hair or a reduction in muscle mass (see ‘Energy management and ageing’). Picard and his colleagues call this concept the ‘brain–body energy-conservation model’. And although many parts of the hypothesis are still untested, scientists are working to decipher the precise mechanisms that connect the brain to processes associated with ageing, such as senescence, inflammation and the shortening of telomeres — the stretches of repetitive DNA that cap the ends of chromosomes and protect them. © 2025 Springer Nature Limited

Keyword: Obesity; Stress
Link ID: 29836 - Posted: 06.18.2025

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

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

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

By Andrew Jacobs When Gov. Greg Abbott of Texas approved legislation this week to spend $50 million in state money researching ibogaine, a powerful psychedelic, he put the spotlight on a promising, still illegal drug that has shown promise in treating opioid addiction, traumatic brain injury and depression. Interest in ibogaine therapy has surged in recent years, driven in large part by veterans who have had to travel to other countries for the treatment. The measure, which passed the Texas Legislature with bipartisan support, seeks to leverage an additional $50 million in private investment to fund clinical trials that supporters hope will provide a pathway for ibogaine therapy to win approval from the Food and Drug Administration, a process that could take years. The legislation directs the state to work with Texas universities and hospitals and tries to ensure that the state retains a financial stake in any revenue from the drug’s development. “You can’t put a price on a human life, but if this is successful and ibogaine becomes commercialized, it will help people all across the country and provide an incredible return on investment for the people of Texas,” said State Senator Tan Parker, a Republican who sponsored the bill. The initiative, one of the largest government investments in psychedelic medicine to date, is a watershed moment for a field that continues to gain mainstream acceptance. Regulated psilocybin clinics have opened in Oregon and Colorado, and ketamine has become widely available across the country as a treatment for depression and anxiety. There have been speed bumps. Last year, the F.D.A. rejected MDMA-assisted therapy for PTSD, the first psychedelic compound to make it through much of the agency’s rigorous drug review process. © 2025 The New York Times Company

Keyword: Drug Abuse; Stress
Link ID: 29833 - 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 Amber Dance The experiment was a striking attempt to investigate weight control. For six weeks, a group of mice gorged on lard-enriched mouse chow, then scientists infected the mice with worms. The worms wriggled beneath the animals’ skin, migrated to blood vessels that surround the intestines, and started laying eggs. Bruno Guigas, a molecular biologist at the Leiden University Center for Infectious Diseases in the Netherlands, led this study some years back and the results, he says, were “quite spectacular.” The mice lost fat and gained less weight overall than mice not exposed to worms. Within a month or so, he recalls, the scientists barely needed their scale to see that the worm-infested mice were leaner than their worm-free counterparts. Infection with worms, it seems, reversed obesity, the researchers reported in 2015. While it’s true that worms gobble up food their hosts might otherwise digest, that doesn’t seem to be the only mechanism at work here. There’s also some intricate biology within the emerging scientific field of immunometabolism. Over the past couple of decades, researchers have recognized that the immune system doesn’t just fight infection. It’s also intertwined with organs like the liver, the pancreas and fat tissue, and implicated in the progression of obesity and type 2 diabetes. These and other metabolic disorders generate a troublesome immune response — inflammation — that worsens metabolism still further. Metabolic disease, in other words, is inflammatory disease. Scientists have also observed a metabolic influence of worms in people who became naturally infected with the parasites or were purposely seeded with worms in clinical trials. While the physiology isn’t fully understood, the worms seem to dampen inflammation, as discussed in the 2024 Annual Review of Nutrition.

Keyword: Obesity; Neuroimmunology
Link ID: 29828 - 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

Myrian Wares for Quanta Magazine You’ve just gotten home from an exhausting day. All you want to do is put your feet up and zone out to whatever is on television. Though the inactivity may feel like a well-earned rest, your brain is not just chilling. In fact, it is using nearly as much energy as it did during your stressful activity, according to recent research. Sharna Jamadar (opens a new tab), a neuroscientist at Monash University in Australia, and her colleagues reviewed research from her lab and others around the world to estimate the metabolic cost of cognition (opens a new tab) — that is, how much energy it takes to power the human brain. Surprisingly, they concluded that effortful, goal-directed tasks use only 5% more energy than restful brain activity. In other words, we use our brain just a small fraction more when engaging in focused cognition than when the engine is idling. It often feels as though we allocate our mental energy through strenuous attention and focus. But the new research builds on a growing understanding that the majority of the brain’s function goes to maintenance. While many neuroscientists have historically focused on active, outward cognition, such as attention, problem-solving, working memory and decision-making, it’s becoming clear that beneath the surface, our background processing is a hidden hive of activity. Our brains regulate our bodies’ key physiological systems, allocating resources where they’re needed as we consciously and subconsciously react to the demands of our ever-changing environments. “There is this sentiment that the brain is for thinking,” said Jordan Theriault (opens a new tab), a neuroscientist at Northeastern University who was not involved in the new analysis. “Where, metabolically, [the brain’s function is] mostly spent on managing your body, regulating and coordinating between organs, managing this expensive system which it’s attached to, and navigating a complicated external environment.” © 2025 Simons Foundation.

Keyword: Attention; Brain imaging
Link ID: 29825 - Posted: 06.07.2025

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

Anna Bawden Health and social affairs correspondent Weight loss drugs could at least double the risk of diabetic patients developing age-related macular degeneration, a large-scale study has found. Originally developed for diabetes patients, glucagon-like peptide-1 receptor agonist (GLP-1 RA) medicines have transformed how obesity is treated and there is growing evidence of wider health benefits. They help reduce blood sugar levels, slow digestion and reduce appetite. But a study by Canadian scientists published in Jama Ophthalmology has found that after six months of use GLP-1 RAs are associated with double the risk of older people with diabetes developing neovascular age-related macular degeneration compared with similar patients not taking the drugs. Academics at the University of Toronto examined medical data for more than 1 million Ontario residents with a diagnosis of diabetes and identified 46,334 patients with an average age of 66 who were prescribed GLP-1 RAs. Nearly all (97.5%) were taking semaglutide, while 2.5% were on lixisenatide. The study did not exclude any specific brand of drugs, but since Wegovy was only approved in Canada in November 2021, primarily for weight loss, it is likely the bulk of semaglutide users in the study were taking Ozempic, which is prescribed for diabetes. Each patient on semaglutide or lixisenatide was matched with two patients who also had diabetes but were not taking the drugs, who shared similar characteristics such as age, gender and health conditions. The researchers then compared how many patients developed neovascular age-related macular degeneration over three years. © 2025 Guardian News & Media Limited

Keyword: Vision; Obesity
Link ID: 29822 - 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