By Emily Baumgaertner Nunn Are you naturally anxious? Highly adventurous? More argumentative than you’d like to admit? Those tendencies are often measured through what psychologists call the “Big Five” dimensions of personality: extroversion, agreeableness, conscientiousness, neuroticism and openness to experience. Each trait exists on a continuum and tends to remain fairly stable throughout adult life. But what determines where you land on those spectra? Scientists have long known that personality is influenced by a host of factors — including DNA. The challenge has been deciphering the specific pathways through which a genetic blueprint nudges the direction of a person’s life. To map this sprawling architecture, a group of experts formed a research consortium and analyzed more than one million genomes, searching for variants associated with personality. The researchers also compared the genes of thousands of siblings and parent-child pairs to rule out other factors that could be at play. With data from 46 different study cohorts, they found a symphony of 1,260 genetic markers tied to personality, nearly two-thirds of them identified for the first time. The findings, published on Wednesday in the journal Nature, reaffirmed scientists’ understanding that temperament and disposition are shaped not by a few particular genes, but by thousands of tiny variants that can be expressed in different circumstances. The sheer scale of the project also brought new statistical power to the study of personality genetics, giving researchers a tool kit to investigate the biological mechanisms behind how we think, feel and behave. “I view the 1,260 variants as kind of a testament to the fact that we’ve now got the power to answer all of these other questions that we couldn’t answer before,” said Elliot Tucker-Drob, a professor of psychology at the University of Texas at Austin and a leader of the study. © 2026 The New York Times Company

Keyword: Emotions; Genes & Behavior
Link ID: 30395 - Posted: 09.05.2026

By Erik Vance Imagine two athletes: a soccer player and a Formula 1 driver. While the soccer player may be blisteringly fast on the field, she still moves at a humanlike speed. She may be quicker than anyone and be able to pivot with incredible dexterity, but it’s always at a pace that the human brain can follow. Now think of the racecar driver, going about 220 miles per hour on the straights and 180 on the corners. No land animal, living or dead, has ever run even half that quickly. It’s simply too fast for any mortal’s brain to keep up with. So, how do they do it? How does a human mind navigate a sport that’s faster than it can follow? “There is a limit, like a physiological limit,” said Otto Lappi, a senior university lecturer at the University of Helsinki in Finland. “But there is less limit to how much cleverness your brain can build in — to know the environment and figure out right now what I need to do not to kill myself.” Scientists have long studied elite athletes as a way to understand the inner workings of the human brain. But Formula 1 drivers offer them a unique window: how the brain adapts to impossible speeds. The first thing to know is that while reflexes are important, they are not what distinguishes a truly elite driver. “This is something that people don’t realize when they think of racing drivers living off their reflexes,” said Dr. Lappi, who studies eye movements of various types of athletes. “Most of their skill is anticipation. The anticipation is how the brain buys itself time.” © 2026 The New York Times Company

Keyword: Learning & Memory
Link ID: 30393 - Posted: 09.05.2026

By Carl Zimmer and Azeen Ghorayshi Scientists have uncovered a wealth of clues about how genetic mutations lead to severe forms of autism, offering opportunities for testing drugs that could treat the condition, according to a study published Thursday. The researchers charted how mutations change the way proteins work together in cells, altering the development of the brain. “This is making maps of unknown territories that’s really necessary to move the biology forward,” said Dan Geschwind, a neurogeneticist at the University of California, Los Angeles, who was not involved in the study. Researchers have been studying autism for over 80 years, but it has only been in recent years that they have been able to explore its molecular biology. One reason that progress has been so slow is that autism is not just one condition, but a broad constellation of them. People with autism can have difficulty with language and making social connections, and often display restricted or repetitive behaviors. While many children with an autism diagnosis can grow up to lead independent adult lives, others may be nonspeaking, have intellectual disabilities, and require round-the-clock care. But in around 30 percent of people diagnosed with autism, typically those with the most severe disabilities, scientists have identified single gene mutations that are almost guaranteed to cause the disorder. When those genes started coming to light 20 years ago, scientists eagerly hoped they could find precise treatments for severe autism. In some studies, they engineered mice with the mutations and then tried different drugs to reverse their autism-like symptoms. But those efforts have not led to any effective treatment targeting a specific gene. © 2026 The New York Times Company

Keyword: Autism; Genes & Behavior
Link ID: 30390 - Posted: 08.29.2026

By Claudia López Lloreda The proteins encoded by 100 genes involved in autism form an interconnected network consisting of multiple protein complexes that serve different cellular functions, according to a study published today in Science. Autism-associated variants may cause this network to rewire, the study also found. Even though autism is a genetically heterogeneous condition, “when you look at the proteins encoded by the genes, and also the specific mutations and the interfaces of protein interactions, the biology starts to converge,” says Kasper Lage, managing director of the Novo Nordisk Foundation Center at the Broad Institute, who was not involved in the work. Many of the proteins the study considered converge on complexes already associated with autism and that are involved in processes such as neural progenitor proliferation and differentiation and neuronal migration, the researchers found. The idea behind the work was to go beyond the genetic studies, which have linked about 250 genes to autism, says study investigator Belinda Wang, assistant professor of psychiatry at the University of California, San Francisco. “Genes can tell us where autism risk begins, but proteins do a lot of the work inside the cells, and so by studying autism at the protein level, maybe this can give us a more direct view of the underlying biology.” Previous network analyses did not reach this magnitude, Lage says. “When you get to the scale that they’re doing in this paper, you can start to do really interesting secondary analysis and pathway and discovery.” © 2026 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 30388 - Posted: 08.29.2026

By Michele Patterson Ford When survivors of trauma recount their experiences, they are often questioned because of how they relay their stories. They may have problems remembering what happened, or their memories may be jumbled or even contradictory. People hearing those stories—attorneys, reporters, healthcare workers or friends—may expect a clearer, linear narrative. Those unaffected by trauma may also be surprised to hear how the person acted in the moment. It’s easy to assume that someone experiencing a traumatic event would have a “fight or flight” response, instinctively fighting off a perpetrator or fleeing the scene—but that might not be the case. Understanding the science of how trauma affects memory and behavior reveals why these responses can actually be expected and are not contradictory. In both my academic and clinical work as a psychologist, I have witnessed the impact trauma has on people’s memories and behaviors, especially when an event in their present life triggers something from their past. Research shows that taking a trauma-informed approach, which prioritizes understanding and curiosity about someone’s experience as opposed to judgment or critical evaluation, increases empathy for survivors’ thoughts, feelings and behaviors. According to the World Health Organization, approximately 70 percent of people worldwide report experiencing a traumatic event in their lifetime. The majority of these people do not develop PTSD, a clinical diagnosis of symptoms, such as having nightmares and flashbacks about the event, avoiding places that are reminders of it, and increased arousal that can make concentration and sleep difficult. Many survivors don’t meet criteria for PTSD but struggle with feeling distressed, depressed or anxious. © 2026 SCIENTIFIC AMERICAN INC.

Keyword: Learning & Memory; Stress
Link ID: 30383 - Posted: 08.22.2026

By Claudia López Lloreda For five years, several small batches of cortical organoids grew in an isolated incubator, away from possible contamination and doted upon by a Harvard University research team. The organoids didn’t merely survive, though—they generated diverse neurons and glia and acquired transcriptional and epigenetic features of postnatal brains, all on a human-like schedule, according to a new study published today in Nature. Organoids typically model only pre- and perinatal brains and notoriously lack robust electrical activity, says In-Hyun Park, associate professor of neuroscience and genetics at Yale University, who was not involved with the study. The new work provides an avenue to study postnatal stages of development, he says. However, the long-lived organoids started losing neuronal signals around the one-year mark, which continued as they aged, the team found. “Yes, the organoid was maturing, everything was great, but the neurons were suffering,” says study investigator Paola Arlotta, professor of stem cells and regenerative biology at Harvard. Modifying the culture medium enabled the team to grow a new set of organoids that had more mature excitatory neurons, greater neuronal complexity and enhanced electrical activity. “If you want to move forward with more network activity, mature human neurons, you need to adapt your tissue culture,” says Alysson Muotri, professor of pediatrics and cellular and molecular medicine at the University of California, San Diego, who was not involved with the study. “I think it’s an important message.” © 2026 Simons Foundation

Keyword: Development of the Brain
Link ID: 30382 - Posted: 08.22.2026

By Aimee Cunningham In 2025, the number of children receiving a drug promoted — but unproven — for autism treatment grew, especially toward the end of the year. A new study suggests the late rise was influenced by a Trump administration announcement. At a White House briefing on September 22, 2025, President Trump touted the drug leucovorin as a potential therapeutic for autism. The week before the announcement, roughly 5 children per 100,000 received leucovorin via a prescription in the United States. The week of the announcement, the pharmacy dispensing rate climbed to roughly 7 children per 100,000. By the end of the year, the rate rose to 8 children per 100,000, researchers reported August 12 in the New England Journal of Medicine. “Our study demonstrates the power of the federal government to influence clinical practice,” says Kao-Ping Chua, a pediatrician and health policy researcher at the University of Michigan Medical School in Ann Arbor. If administration communications and decisions are not based on rigorous scientific evidence, it could lead to harms “including giving people false hope and potentially exposing them to the side effects of ineffective medical treatments.” Leucovorin is a form of the essential vitamin folic acid. The drug is prescribed when the body’s method for breaking down folic acid from food is impaired. The U.S. Food and Drug Administration had approved leucovorin for use with certain genetic disorders and to help reduce the side effects of chemotherapy drugs that disrupt that break down. The American Academy of Pediatrics does not recommend leucovorin for autism because of the lack of evidence surrounding dosing, effectiveness and safety. © Society for Science & the Public 2000–2026.

Keyword: Autism
Link ID: 30380 - Posted: 08.22.2026

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 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 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 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 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 Alissa de Chassey A long-standing model of the hippocampus’s role in memory needs to be revised, according to a new preprint. For more than half a century, memory theories treated the CA3 region of the hippocampus as a uniform population of pyramidal neurons that form one broad recurrent, or autoassociative, network; the cells synapse onto each other and also send signals to the CA1 region. The network stores memories as synapses strengthen among coactivated cells, each encoding a different piece of the memory. And because of this architecture, a partial cue can reactivate a full memory, such as when the taste of a madeleine sparks a flood of childhood memories for the narrator of Marcel Proust’s “In Search of Lost Time.” But it turns out that picture may be wrong. The CA3 instead comprises two distinct types of pyramidal neurons arranged in two layers, with different morphology, physiology and connectivity patterns, the preprint suggests. The findings were posted on bioRxiv in July. “These two cell types are very different, and one of them is totally breaking what the textbook would say,” says study investigator Jake Watson, a postdoctoral researcher in Peter Jonas’ lab at the Institute of Science and Technology Austria. A single transcription factor, ST18, distinguishes the two populations, the study reveals: A set of superficial CA3 neurons that express ST18 forms a recurrent network as predicted by the classical model, and a deeper set, which does not express ST18, regulates the superficial one. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30359 - Posted: 08.05.2026

By RJ Mackenzie LONDON — A protein marker of Alzheimer’s disease in the brain may also help diagnose cases of the brain condition chronic traumatic encephalopathy, or CTE, early data suggest. The condition, which is linked to repeated head trauma, currently can be identified only in autopsies. But measurements of an Alzheimer’s-associated protein, eMTBR-tau243, might one day bring testing to the living: In confirmed CTE cases, levels of the protein increased the more advanced the disease had been at death, researchers reported July 15 at the Alzheimer’s Association International Conference. The data, which have yet to be peer-reviewed, suggest a path toward a first way of diagnosing CTE in living people, says Chihiro Sato, a neuroscientist at Washington University in St. Louis. While the results would need to be confirmed in a larger dataset, “we think there’s potential.” The ability to diagnose patients while they are still alive would provide clarity to patients about their well-being and be invaluable to getting them involved in future trials of any CTE treatments, says John Arena, a neurosurgeon at the University of Pennsylvania who was not involved in the research. Diagnosing CTE currently requires a careful examination of the brain after death, which has complicated efforts to identify how many people are affected by the condition. A 2018 study found that CTE-like damage affected 1 of 164 donated brains. But CTE is far more common in people repeatedly exposed to head trauma, like athletes in contact sports. In 2023, the Boston University CTE Center reported that CTE pathology was present in more than 90 percent of brains in a sample of 376 former NFL players. © Society for Science & the Public 2000–2026.

Keyword: Brain Injury/Concussion; Alzheimers
Link ID: 30355 - Posted: 08.01.2026

By Natalia Mesa Theoretical models of the brain often treat neurons as single, homogenous units. But dendrites can store information about the past and make predictions about the future independently of the cell body, according to a new study. “In the artificial-intelligence community, dendrites are underappreciated,” says Eilif Muller, associate professor of neurosciences at the University of Montreal, who was not involved in the study. “In this paper, and as we study dendrites more, we’re getting a glimpse into mechanisms that allow us to learn rapidly but stably.” Dendritic activity can dissociate from cell body activity, depending on an animal’s goal, the new work shows. The findings are the first in-vivo evidence of the long-standing theoretical prediction that a neuron’s dendrites play a separate role from cell bodies in neural computations. The study was published in Science earlier this month. “There’s been decades of studies on how dendrites function: Are they passive, or do they play a more active role in cognitive processes?” says study investigator Attila Losonczy, professor of neuroscience at the University of Texas Southwestern Medical Center. Action potentials generated at the soma can backpropagate into the dendrites, making the two compartments’ activity hard to tease apart. Losonczy and his colleagues used ultrafast voltage imaging to record electrical activity in the dendrites of pyramidal place cells in the CA3 region of the hippocampus of mice as the animals moved around in a virtual environment and received a sip of water in certain locations; the place cells fire when a mouse is in a specific location in space. When the reward locations changed, dendrites retained information about the original sites. But when the entire virtual environment changed, dendrites were the first to encode new locations of rewards—the cell body caught up later. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30353 - Posted: 08.01.2026

By Ailie McWhinnie On a research trip to Indonesia in 2007, Yosuke Kaifu saw for himself the skull of “Flo”—the skeletal remains first discovered 4 years earlier that heralded the existence of a diminutive human relative called Homo floresiensis. These so-called “Hobbits,” which stood about 1 meter tall, lived on the Indonesian island of Flores until about 50,000 years ago. The University of Tokyo anthropologist was drawn to one anatomical peculiarity: The skull’s right side is slightly smooshed. Some researchers had previously attributed this abnormality to disease, others to distortion after burial. But when Kaifu showed it to a clinician back in Japan, he received a surprising response: It looked like a harmless condition known as deformational plagiocephaly, or flattening of the skull, that occurs today in about one in six babies. Usually, the skull rounds out over time, but in some cases, it can persist into adulthood. The condition arises because the human skull remains soft for the first months of life to allow for the enormous amount of brain growth that occurs after birth. Repeated pressure on one side can cause flattening, and because babies cannot hold up their own heads, they are prone to resting it on one side when put down. Such helplessness is thought to be a concession to babies’ brains being relatively underdeveloped at birth to allow them to fit through the birth canal. Kaifu reasoned that deformational plagiocephaly in the skulls of ancient hominins could be a good indicator that they, too, were helpless as infants. After examining hundreds of skulls, they conclude today in the Proceedings of the Royal Society B that at least two other lineages of humans shared this trait with us, suggesting it has deep evolutionary origins. “I thought it was a very ingenious study,” says Lia Betti, an anthropologist at University College London. © 2026 American Association for the Advancement of Science.

Keyword: Evolution; Development of the Brain
Link ID: 30352 - Posted: 08.01.2026

By Emily Anthes One day last summer, a curious white-faced capuchin encountered a strange contraption in the forest. There, in the middle of the Taboga Forest Reserve in Costa Rica, sat a 15-inch touch screen, mounted in a wooden frame. As the monkey, an alpha male named Papi, began investigating — poking the device here, prodding it there — his fingers landed on the screen. Suddenly, a piece of dried banana dropped into a tray below the frame. Before long, Papi learned the basic rules of the device: touch the screen, get a dried banana slice. He also provided proof of concept for CapuchinAI, a new device designed to assess the cognitive abilities of monkeys in the wild. The testing apparatus, which the researchers described in a new paper, used A.I.-powered facial recognition software to detect capuchins in real time and record their responses to a simple learning task. The scientists hope that more sophisticated versions of the device, which they will begin testing in the coming weeks, will shed new light on primate evolution and intelligence, and answer questions that would be impossible to study in a lab, such as how a monkey’s smarts affect its success and survival. “If we really want to understand how primates make decisions, if we want to understand how they’re using these large brains that they evolved, we have to really put it in the context of the world in which they’re navigating,” said Marcela Benítez, a primatologist at Emory University and an author of the new paper, which was published in the American Journal of Primatology on Tuesday. “But that is a lot easier said than done.” Dr. Benítez has been studying the white-faced capuchins at Taboga for years, logging their behavior, recording their vocalizations and measuring their hormone levels. For the new study, she and her colleagues used images of some of these monkeys to train an artificial intelligence model to identify capuchins and distinguish them from the other animals roaming the forest. Then they built a portable testing station equipped with a touch screen, webcam and 3-D-printed food dispenser. © 2026 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 30349 - Posted: 07.29.2026

By Liz Seegert More than one in 10 Americans takes a GLP-1 medication for weight loss. As more people take a GLP-1, or glucagonlike peptide 1, receptor agonist, such as Wegovy, so, too, do more older adults—and those numbers are set to skyrocket. Last week the Trump administration launched the Medicare GLP-1 Bridge program, a new initiative that would set the cost of three weight-loss medications— Wegovy, the KwikPen version of Zepbound (tirzepatide) and Foundayo (orforglipron)—at $50 a month. That may be welcome news for the estimated 38.9 percent of adults aged 60 and up in the U.S. who are living with obesity. But it could also supercharge an ongoing and risky experiment in growing old on weight-loss drugs. For years, clinicians have had few good options to safely treat obesity in older adults. But while GLP-1s, long used to treat diabetes, are now approved for weight loss, the evidence supporting their use in the age-60-and-older population is limited. Someone in their 70s may benefit as much from weight loss as a person in their 30s but may respond very differently to these drugs’ side effects; we simply don’t have enough evidence yet to make informed conclusions, experts advise. “Eligibility doesn’t mean benefit automatically,” says Ruchi Gaba, an associate professor of endocrinology at Baylor College of Medicine. “We have to individualize.” And within the 60-and-older group, there is huge variety: a healthy, active 68-year-old with obesity and sleep apnea is a very different patient than an 88-year-old who’s frail, has poor appetite and is at risk of falls, Gaba says. Older adults are underrepresented in the clinical trials for GLP-1 drugs. Despite the high prevalence of obesity among this age group, only about one in 10 participants in early GLP-1 trials was age 65 or older, says Alissa Chen, a primary care physician and a researcher at the Yale School of Medicine, who specializes in obesity. Older adults are more heterogeneous than people in younger age groups in terms of chronic conditions and multiple medications, Chen says, which can pose challenges with both prescriptions and side effects. © 2026 SCIENTIFIC AMERICAN

Keyword: Obesity; Development of the Brain
Link ID: 30334 - Posted: 07.22.2026

By Dylan Loeb McClain Susumu Tonegawa, a Japanese molecular biologist who won the Nobel Prize in 1987 for figuring out how the body can produce sufficient antibodies to combat a multitude of infections, and who later advanced the understanding of how the brain works by discovering how memories are stored, died on July 11 at his home in San Mateo, Calif. He was 86. The Massachusetts Institute of Technology, where Dr. Tonegawa was a professor, announced his death. “Few scientists have reshaped our understanding of biology as profoundly,” Myriam Heiman, the director of M.I.T.’s Picower Institute for Learning and Memory, which Dr. Tonegawa founded in 1994, said in a statement. “His intellectual fearlessness, extraordinary creativity and relentless pursuit of fundamental questions opened entirely new frontiers in both immunology and neuroscience.” For decades, scientists were confounded by the antibodies created in the white blood cells known as B lymphocytes. Those antibodies, which fight disease, are shaped like Y’s, with two long and two short symmetrical chains of proteins built from amino acids, all bound together by bridges of sulfur atoms. Most of the long proteins and some of the short ones are considered constants because they are the same in all antibodies. At the end of each strand are variable amino acids that allow the antibodies to bind to antigens on an array of infections, disabling them. A common analogy is that the constant amino acids are like the shaft of a key, and the variable ones are the notches that turn the lock. As with a key, each combination of notches is unique. Even so, scientists were puzzled by how the antibodies could create enough combinations to fight millions of infections. © 2026 The New York Times Company

Keyword: Learning & Memory
Link ID: 30333 - Posted: 07.22.2026