By Amanda Heidt Earlier this month, the US Food and Drug Administration approved the first drug designed to treat the root cause of narcolepsy, a condition that affects millions of people by causing extreme sleepiness during the day and wakefulness at night. The success of the drug, called oveporexton and marketed as Orzeyful, is being celebrated by those who struggle with narcolepsy. “It’s the best thing that has ever happened to me,” says Tyler Chapman, who volunteered for one of the clinical trials that contributed to the drug’s approval. But it’s also being watched with anticipation by researchers, who see it as the first in a line of therapies for sleep disorders that are likely to be approved in the coming years. These emerging treatments, known as orexin agonists, are exciting because they promise not just to alleviate symptoms of narcolepsy but also to target the disease’s biological cause — and might even have implications for other neuropsychiatric disorders. With this new strategy against narcolepsy, pharmaceutical companies have jumped at the chance to tap into a market that is projected to top US$6.4 billion annually by the early 2030s. “This is a tremendously exciting time for patients and for clinicians and scientists who have been working towards this for many years,” says Barry Lubarsky, the vice-president of medical affairs at the pharmaceutical company Alkermes, which is based in Dublin and is developing its own narcolepsy treatment. A chance to feel normal For Chapman, a 19-year-old student at the University of Tennessee, Knoxville, the milestone is life changing. Chapman had long struggled with his condition, at times sleeping for 16 hours a day, struggling in school and relying heavily on coffee. When he laughed, it would sometimes trigger his body to collapse, even though he remained fully conscious — a symptom known as cataplexy. Instead of experiencing all that university life has to offer, Chapman says that he rarely went out. © 2026 Springer Nature Limited

Keyword: Narcolepsy; Sleep
Link ID: 30379 - Posted: 08.19.2026

By Jake Buehler This nose grows. During harsh Japanese winters, long-clawed shrews’ snouts temporarily expand. The seasonal swelling is the opposite of the previously known winter pattern in shrews, in which the brain and surrounding cranium shrink. The findings complicate our understanding of an already extreme adaptation for harsh, frigid conditions, researchers report August 19 in Proceedings of the Royal Society B. The temporary dwindling and regrowth of the brain and skull tissue in shrews is part of Dehnel’s phenomenon, first described by Polish zoologist August Dehnel in 1949. The phenomenon involves winter reductions in body size and internal organ mass. It’s thought to be an adaptation for surviving winter. Paring back tissues cuts food energy costs, which is useful when calories are scarce. The new findings add an unexpected wrinkle to our understanding of the phenomenon. Yugo Ikeda, a mammalogist at Toyo University in Tokyo, and his colleagues knew about these “mind-boggling” seasonal shifts. Some other animals like weasels, voles and moles experience similar winter changes. But scientists didn’t know if any shrews outside of Europe also went through these changes. Northeast Asia, for instance, has extreme, snowy winters that might present a challenge to local small mammals. The researchers carefully measured the dimensions of 136 skulls from museum specimens of long-clawed shrews (Sorex unguiculatus), a species native to the region. The shrews were collected between 1948 and 1988 on the Japanese island of Hokkaido. Ikeda and his colleagues took photos of the skulls and used software to measure dozens of physical landmarks across them. The team then compared the skull dimensions with the season in which the shrews were collected. © Society for Science & the Public 2000–2026.

Keyword: Biological Rhythms; Chemical Senses (Smell & Taste)
Link ID: 30378 - Posted: 08.19.2026

By Zoe Beketova Efforts to explain rising rates of myopia, or nearsightedness, in children worldwide have made two things clear: More time spent outdoors seems protective, and more time spent indoors increases risk. A new study in tree shrews now suggests a key to preventing myopia may be the indigo portion of sunlight. Adding this part of the light spectrum to the animals’ environment prevented them from developing myopia, researchers report today in Cell Reports Medicine. The findings have not yet been confirmed in humans, but some researchers are cautiously optimistic that increasing children’s exposure to indigo wavelengths could preserve their developing vision as well. “No one knows why outdoor light is good for kids’ eyes,” says Lisa Ostrin, a vision scientist at the State University of New York College of Optometry, who was not involved in the study. “If it turns out to be [the presence of certain wavelengths], it could be so simple to just add in overhead lights and enhance them with additional short wavelengths.” But she stresses that more research is needed to draw that conclusion. Myopia, or nearsightedness, affects almost 3 billion people worldwide, and this number is projected to climb to almost 5 billion by 2050. The condition occurs when the eyeball grows too long in childhood, instead of developing its typical spherical shape. This causes light to focus in front of the retina, the light-sensing layer of tissue along the back of the eye, instead of directly on it, making the resulting image transmitted to the brain unclear. Human genetics do not change fast enough over time to account for the rising rates, which some have blamed on increased reading or computer screen use. Others have said greater exposure to indoor light, with its more limited spectrum of wavelengths compared with outdoor light, could be the problem. © 2026 American Association for the Advancement of Science.

Keyword: Vision; Development of the Brain
Link ID: 30377 - Posted: 08.19.2026

By Sarah Thau Sound the alarm! Activating a subset of neurons in the medulla promotes anxiety in mice, a study published in Neuron finds. Anxiety is typically thought of as a set of “complex, social, environmental, biological, neurobiological interactions” involving multiple regions across the brain, says Oliver Robinson, professor of neuroscience and mental health at University College London, who was not involved in this work. So he was “surprised that you can have such dramatic effects by just looking at a single cell type.” The role of medullary neurons in anxiety adds to a growing body of work on anxiety circuitry, says study investigator Carlos Fernández-Peña, assistant professor of neurological sciences at the University of Nebraska. “It was already complex. Now let’s add some more.” Two sets of neurons—C1 and A1—in the rostral ventrolateral medulla (RVLM) produce catecholamines that could drive anxiety, but only C1 neurons are activated when mice are stressed, Fernández-Peña says. The challenge, then, was to study only C1 neurons, which are intermingled with A1 neurons, in awake mice to uncover their role in anxiety-like behaviors, he says. He and his colleagues employed two different genetic recombination tools—one called INTRSECT and another called ConVERGD—for the first time, according to study investigator Lindsay Schwarz, associate member of the St. Jude Children’s Research Hospital faculty, who co-developed the latter tool. This pairing enabled them to make transgenic mice in which they could optogenetically modulate only the C1 neurons and not the A1 cells, using careful genetic logic. © 2026 Simons Foundation

Keyword: Emotions
Link ID: 30376 - Posted: 08.19.2026

Emily Mullin Erin McNulty had been missing for weeks when her mother, Linda, sat down on a chair in her living room, exhausted. Linda had put in her usual seven-day workweek at the antiques shop she runs near Burlington, Vermont. She’d spent her free evenings driving around, trying to track down her daughter. Erin, 45 at the time, had been using methamphetamine for years. Her substance use started in high school—first alcohol, then marijuana, and eventually heroin. Erin’s brother used heroin, too. When Linda found out, she started driving her kids to a methadone clinic three hours away in Massachusetts. The methadone helped, but it made Erin feel tired all the time, so she started using cocaine to stay awake. There were stretches of sobriety—she had her daughter during one of them, in 2008. The family took trips to the Great Escape waterpark in New York and Hampton Beach in New Hampshire. There were also several overdoses and attempts at rehab. Eventually, Erin switched to suboxone and stopped using heroin. But when a friend introduced her to meth, Linda says, “Erin was gone.” Linda turned on the TV and was flipping through the channels when a 60 Minutes segment caught her attention. It was early 2024, and the show focused on a procedure that might help people with substance use disorders. Linda immediately thought of her daughter. The procedure involved beaming ultrasound through the skull to treat the brain. Researchers at West Virginia University were testing it on people with Alzheimer’s disease and addiction. The neurosurgeon behind the procedure, Ali Rezai, was a pioneer in the field of deep brain stimulation, which involves cutting into the skull to implant electrodes that can reach neurons deep in the brain. He was excited by the ability of ultrasound—the imaging tool best known for observing fetal development during pregnancy—to reach into the same brain structures without breaking the skin. There would be no drilling into the skull, no poking or prodding the brain’s delicate tissue. The ultrasound could be delivered in 20 minutes, and patients could go home the same day. © 2026 Condé Nast.

Keyword: Drug Abuse; Biomechanics
Link ID: 30375 - Posted: 08.15.2026

By Kristen French When evolutionary anthropologist David Samson was living and working among the Hadza tribe in northern Tanzania, he noticed something puzzling: Their sleep was highly fragmented, short in duration, and low in “efficiency,” or actual time spent sleeping versus time in bed. This broken sleep was partly the consequence of activity and noise well into the night in the camps. People stayed up late telling stories, sharing food, and dancing. Yet, the Hadza uniformly reported high satisfaction with their sleep. It challenged the so-called Paleo sleep hypothesis, the notion that hunter-gatherer sleep must be optimally long and deep, but also ran counter to the medical orthodoxy that unbroken sleep is essential to a good night’s rest. Samson traveled to Tanzania to hang out with the Hadza because he was trying to untangle what he calls the sleep paradox: Sleep is critical to human functioning, and yet, we sleep fewer total hours than any other ape, and are still arguably the most evolutionarily successful of the primates. This riddle sent him climbing into chimpanzee nests high in the trees and exploring the sleeping huts and practices of communities around Africa and Madagascar. The stories he collected, people he met, and research findings he uncovered are vividly described in his new book The Sleepless Ape: The Story of Sleep in Human Evolution. I spoke with Samson about what we really need for a good night’s sleep, why we may be on the cusp of a “sleep enlightenment,” and the origins of what he calls the “lie-down-and-die” model of Western sleep. What is the paradox of human sleep? You can just say, “Oh, here’s where humans are relative to other primates on sleep.” But that misses the deeper evolutionary story. When I was a postdoc at Duke University about a decade ago, new data was emerging showing that even after controlling for brain size, body size, social order, and actual phylogenetic relatedness, humans are weird outliers—we’re the shortest sleeping primates, yet we pack in the most REM sleep relative to this short duration.

Keyword: Sleep; Evolution
Link ID: 30374 - Posted: 08.15.2026

By Siddhant Pusdekar Visual experiences during early life famously shape cortical circuits. Animals deprived of vision in one eye rewire their cortex to favor the other eye, according to Nobel Prize-winning work by Hubel and Wiesel. And animals raised in controlled visual environments—surrounded by vertical stripes or horizontal ones, for example—adjust their cortical neurons’ orientation tuning. This kind of experience-dependent plasticity also occurs in the retina itself, leading to lasting changes in behavior, according to a recent zebrafish study in Neuron. The sensory structure had long been thought to be hardwired. “The field in general doesn’t think that activity has any effect on the retina, and it’s always [acting] downstream,” says Marla Feller, professor of neuroscience at University of California Berkeley, who wasn’t involved in the study. Previous research suggests that waves of spontaneous neuronal activity in the retina that begin prenatally and continue till mice open their eyes help shape visual circuitry. The new work is the first to show that what an animal sees can prompt retinal activity that changes the shape and function of its interneurons, altering downstream processes including behavior, Feller says. Vertebrates share many aspects of wiring in the retina, where layers of interneurons transform the pixel-like input from photoreceptors into distinct information channels encoding features of the visual environment. This commonality includes amacrine cells, which are one of the most diverse kinds of interneurons, says Robert Hindges, professor of developmental neurobiology at King’s College London and an investigator on the new study. © 2026 Simons Foundation

Keyword: Development of the Brain; Vision
Link ID: 30373 - Posted: 08.15.2026

By Jennie Erin Smith In the past decade, as opioids claimed nearly half a million lives across the United States, surgeons, dentists, and other clinicians have pined for pain relievers that work as well as hydrocodone or oxycodone but without the high risk of addiction and overdose. Last year, the U.S. Food and Drug Administration (FDA) approved suzetrigine, the first in a new class of drugs that promised pain relief approaching that of opioid pills without those concerns. Many expected to see even more powerful drugs emerge from this class of agents, known as Nav1.8 inhibitors, which block sodium channels on pain-sensing neurons to quell their activity. But efforts to improve on suzetrigine—which has been shown to offer consistent but moderate effects on acute pain—have not produced stronger relief. Recent research has aimed to explain what seems to be a ceiling to the drugs’ benefits, and to get a better handle on their real-world limits. Nav1.8 inhibitors are a needed advance, pain researchers agree, as federal guidance has sought to curb use of opioid painkillers. “Almost everyone you talk to either has a friend or family member that’s been affected by the opioid crisis,” says independent pharmacologist Paul Desjardins, who designed some of the widely used surgical protocols for testing pain drugs and consults for companies developing Nav1.8 inhibitors. But “the data to this point don’t convince me that any of the sodium channel blockers that I’ve seen are better than ibuprofen or naproxen or acetaminophen when they are combined.” The origin story of the drug class led to high hopes. Starting in the late 1990s, genetic studies of people with rare syndromes marked by chronic or excessive pain flagged mutations that caused peripheral sensory neurons, which relay pain signals to the brain, to become hyperactive. The syndromes were linked to changes in the function of two proteins, Nav1.7 and Nav1.8, that regulate neuronal activity by allowing sodium to flow into the cells. Blocking these channels offered a more precise painkilling strategy compared with drugs such as lidocaine, which blocks sodium channels more broadly and has too many toxic effects to be given systemically. © 2026 American Association for the Advancement of Science.

Keyword: Pain & Touch
Link ID: 30372 - Posted: 08.15.2026

By Erin Garcia de Jesús In The Sheep Detectives, Mopple has a superpower: The anthropomorphic sheep can’t forget anything. He joins a long line of fictional characters with some version of photographic memory — a strikingly useful skill, or at least a key plot device. Sherlock Holmes uses perfect recall to solve crimes (as long as, in the case of the BBC television series, it’s in his mind palace). And medical student Joy Kwon’s ability comes to the rescue in The Pitt, remembering patient room numbers, symptoms and treatments after the ER loses access to electronic medical records. “A lot of people [believe] that our memory acts like a video recorder, that it exactly captures reality, it holds on to it perfectly,” says Gabrielle Principe, a developmental psychologist at College of Charleston in South Carolina. To debunk that idea, she has a simple task for her students: Draw a penny from memory. None can. Some rare people, mostly children, claim to have what’s called eidetic imagery, or an ability to conjure up mental images of objects even after they’ve been removed from sight. But those images are not perfect and are still temporary. Though exceptional memories exist, everyone forgets. And that is not a flaw. In fact, human brains can’t retain everything. “If we did, we would live in a very cluttered place,” says Simona Ghetti, a developmental psychologist at the University of California, Davis. Our brains wouldn’t know which memories to prioritize, affecting our ability to recall the events or details that matter over unimportant particulars. The ability to retrieve memories of experiences usually starts around age 3, although most early memories are ultimately lost. “There’s always the occasional person who thinks that they remember going through the birth canal,” Ghetti says. But these claims often fall apart upon careful questioning. © Society for Science & the Public 2000–2026.

Keyword: Learning & Memory
Link ID: 30371 - Posted: 08.15.2026

Elie Dolgin The video opens with a man in his 80s slumped in a hospital bed, his face hollow as he scrunches his eyes. A jump cut advances the scene three days: the man is alert now, words gathering as he identifies his son. Six months later, he is pictured sitting upright, engaged in conversation. His gaze is animated. At eight months, the man walks briskly down a hospital corridor. He recites a near-century-old Maoist military anthem from memory. He is practically unrecognizable from the withered figure in the opening frame. The footage records the recovery of a man who, in September 2020, became the first person in the world to undergo a surgery known as deep cervical lymphatic-venous anastomosis (dcLVA) to treat Alzheimer’s disease. The procedure involves connecting tiny lymphatic vessels in the neck — part of the drainage system that carries waste away from the brain — to nearby veins, creating a route that, in theory, allows fluid and waste proteins to flow more easily into the bloodstream. The treatment was first reported1 in 2022 in a Chinese-language journal by microsurgeon Qingping Xie, president of the Qiushi Hospital in Hangzhou, China. At the time, it drew little notice. But that changed the following year, when Wei Chen, a lymphatic microsurgeon at the Cleveland Clinic in Ohio, began showing the footage (with consent from Xie and the man’s family) at surgical meetings around the world. “A lot of jaws dropped,” recalls Chen. “It basically started a frenzy of this surgery being performed left and right.” Almost all of the surgeries took place in China, where hundreds of hospitals were soon offering the experimental procedure. Propelled by viral testimonial videos and aggressive marketing campaigns on social-media platforms such as Douyin and WeChat, it was sought out by thousands — with many people paying more than 200,000 yuan (US$30,000) for a chance of recovery. © 2026 Springer Nature Limited

Keyword: Alzheimers
Link ID: 30370 - Posted: 08.12.2026

By Meghan Rosen Dogs may be even more attuned to people’s feelings than we think. Man’s best friend has a knack for knowing what humans are thinking, reading signs as subtle as jangling keys or a dangling leash. But a new brain-imaging study suggests that dogs may even be able to distinguish between certain negative emotions without using clues like our body language, odor or words. Just looking at people’s faces may be enough, scientists report August 10 in iScience. The results offer a new peek at what’s going on in canine brains. That could help scientists better understand how dogs’ emotion-sensing abilities evolved, says Laura Cuaya, a neuroscientist at the University of Vienna in Austria. In the meantime, the work provides yet another reason to smile at any pup that crosses your path, she says — perhaps they’ll understand. Previous studies have revealed much about dogs’ perception of emotion. They can tell whether a human face is displaying positive or negative emotions, for example. And such emotions seem to arouse different areas of the brain. But many questions remained. Can dogs’ brains differentiate between two negative emotions, such as anger versus fear? Do the faces need to be familiar? Who’s a good boy? Odin and Kun-Kun (right) are two canine participants in a project that examined dogs’ brain activity. Researchers trained the pups to sit still inside an MRI machine while looking at images of human faces. The dogs’ brains lit up in different patterns depending on what emotions people’s faces displayed. © Society for Science & the Public 2000–2026

Keyword: Emotions; Evolution
Link ID: 30369 - Posted: 08.12.2026

By Holly Barker Individual structural MRI studies fail to identify reproducible brain signatures for autism and other neuropsychiatric conditions, a new study finds. Brain scans of people with autism, depression and bipolar disorder rarely show consistent differences in cortical thickness or grey matter volume across independent studies, according to the analysis. The study suggests that these structural measures are unlikely to provide reliable biomarkers of those conditions and that different approaches are needed. “The findings are really a wake-up call. We’ve all been operating under the assumption that if we keep doing these studies enough, eventually the noise will wash out and we will converge on some consensus of what the brain changes in a particular disorder are,” says study investigator Alex Fornito, professor of psychology at Monash University. “Our findings suggest if we keep doing that business as usual, that’s not going to happen.” Structural MRI studies have long produced conflicting results. Some have identified greater cortical thickness of select brain regions in people with autism than those without the condition, while others have reported the opposite. Until now, it was unclear whether such discrepancies reflected differences in study design and analysis, or whether structural brain signatures for these conditions do not exist. To address that question, Fornito and his colleagues analyzed MRI scans from thousands of people with neuropsychiatric conditions—including depression, schizophrenia, schizoaffective disorder, autism and bipolar disorder—as well as from people with Alzheimer’s disease. They calculated cortical thickness or grey matter volume using the same analysis pipeline across all datasets and then compared how consistently brain changes were reproduced between independent study sites. © 2026 Simons Foundation

Keyword: Brain imaging; Schizophrenia
Link ID: 30368 - Posted: 08.12.2026

Will Stone A few times, Dr. Jamin Brahmbhatt suspected he might have low testosterone. But when he checked his numbers, he discovered they were within a normal range. "Turns out it was more so my sleep and stress and everything else," says Brahmbhatt, a urologist at Orlando Health in Florida. Brahmbhatt treats men with low testosterone every day — meaning he's on the front lines of the current cultural fixation with testosterone. Social media is overflowing with testosterone content, from fears of "low T" to "T-maxxing" tutorials. Influential voices, including the podcaster Joe Rogan and Health Secretary Robert F. Kennedy Jr., are openly discussing their own use of testosterone therapy. And there's a huge industry of online clinics that make it easy for anyone to get a prescription. Brahmbhatt welcomes the increased attention to men's health — and hormone replacement therapy specifically — which he says has been "ignored" for too long. But he also sees men who've spent hours in online forums like Reddit, convinced they need testosterone even before they've spoken to a doctor or had their levels tested. "Not every guy needs to be on it," Brahmbhatt says. "Testosterone has gotten a bad rap because … you can walk into these clinics, go online, and get a prescription, they don't do all the testing, they don't do the follow up. That is the unsafe territory." © 2026 npr

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 30367 - Posted: 08.12.2026

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

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

By Sara Reardon The protein tau is best known for its potential to clog the brain. In neurodegenerative conditions including Alzheimer’s disease, chains of the molecule twist into tangles inside neurons and choke out the cells. But a new study suggests tau may play an earlier and more fundamental role in neurodegeneration: sneaking into the cell’s power-generating mitochondria—the cell’s power generators—and interfering with aging neurons’ energy production. If this process gets out of control, it creates tangle-prone forms of tau and other toxic byproducts that damage neurons, long before a person’s cognitive symptoms start. The research, published today in Neuron, also showed interrupting this process can prevent brain damage and disease symptoms in mice. “It really is opening up something we’ve needed for a while, which is some really new ideas and fresh directions” for understanding neurodegenerative diseases, says Kenneth Kosik, a neuroscientist at the University of California, Santa Barbara who was not involved in the research. “I think this paper will reinvigorate the idea that [modifying tau] is going to be a possible therapeutic approach.” Researchers and companies developing treatments for Alzheimer’s have long seen tau as a potential drug target. One recent clinical trial, for instance, showed lowering the levels of tau in the brains of people with Alzheimer’s reduced their rate of cognitive decline by as much as 26%. Other approaches have tried to prevent enzymes from adding chemical tags called phosphate groups to tau proteins. These phosphorylated forms of tau (p-tau) are especially prone to misfolding and clumping into tangles. But tau therapies have seen limited success so far, leading researchers to wonder whether the protein actually drives neurodegeneration or is merely a sign of it. So geneticist Bingwei Lu of Stanford University and his colleagues set out to find specific ways in which p-tau affects cells. Previous research has suggested Alzheimer’s and other so-called tauopathies, including frontotemporal dementia and Parkinson’s disease, all involve problems with energy production in the brain’s mitochondria © 2026 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 30365 - Posted: 08.08.2026

By Camille Bromley When Cameron LaBar was a kid, he was a towhead with bright blue eyes and big feelings. He seemed to sense things more strongly than other children. His family lived in Southern California, and when he was at the beach or playing in the yard, they’d put him on a double layer of towels so he wouldn’t scream when he got sand on his hands or was poked by the grass. Susan LaBar, his mother, called him the flip-top baby. He’d build up to a certain pressure, then erupt in tears. Around the age of 5, his face and body began repetitively twitching in ways he couldn’t control. Ms. LaBar bought books on Tourette’s syndrome and started highlighting things she recognized — until she was almost coloring in whole pages. In fourth grade, his teacher called her and said that he had gotten overwhelmed with instructions on an assignment and froze at his desk. She took him to a pediatric neurologist, who diagnosed him with Tourette’s syndrome, obsessive-compulsive disorder and generalized anxiety disorder. Of her five children, Ms. LaBar thought, he was the most like her: anxious and sensitive. “He can’t take a deep breath,” she told the doctor. “He’s so knotted up.” The doctor suggested that Paxil, an antidepressant in the category known as S.S.R.I.s, could level things out for him. The doctor told her that Paxil would adjust what was going on in his head so he could do what he needed to do: relax, sit down in class and complete his homework. Giving her son psychiatric medication at 9 years old was not a decision Ms. LaBar took lightly. She thought about it every night for a week, then called the doctor and asked for a prescription at the lowest dose that would help him get unstuck from inside his own head. More than 20 years later, as an adult, Mr. LaBar looks back on that moment with ambivalence and regret. It was the start of a prolonged pharmaceutical spiral that kept him on medication without egress. He believes that the years he spent on antidepressants kept him from feeling the full range of his emotions — from living a full authentic life, even. He was not alone: When he described his experience online, he encountered a multitude of others who had a similar story. © 2026 The New York Times Company

Keyword: Depression
Link ID: 30364 - Posted: 08.08.2026

By Cody Cottier The twittering of songbirds may bear little resemblance to human speech, but new research on Bengalese finches shows that their vocalizations do follow a fundamental structural principle found in all languages. Zipf’s law states that a handful of words—or, in this case, chirps, whistles and trills—occur frequently, while most are rare. Specifically, the most common word (“the,” in English) appears roughly twice as often as the second-most common (“of”), three times as often as the third most common (“and”), and so on. This peculiar frequency distribution was also documented last year in humpback whale song, meaning it has emerged in at least three evolutionary lineages that are separated by millions of years. Though these wordlike units in songbirds and whales probably don’t convey specific meaning in the way that human words do, these discoveries challenge the notion that human language is wholly unique, says Simon Kirby, a cognitive scientist at the University of Edinburgh and a co-author of both the whale and songbird studies. “We suddenly have these unrelated species that do something similar to what humans do,” he says. “This gives us a new dividing line, a new way of carving up communication systems in the world.” The dividing line, as Kirby sees it, lies between species that learn their vocal signals culturally and those whose calls are genetically built-in. Much like language, the songs of humpbacks and many songbirds get transmitted from one generation to the next. Because so-called Zipfian word distribution is known to help human infants pick up language from the adults around them, it stands to reason that similar patterns may aid learning in young birds and whales, too. © 2026 SCIENTIFIC AMERICAN INC.

Keyword: Animal Communication; Language
Link ID: 30363 - Posted: 08.08.2026

By Natalia Mesa As an animal navigates the world, cells in the hippocampus and entorhinal cortex produce rapid, repeating bursts of activity called theta sweeps: Grid and place cells fire in a specific sequence, first plotting the location the animal has just passed, then where it is currently and lastly what lies ahead. Whether these theta sweeps simply scan the surrounding environment or instead represent the deliberation and planning needed for goal-directed movement is “something that people have been arguing about for 30 years,” says David Redish, professor of neuroscience at the University of Minnesota. That debate may now be over: Theta sweeps serve both functions, depending on the situation, according to three new studies by independent teams. The brain produces systematic sweeps by default to passively sample an environment, but it switches to active, targeted sweeps whenever an animal is pursuing a goal or focused on something specific, the studies show. “It changes our conception of what theta sweeps do,” says Edvard Moser, professor of neuroscience at the Norwegian University of Science and Technology and an investigator on one of the new studies, published today in Science. The other two studies appeared last month in Nature Neuroscience. Theta sweeps occur within individual theta wave cycles, which are around 125-250 milliseconds long. The teams were able to detect the sweeps’ trajectories by recording hundreds of individual neurons at once in 10-millisecond blocks, a time resolution fine enough to see individual theta cycles, Moser says, adding that they are “invisible if you only look at the average.” © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30362 - Posted: 08.08.2026

By Jake Buehler A craving for sweets may have helped set the stage for the evolution of the human brain. Over 4 million years, our lineage’s brains grew from about 300 grams to 1,500 grams. Much of the brain growth occurred before early humans had mastered both fire and cooking, which would have unlocked access to the energy of starches. A new analysis of existing data from human ancestors, as well as chimps, suggests that a large proportion of that energy probably came from sugary foods like fruits and honey. These simple carbohydrates may have played an important, overlooked role in humankind’s evolutionary story, researchers argue August 6 in Science. A major part of the story of diet and human evolution revolves around meat-eating: Around 2.5 million years ago, our hominid ancestors began increasing their intake of animal food. This influx of protein and fat is seen as instrumental in fueling our ancestors’ ever-expanding brains. But Jennie Brand-Miller, a human nutrition scientist at the University of Sydney, was interested in how dietary sugars factored into the lives and overall evolution of our early ancestors. A 2017 study suggested that fruit-eating primates had bigger brains than leaf-eating species. Other researchers had hypothesized in the 1990s that the cognitive demands of fruit eating may have kick-started the evolution of big brains in humans. “You need to remember when various species of ripe fruit begin to ripen, then you need to remember where it is in the forest,” Brand-Miller says. “Your memory is associated with a bigger brain.” © Society for Science & the Public 2000–2026.

Keyword: Obesity; Evolution
Link ID: 30361 - Posted: 08.08.2026

By Jake Currie No one knows what causes Alzheimer’s disease. There are plenty of risk factors associated with the neurodegenerative disease, like inflammation, smoking, and genetics, but so far no single culprit has emerged. A new study published in Translational Psychiatry, however, investigated the link between Alzheimer’s and another risk factor, depression, leading to some surprising results. Neuroscientists led by a team from the University of Southern California analyzed high-resolution MRI scans from more than 2,000 healthy adults between the ages of 50 and 90. Around a third of them (630) had been diagnosed with depression, and these subjects showed a significant decrease in volume in their hippocampus. The entire hippocampus wasn’t affected, though, just a smaller subfield responsible for retrieving memories, reconstructing memories from partial information, and distinguishing between similar experiences. “This study shows why it’s important to look beyond the total size of the hippocampus,” study co-author Meredith N. Braskie said in a statement. “Depression wasn’t related to smaller volume throughout the entire region. The association was concentrated in a particular set of subfields, giving us a more precise picture of how depression may relate to brain health during aging.” © Copyright 2026

Keyword: Depression
Link ID: 30360 - Posted: 08.08.2026