By Tim Vernimmen On a rainy day in July 2024, Tim Bliss and Terje Lømo are in the best of moods, chuckling and joking over brunch, occasionally pounding the table to make a point. They’re at Lømo’s house near Oslo, Norway, where they’ve met to write about the late neuroscientist Per Andersen, in whose lab they conducted groundbreaking experiments more than 50 years ago. The duo only ever wrote one research paper together, in 1973, but that work is now considered a turning point in the study of learning and memory. Published in the Journal of Physiology, it was the first demonstration that when a neuron — a cell that receives and sends signals throughout the nervous system — signals to another neuron frequently enough, the second neuron will later respond more strongly to new signals, not for just seconds or minutes, but for hours. It would take decades to fully understand the implications of their research, but Bliss and Lømo had discovered something momentous: a phenomenon called long-term potentiation, or LTP, which researchers now know is fundamental to the brain’s ability to learn and remember. Today, scientists agree that LTP plays a major role in the strengthening of neuronal connections, or synapses, that allow the brain to adjust in response to experience. And growing evidence suggests that LTP may also be crucially involved in a variety of problems, including memory deficits and pain disorders. Bliss and Lømo never wrote another research article together. In fact, they would soon stop working on LTP — Bliss for about a decade, Lømo for the rest of his life. Although the researchers knew they had discovered something important, at first the paper “didn’t make a big splash,” Bliss says. By the early 1970s, neuroscientist Eric Kandel had demonstrated that some simple forms of learning can be explained by chemical changes in synapses — at least in a species of sea slug. But scientists didn’t yet know if such findings applied to mammals, or if they could explain more complex and enduring types of learning, such as the formation of memories that may last for years.

Keyword: Learning & Memory
Link ID: 29694 - Posted: 03.05.2025

Five years ago Italian researchers published a study on the eruption of Mount Vesuvius in A.D. 79. that detailed how one victim of the blast, a male presumed to be in his mid 20s, had been found nearby in the seaside settlement of Herculaneum. He was lying facedown and buried by ash on a wooden bed in the College of the Augustales, a public building dedicated to the worship of Emperor Augustus. Some scholars believe that the man was the center’s caretaker and was asleep at the time of the disaster. In 2018, one researcher discovered black, glossy shards embedded inside the caretaker’s skull. The paper, published in 2020, speculated that the heat of the explosion was so immense that it had fused the victim’s brain tissue into glass. Vesuvius Erupted, but When Exactly? March 2, 2025 Forensic analysis of the obsidian-like chips revealed proteins common in brain tissue and fatty acids found in human hair, while a chunk of charred wood unearthed near the skeleton indicated a thermal reading as high as 968 degrees Fahrenheit, roughly the dome temperature of a wood-fired Neapolitan pizza oven. It was the only known instance of soft tissue — much less any organic material — being naturally preserved as glass. On Thursday, a paper published in Nature verified that the fragments are indeed glassified brain. Using techniques such as electron microscopy, energy dispersive X-ray spectroscopy and differential scanning calorimetry, scientists examined the physical properties of samples taken from the glassy fragments and demonstrated how they were formed and preserved. “The unique finding implies unique processes,” said Guido Giordano, a volcanologist at the Roma Tre University and lead author of the new study. Foremost among those processes is vitrification, by which material is burned at a high heat until it liquefies. To harden into glass, the substance requires rapid cooling, solidifying at a temperature higher than its surroundings. This makes organic glass formation challenging, Dr. Giordano said, as vitrification entails very specific temperature conditions and the liquid form must cool fast enough to avoid being crystallized as it congeals. © 2025 The New York Times Company

Keyword: Brain imaging
Link ID: 29690 - Posted: 03.05.2025

By Holly Barker Hunched over a microscope more than a century ago, Santiago Ramón y Cajal discovered that distinct types of neurons favor different brain regions. Looking at tissue from a pigeon’s cerebellum, he drew Purkinje cells, their dendrites outspread and twisted like a ravaged oak. And drawing from another sample—the first cortical layer of a newborn rabbit’s brain—he traced the tentacled nerve cells that would later bear his name. But the brain’s cellular organization is even more ordered than Ramón y Cajal could have imagined, a new study suggests. Different functional networks—measured using functional MRI—involve distinct blends of cell types, identified from their transcriptional profiles. And a machine-learning tool trained on cell distributions in postmortem tissue can identify functional networks based on these cellular “fingerprints,” the researchers found. The findings could address the gulf between neuroimaging and cell-based research, says the study’s principal investigator, Avram Holmes, associate professor of psychiatry at Rutgers University. “In-vivo imaging studies are almost never linked back to the underlying biological cascades that give rise to the phenotypes,” he says. But the new approach “lets you jump between fields of study—that was very difficult to do in the past.” Using bulk gene-expression data from postmortem human brain tissue—obtained from the Allen Human Brain Atlas—Holmes and his colleagues classified 24 different types of cells. They then mapped the cells’ spatial distribution to two features of large-scale brain organization derived from a popular fMRI atlas: networks, and those networks’ position in the cortical gradient, which is based on location, style of information processing and connectivity pattern. Unimodal sensorimotor networks—those that perceive stimuli and act on them—anchor one end of the gradient, and the other end is occupied by transmodal systems, such as the default mode network, that integrate multiple information streams across the cortex. The remaining networks are parked between these two extremes. © 2025 Simons Foundation

Keyword: Brain imaging
Link ID: 29689 - Posted: 03.01.2025

By Donna L. Maney It’s springtime in your backyard. You watch a pair of little brown songbirds flit about, their white throats flashing in the sun. One of the birds has striking black and white stripes on its crown and occasionally belts out its song, “Old Sam Peabody, Peabody, Peabody.” Its partner is more drab, with tan and gray stripes on its head and brown streaks through its white throat. Knowing the conventional wisdom about songbirds—that the males are flashy show-offs and the females more camouflaged and quiet—you decide to name the singer with bright plumage Romeo and the subtler one Juliet. But later that day you notice Juliet teed up on the fence, belting out a song. Juliet’s song is even louder and showier than Romeo’s. You wonder, Do female birds sing? Then you see Romeo bringing a twig to the pair’s nest, hidden under a shrub. Your field guide says that in this species the female builds the nest by herself. What is going on? Turns out, when you named Romeo and Juliet, you made the same mistake 19th-century artist and naturalist John Audubon did when, in his watercolor of this species, he labeled the bright member of the pair “male” and the drab one “female.” Romeo might look male, even to a bird expert such as Audubon, but will build a nest and lay eggs in it. Juliet, who might look female, has testes and will defend the pair’s territory by singing both alone and alongside Romeo, who also sings. Juliet and Romeo are White-throated Sparrows (Zonotrichia albicollis). At first glance, members of this species of songbird might look rather ordinary. For example, like many other songbirds, one member of each breeding pair of these sparrows has more striking plumage—that is, its appearance is what we would traditionally consider malelike for songbirds. The other bird in the pair is more femalelike, with drabber plumage. © 2024 SCIENTIFIC AMERICAN

Keyword: Sexual Behavior; Evolution
Link ID: 29686 - Posted: 02.26.2025

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

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

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

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

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 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 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

By Emily Anthes The English language is full of wonderful words, from “anemone” and “aurora” to “zenith” and “zodiac.” But these are special occasion words, sprinkled sparingly into writing and conversation. The words in heaviest rotation are short and mundane. And they follow a remarkable statistical rule, which is universal across human languages: The most common word, which in English is “the,” is used about twice as frequently as the second most common word (“of,” in English), three times as frequently as the third most common word (“and”), continuing in that pattern. Now, an international, interdisciplinary team of scientists has found that the intricate songs of humpback whales, which can spread rapidly from one population to another, follow the same rule, which is known as Zipf’s law. The scientists are careful to note that whale song is not equivalent to human language. But the findings, they argue, suggest that forms of vocal communication that are complex and culturally transmitted may have shared structural properties. “We expect them to evolve to be easy to learn,” said Simon Kirby, an expert on language evolution at the University of Edinburgh and an author of the new study. The results were published on Thursday in the journal Science. “We think of language as this culturally evolving system that has to essentially be passed on by its hosts, which are humans,” Dr. Kirby added. “What’s so gratifying for me is to see that same logic seems to also potentially apply to whale song.” Zipf’s law, which was named for the linguist George Kingsley Zipf, holds that in any given language the frequency of a word is inversely proportional to its rank. There is still considerable debate over why this pattern exists and how meaningful it is. But some research suggests that this kind of skewed word distribution can make language easier to learn. © 2025 The New York Times Company

Keyword: Language; Evolution
Link ID: 29662 - Posted: 02.08.2025

By Avery Schuyler Nunn Migratory songbirds may talk to one another more than we thought as they wing through the night. Each fall, hundreds of millions of birds from dozens of species co-migrate, some of them making dangerous journeys across continents. Come spring, they return home. Scientists have long believed that these songbirds rely on instinct and experience alone to make the trek. But new research from a team of ornithologists at the University of Illinois suggests they may help one another out—even across species—through their nocturnal calls. “They broadcast vocal pings into the sky, potentially sharing information about who they are and what lies ahead,” says ornithologist Benjamin Van Doren of the University of Illinois, Urbana-Champaign and a co-author of the study, published in Current Biology. Using ground-based microphones across 26 sites in eastern North America, Van Doren and his team recorded over 18,300 hours of nocturnal flight calls from 27 different species of birds—brief, high-pitched vocalizations that some warblers, thrushes, and sparrows emit while flying. To process the enormous dataset of calls, they used machine-learning tools, including a customized version of Merlin, the Cornell Lab of Ornithology’s bird-call identification app. The analysis revealed that birds of different species were flying in close proximity and calling to one another in repeated patterns that suggested a kind of code. Flight proximity was closest between migrating songbirds species that made similar calls in pitch and rhythm, traveled at similar speeds, and had similar wing shapes. © 2025 NautilusNext Inc.,

Keyword: Language; Evolution
Link ID: 29661 - Posted: 02.08.2025

Nell Greenfieldboyce People are constantly looking at the behavior of others and coming up with ideas about what might be going on in their heads. Now, a new study of bonobos adds to evidence that they might do the same thing. Specifically, some bonobos were more likely to point to the location of a treat when they knew that a human companion was not aware of where it had been hidden, according to a study which appears in the Proceedings of the National Academy of Sciences. The findings add to a long-running debate about whether humans have a unique ability to imagine and understand the mental states of others. Some researchers say this kind of "theory of mind" may be practiced more widely in the animal kingdom, and potentially watching it in action was quite the experience. "It's quite surreal. I mean, I've worked with primates for quite some years now and you never get used to it," says Luke Townrow, a PhD student at Johns Hopkins University. "We found evidence that they are tailoring their communication based on what I know." Hmmm, where is the grape? To see what bonobos might know about what humans around them know, Townrow worked with Chris Krupenye of Johns Hopkins University to devise a simple experiment. "It's always a challenge for us, that animals don't speak, so we can't just ask them what they're thinking. We have to come up with creative, experimental designs that allow them to express their knowledge," says Krupenye. © 2025 npr

Keyword: Attention; Consciousness
Link ID: 29658 - Posted: 02.05.2025

By Laura Hercher edited by Gary Stix It is impossible, of course, to identify the precise moment we first suspected the changes in my mother were something other than normal aging. In my own imperfect memory, what rises up is the first morning of a weeklong trip to Rome, when my mother woke up at 2 A.M., got dressed and went down for breakfast. A hotel employee found her wandering from room to room, looking for toast and coffee. She was jet-lagged, my brother and I told each other uneasily. It could happen to anyone. But weren’t there cues? Didn’t she notice the darkened lobby, the stillness, the clock? If we had known then, would it have helped? To date, no U.S. Food and Drug Administration–­approved therapy exists for asymptomatic people at risk of Alzheimer’s disease (AD). My mother was not a smoker, drank in moderation, read books, took classes, and spent that week in Italy soaking up everything the tour guide told her about Caravaggio and Bernini like she was prepping for a quiz. Five years passed after that trip before my mother received a diagnosis of dementia. Today, a simple blood test can detect changes in the brain that predict AD up to 15 years before the first symptoms emerge. For researchers, tools for early detection give a peek at the full spectrum of AD, pinpointing early seeds of pathology deep inside the brain. Cognitive decline—what we typically think of as the disease itself—is merely the illness’s denouement. “Dementia is a result. Dementia is a symptom,” explains Clifford R. Jack, Jr., a neuroradiologist at the Mayo Clinic in Rochester, Minn., and chair of the Alzheimer’s Association (AA) working group responsible for recent, controversial guidelines for the diagnosis of AD based on underlying biology, not clinical presentation. Scientific American is part of Springer Nature,

Keyword: Alzheimers
Link ID: 29657 - Posted: 02.05.2025

Damian Carrington Environment editor The exponential rise in microplastic pollution over the past 50 years may be reflected in increasing contamination in human brains, according to a new study. It found a rising trend in micro- and nanoplastics in brain tissue from dozens of postmortems carried out between 1997 and 2024. The researchers also found the tiny particles in liver and kidney samples. The human body is widely contaminated by microplastics. They have also been found in blood, semen, breast milk, placentas and bone marrow. The impact on human health is largely unknown, but they have been linked to strokes and heart attacks. The scientists also found that the concentration of microplastics was about six times higher in brain samples from people who had dementia. However, the damage dementia causes in the brain would be expected to increase concentrations, the researchers said, meaning no causal link should be assumed. “Given the exponentially rising environmental presence of micro- and nanoplastics, this data compels a much larger effort to understand whether they have a role in neurological disorders or other human health effects,” said the researchers, who were led by Prof Matthew Campen at the University of New Mexico in the US. Microplastics are broken down from plastic waste and have polluted the entire planet, from the summit of Mount Everest to the deepest oceans. People consume the tiny particles via food, water and by breathing them in. A study published on Thursday found tiny plastic pollution to be significantly higher in placentas from premature births. Another recent analysis found that microplastics can block blood vessels in the brains of mice, causing neurological damage, but noted that human capillaries are much larger. © 2025 Guardian News & Media Limited

Keyword: Neurotoxins
Link ID: 29656 - Posted: 02.05.2025