By Elie Dolgin Jeff Carroll was in his mid-twenties, fresh out of the U.S. Army, when a genetic test confirmed his worst fear: He was going to develop Huntington’s disease. He had watched his mother’s illness for years; the tremors first, small enough to explain away, then the involuntary movements that looked almost like dancing. The test revealed that the same mutation that caused her disease lived in him: a stretch of three DNA letters in a gene called HTT, repeated over and over again dozens of times. Carroll himself was not sick yet. He would not get sick for many years. But the countdown had begun. In fact, it had likely been running all his life, deep inside vulnerable neurons in his brain. There, the mutant HTT gene was slowly growing longer, its internal repeats piling up toward a threshold that, once crossed, would tip the cell into disarray. The first outward signs of Huntington’s often begin with mood changes and subtle cognitive effects. The hallmark jerky movements come later. Eventually, and relentlessly, patients lose the ability to speak, swallow or move. Most people die within a decade or two of symptom onset. Huntington’s disease is rare, affecting roughly 1 in 20,000 people worldwide. Yet because each child of an affected parent has a 50 percent chance of inheriting the mutation, the disease can haunt families for generations. It had already claimed Carroll’s grandmother and would take his mother at age 54. Without a therapy capable of altering its course, Carroll — along with three of his five siblings who also inherited the mutation — seemed fated to follow his ancestors into an early grave. Carroll decided the only rational response was to become one of the scientists seeking ways to beat the disease. He was midway through his undergraduate studies when he learned, in 2003, that he carried the mutation. He pressed on, earning a Ph.D. and completing postdoctoral training before establishing his own research group devoted to understanding and slowing the disease stalking him from within. © Society for Science & the Public 2000–2026.

Keyword: Huntingtons
Link ID: 30332 - Posted: 07.18.2026

By Jennie Erin Smith Alzheimer’s disease has long been seen as a tale of two proteins: beta amyloid, which forms sticky plaques in the brain, and tau, which in its diseased state creates tangles inside neurons. Antibodies that clear beta amyloid have been approved to treat Alzheimer’s, but it was tau that made headlines this week, as researchers presented key new details about a drug that reduced production of the protein and slowed cognitive decline in a recent clinical trial. At the Alzheimer’s Association International Conference, neurologist Catherine Mummery of University College London presented results from a phase 2 trial testing diranersen, a drug developed by Biogen to lower the body’s production of tau, in more than 400 patients with early-stage Alzheimer’s. On the study’s main measure of cognition, participants getting diranersen saw as much as a 26% slowing of decline—about on par with the effect seen in earlier trials of approved antiamyloid drugs. (Biogen had announced in May the drug slowed cognitive decline but did not say by how much.) Although the presentation sparked enthusiasm from Alzheimer’s researchers, it also drew attention to puzzling aspects of the trial results. A potentially worrisome side effect emerged at high doses, and contrary to expectations, patients taking the lowest of three possible doses saw the greatest benefit. For these reasons, the findings represent “a double, not a home run,” says neurologist Adam Boxer of the University of California San Francisco, who this month launched a clinical trials platform to try different antitau therapies in Alzheimer’s. Diranersen belongs to a class of drugs known as antisense oligonucleotides, strands of RNA that dampen activity of specific genes. It interrupts production of tau by binding to the messenger RNA that encodes instructions for producing the protein, and must be injected directly into the cerebrospinal fluid to reach the brain. After 18 months, participants in all three dose groups had between one-third and one-half as much tau in their cerebrospinal fluid as when they started the trial, whereas levels increased slightly among people receiving placebo. Imaging done on a subgroup of participants showed the drug also reduced tau tangles in the brain. © 2026 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 30329 - Posted: 07.18.2026

By Laura Sanders Babies are born with a natural preference for using their left or right side. Now, a new study suggests that preference alone doesn’t explain the dominant side’s superior skills: They come from practice. The results, published June 30 in the Proceedings of the National Academy of Sciences, show how flexible human brains can be when learning new motor skills. A deeper understanding of how the brain generates movements could help illuminate what happens when that process goes awry, such as after a stroke. Even before birth, babies tend to move one hand more than the other, an early sign of whether a person will be left- or right-handed. This preference probably comes from a mix of genetics and quirks of brain development. But this origin story isn’t what interested researchers. Instead, they wondered why a person’s dominant side — left or right — is more talented. It could be that one half of the brain is just better at controlling movement. Or, as neurologist and neuroscientist Ahmet Arac now suspects, it could all come down to practice. To tease these two ideas apart, Arac and his colleagues had 11 people write the letter A and the number 8 with either their dominant or nondominant hand. The results were exactly what you’d expect; dominant hands wrote the figures better. Then, Arac, of the David Geffen School of Medicine at UCLA, and his colleagues threw these folks a curveball by asking them to write with a pen taped to an elbow. Half the people wrote with their dominant elbow, and the other half wrote with their nondominant elbow. Neither elbow — dominant or nondominant — was very good. © Society for Science & the Public 2000–2026.

Keyword: Laterality; Learning & Memory
Link ID: 30325 - Posted: 07.15.2026

By RJ Mackenzie LONDON — An experimental drug can sweep tangles of tau from the brain, raising hopes that the treatment could help Alzheimer’s disease patients, according to clinical trial data released July 14. The compound, called diranersen and developed by pharma giant Biogen, reduced tau levels in patients’ cerebrospinal fluid by between 50 and 65 percent as compared with the start of the trial. The drug also seemed to slightly slow people people’s cognitive decline compared with those given a placebo. But it’s unclear whether a change of this size will help patients. And the results raised a puzzling conundrum: Contrary to expectations, the patients who had the biggest reductions in their levels of tau didn’t benefit the most in cognitive testing. “This story has been almost a decade in the telling,” said neurologist Catherine Mummery, who presented data on the drug to a packed conference room at the Alzheimer’s Association International Conference. Mummery, head of novel therapeutics at the University College London Dementia Research Center, began the first diranersen trial in October 2017. The results are a “significant step forward,” says molecular neuroscientist Heather Snyder of the Chicago-based Alzheimer’s Association. Over seven million people ages 65 and older in the United States have Alzheimer’s, and treatments to slow its progression, much less cure it, have been hard to come by. Diranersen is what’s called an antisense oligonucleotide — a synthetic chunk of DNA that silences genes. It binds to the MAPT gene, which produces tau, a protein that’s been implicated in Alzheimer’s disease. In the condition, tau goes haywire, forming into tangles which damage nerve cells. © Society for Science & the Public 2000–2026.

Keyword: Alzheimers
Link ID: 30323 - Posted: 07.15.2026

By Dana G. Smith In theory, taking an omega-3, or fish oil, supplement makes a lot of sense. Omega-3 fatty acids are vital for brain health: They are used to build brain cells, keeping the cell walls flexible and enabling the neurons to sprout new connections and communicate with other cells. Numerous studies have shown that people with higher levels of omega-3s in their blood have better cognition and healthier looking brains, as well as a lower risk of developing dementia. In contrast, people with Alzheimer’s disease have been shown to have lower omega-3 levels. But there’s a catch: The vast majority of clinical trials have found that taking omega-3 supplements offers virtually no benefit for cognition or dementia symptoms. “It kind of intuitively makes sense” that neurons need fatty acids for their health, so you should take a fatty acid supplement, said Dr. Kristine Yaffe, a professor of psychiatry, neurology and epidemiology at the University of California, San Francisco. “The problem is that most of the evidence, particularly the trial evidence, just doesn’t support it at all,” she said. A study published last month offers a prime example. The scientists who ran the clinical trial tried to cover all their bases: The participants were older adults who didn’t eat a lot of fish (which is rich in omega-3s), suggesting they might benefit the most from a supplement. Roughly half of the participants had an increased genetic risk for Alzheimer’s, which is another group that experts think might need more omega-3s. The researchers even did lumbar punctures on some of the participants to confirm that the supplement caused omega-3 levels in the brain to go up. But compared with a placebo, the supplement didn’t result in any benefit when it came to people’s cognition or brain structure. So what’s behind the disconnect? Scientists have a few hypotheses, and most are connected to diet and lifestyle. © 2026 The New York Times Company

Keyword: Development of the Brain; Alzheimers
Link ID: 30322 - Posted: 07.15.2026

Helen Pearson Sometimes, Kristine Yaffe will hear a poignant question from someone at her memory clinic. “I walk five miles a day, don’t drink and play bridge,” they’ll say, “so why do I have Alzheimer’s disease? Yaffe, a neurologist and dementia specialist at the University of California, San Francisco, finds it difficult to explain that even if someone does everything they can to lower the risk of dementia, there’s no guarantee they’ll avoid the condition. Her struggles mirror a challenge in her field. Studies have identified a list of virtuous lifestyle choices associated with a reduced dementia risk, including a healthy diet, physical exercise and social and cognitive stimulation. Research has also pointed to some less obvious factors linked to lower risk, such as treating vision and hearing loss and, potentially, receiving a shingles vaccine. The trouble is that it’s hard to work out how much doing any — or all — of these things helps to reduce risk in the real world. That’s not for lack of trying. A growing number of ambitious clinical trials have tested the effects of lifestyle interventions, providing people with intensive help to improve their diet, exercise regime, social connections and heart and brain health. These include the FINGER trial1, which involved some 2,650 participants testing a two-year lifestyle overhaul in Finland, and the multimillion-dollar POINTER study2, which tested a similar approach in the United States. These and other studies have suggested that lifestyle programmes can boost cognitive performance. But these intensive interventions seem to help only slightly — a benefit equivalent to a modest boost on some memory tests. None has been shown to reduce the incidence of dementia, and critics argue that such programmes are costly and difficult to scale up. Other trials, including offshoots of the FINGER study in the Netherlands and in 12 Latin American countries, will announce their results this month, and the World Health Organization will release its new dementia risk-reduction guidelines on 16 July. Deciphering the most effective ways to cut risks is important for researchers, clinicians and the public alike — especially given that the number of people with dementia worldwide is expected to soar in decades to come. © 2026 Springer Nature Limited

Keyword: Alzheimers
Link ID: 30321 - Posted: 07.11.2026

Stephanie Dorais You slide your hand into your coat pocket and find an old, folded $100 bill. In the other pocket, you find a coin. Now, here’s the gamble: flip the coin. Heads, you win another $300. Tails, you hand over your $100 bill. Do you take the risk? Mathematically, you should. One coin flip gives you two equally likely futures: in one, heads, you gain $300; in the other, tails, you lose $100. Because each future has a 50 per cent chance of happening, you count half of each outcome: half of $300 is $150, and half of $100 is $50. Balance those against each other, and taking the gamble puts you $100 ahead on average. Decision scientists call this positive expected value. Even when someone grasps the mathematics, however, it’s hard to take the risk. Why? About 50 years ago, the psychologists Amos Tversky and Daniel Kahneman showed that this hesitation is not random. People depart from logic in patterned ways. One of the most durable patterns is loss aversion: our tendency to feel the pain of losing more sharply than the pleasure of an equivalent, or even greater, gain. This is where mindfulness becomes interesting. Mindfulness is usually defined as paying attention to the present moment, on purpose, without immediately judging what is happening. In practice, that can mean noticing a thought before believing it, feeling an emotion before acting on it, or returning attention to the body, the breath, or the world around you. At its simplest, mindfulness creates a pause between what arises in the mind and what we do next. That pause helps because many of our choices are made before we have fully examined them. We may think we are deliberating over the coin toss, but often the body has moved first: recoiling from loss or preserving a decision simply because we have already invested in it. These mental shortcuts are called cognitive biases, and the study of this kind of human misjudgment is central to decision science. © Aeon Media Group Ltd. 2012-2026.

Keyword: Attention; Emotions
Link ID: 30319 - Posted: 07.11.2026

By Azeen Ghorayshi In early June, Ally Betchan and her family made the monthly trek from their small central Texas town to a therapy center in Austin, hoping that she could learn to communicate. Like nearly 30 percent of people with autism, Ally is severely disabled and does not speak. Ally, 22, sat quietly in a small room next to her instructor, Soma Mukhopadhyay, a sprightly 63-year-old who, by contrast, talked almost nonstop. More than 30 years ago, Ms. Mukhopadhyay taught her nonspeaking autistic son, Tito, to write and type independently, creating a communication method that supporters hailed as transformative and critics have challenged ever since. Ms. Mukhopadhyay held up a clear plastic sheet marked with the alphabet, prompting Ally to make up a story. As Ally tugged rhythmically at her purse, she slowly pointed at letters to spell “DONNA KNOWS,” and then seemed to get stuck, pointing to a jumble of letters. “I’m so lost,” Ms. Mukhopadhyay said, shaking the sheet and pressing her to try again. As Ms. Mukhopadhyay occasionally tapped under the letter board on her thigh or leaned in the direction of a letter, Ally eventually spelled: “CARING HURTS.” “‘Donna knows caring hurts’ — that is a life lesson,” Ms. Mukhopadhyay said, nodding in agreement. Then, Ally jabbed many letters in quick succession, but distinctly: “SHE LOVES THOSE WHO CARE FOR HER.” Sitting beside her, Ally’s mother, aunt and grandmother smiled. Ms. Mukhopadhyay’s technique, called the Rapid Prompting Method, or R.P.M., is one of several intended to help nonverbal people learn to communicate using letter boards held in midair by another person. At the core of these assisted spelling methods is a radical assertion: that nonspeaking autistic people, many of whom have been considered intellectually disabled their whole lives, may have typical or even extraordinary cognitive abilities, obscured by motor problems and an overwhelmed sensory system that has cut them off from the world around them. © 2026 The New York Times Company

Keyword: Autism; Language
Link ID: 30314 - Posted: 07.08.2026

By Natalia Mesa To accurately navigate the world, an animal must learn, remember and continually update how its body position relates to what it sees in the world around it. New findings reveal the circuit mechanisms responsible for this process in fruit flies—and upend a widely held assumption that this kind of learning relies on dopamine. The research “solves this long-standing problem of how you learn about landmarks in the world,” says Lisa Giocomo, professor of neurobiology at Stanford University, who was not involved in the study. “Over the last decade, some of the biggest insights into how the brain generates algorithms for navigational systems have come from Drosophila,” she says. “It’s been astonishing to see what’s been possible with that system.” When a neuron in a fly’s internal compass activates at the same time as a cell responding to a visual landmark, a third type of cell called an EL neuron releases the neuromodulator octopamine onto the visual inputs, according to the work, posted as a preprint in December 2025 and presented at the Jane Coffin Childs Symposium in May 2026. Octopamine acts as a signal that modifies the connection between the compass and visual cells, anchoring the fly’s sense of direction to visual cues. To their knowledge, the synaptic and circuit mechanisms the fly uses to update its internal compass work unlike any yet described, the study investigators say. “It’s a completely new learning mechanism, basically,” says Stanley Heinze, senior lecturer of sensory biology at Lund University, who was not involved in the study. Fruit flies, like other animals, have an internal compass made up of head direction cells that selectively activate based on the direction the fly faces. The fly’s internal representation of the world drifts without visual input but quickly reorients when familiar landmarks reappear. © 2026 Simons Foundation

Keyword: Learning & Memory; Evolution
Link ID: 30313 - Posted: 07.08.2026

By Giorgia Guglielmi Neuroscience textbooks have long cast mitochondria as pure neuronal powerhouses: These bean-shaped organelles just crank out a cell’s energy. That picture, however, is starting to look incomplete. Mitochondria do far more than fuel neurons, a growing body of research suggests. They also appear to help synapses communicate, regulate neurotransmitter release and shape social behavior. Mitochondrial function has also been tied to autism and related neurodevelopmental conditions, though that link remains debated. Even memory formation may lean on these tiny, double-membraned structures, according to a study published in Nature Metabolism in February. Increasing mitochondrial metabolism boosted long-term memory in both fruit flies and mice. Mitochondria are “not just permissive but also instructive,” says Ezgi Hacisuleyman, assistant professor of molecular medicine at the Herbert Wertheim UF Scripps Institute for Biomedical Innovation & Technology, who was not involved in the February study. Her unpublished results show that mitochondrial proteins are translated near active synapses, for example. Over the past decade, work from Hacisuleyman and others has fast expanded the repertoire of mitochondria in the brain. Taken together, she adds, the findings put mitochondria “more in the center of how we think about brain function and memory.” Mitochondria may be central to brain function, but they are not central inside neurons. Many synapses sit hundreds of micrometers away from a cell’s soma, so small, mobile mitochondria must travel there to deliver fuel in the form of ATP. In dendrites, mitochondria often linger near spines, and activity recruits them to presynaptic boutons, where they help stabilize neurotransmitter release. © 2026 Simons Foundation

Keyword: Development of the Brain; Obesity
Link ID: 30310 - Posted: 07.04.2026

By Henry Taylor & The Conversation US You know that feeling when you walk into a room and immediately forget why you came in? Maybe you were there to fetch your keys. On your way to the room, you were thinking about grabbing your keys. But once you arrive, your keys have completely disappeared from your mind. This is sometimes known as the doorway effect, since it often strikes when you walk into a new room. Why does it happen? The answer has a lot to do with a faculty called working memory. Information gets stored in working memory when we need it for the tasks that we are engaged in right now (like remembering to grab your keys). What makes working memory so intriguing is its close link to consciousness. The doorway effect suggests that when information is removed from working memory, it immediately seems to leave consciousness. It also suggests that it is easy for information in working memory to be forgotten. The link between working memory and consciousness is getting increasing attention in psychology, philosophy and neuroscience. Could working memory somehow give rise to consciousness? In my new book, I explore the complex relationship between the two. Working memory: both rich and poor To understand the doorway effect, we’ll need to know a bit about working memory. One thing that makes working memory so special is that it’s so rich, both in terms of the information it has access to, and its processing power. According to recent models of working memory, it can draw information from sensory channels (vision, touch, smell etc), as well as from other memory systems such as long-term memory and also the brain’s system for processing language. In other words, working memory is where a lot of the information in your brain comes together. Once working memory has that information, there’s a lot it can do with it. Inside working memory are a host of different smaller systems for specific tasks, including visual and spatial reasoning (like solving a Rubik’s cube) and storing chunks of information (like a phone number). There’s even a “central executive” system (my favorite). The executive is like a merciless boss, assigning tasks to the different systems within working memory and keeping everything under control. © 2026 SCIENTIFIC AMERICAN

Keyword: Consciousness; Learning & Memory
Link ID: 30309 - Posted: 07.04.2026

By Jake Currie Memory loss is by far the most notorious symptom of Alzheimer’s disease, but it might not be the initial sign of the illness. According to a new study published in Nature Communications, there’s an even earlier tell—impaired cognitive flexibility. Cognitive flexibility is one of the brain’s executive functions governing our ability to switch between different tasks, adapt to novel situations, learn new rules, and so on. To study changes in this vital function, neuroscientists at Texas A&M University used mice genetically engineered to produce the amyloid-beta plaques associated with Alzheimer’s disease (5xFAD mice). The team conditioned the mice to learn that a particular action (pulling a lever) led to a reward (a delicious food pellet). They then changed the rules to find out how they reacted. Healthy mice had no trouble adapting to the new regime, but the 5xFAD mice struggled, often repeatedly pulling the original lever without receiving a reward. Importantly, these cognitive flexibility problems surfaced earlier than the kinds of memory problems typically associated with Alzheimer’s. “We found that this function was impaired before we could detect deficits in spatial memory,” study author Jun Wang said in a statement. Taking a closer look into the 5xFAD mice brains, the researchers discovered abnormally high levels of neuroactivity in the medial prefrontal cortex, a region involved in decision-making and behavioral flexibility. Previous research has shown this kind of hyperactivity can lead to amyloid-beta plaques piling up, which in turn makes neurons even more excitable. It basically leads to a positive feedback loop.

Keyword: Alzheimers; Attention
Link ID: 30307 - Posted: 07.04.2026

By Nora Bradford Mirrors are tricky. Even humans aren’t born with an intuitive understanding of them; we have to learn how they work. Now, scientists have discovered that the California two-spot octopus (Octopus bimaculoides) can also learn to use mirrors, researchers report June 3 in Current Biology. When brainstorming octopus experiments, Mary Kieseler, a neuroscientist at the University of Fribourg in Switzerland, had wondered whether the famously smart creatures could pass the mirror test, which evaluates if an animal can identify itself in a mirror. Because of the challenging logistics the mirror self-recognition test would entail underwater, Kieseler and her team decided to first study whether octopuses could use mirrors as a tool to do something they’re already great at. And octopuses are great at hunting prey. The team began by habituating three wild-caught octopuses to a mirror covering half their tank. They let the octopuses hide from the mirror and even explore the other half of the tank behind it. After the octopuses became comfortable with seeing their reflection and eating in front of the mirror, the team gave them a task: Find a hidden jar with a tasty crab inside, placed where the snack could be found using only its reflection in the mirror. Initially, the octopuses approached the mirror, then turned around to find their prey. But after about 10 to 12 trials, each animal learned to crawl directly to the crab without the mirror pit stop. When using real crabs, there was no way to know whether the octopuses might have been relying on smell or another nonvisual sense to hunt, so Kieseler and her team came up with one final test. Rather than using real crabs, the team used virtual ones. © Society for Science & the Public 2000–2026

Keyword: Intelligence; Learning & Memory
Link ID: 30305 - Posted: 07.01.2026

By K. R. Callaway Strutting and fluttering around cities, pigeons have adapted to an ever-shifting environment. But their environment isn’t the only thing that’s constantly changing. New research suggests the birds themselves avoid stability in their decision-making, instead choosing to live “at the edge of chaos.” As model species for learning and behavior, these birds are helping researchers test a century-old law about how humans and other creatures learn. When learning something new, people and animals alike tend to repeat behaviors that are rewarded. First proposed by Edward Thorndike in 1898, this principle is so well established in psychology that it's become known as the law of effect. But the law implies that beyond making a behavior more frequent, rewards also make it more consistent: reducing variability in the specific way behaviors are performed over time. Although scientists have repeatedly tested whether rewards increase the frequency of behaviors, their effect on consistency is less well studied. University of Iowa experimental psychologist Edward A. Wasserman and his colleagues decided to put it to the test in pigeons—a species that has been integral to the study of learning at the university’s Comparative Cognition Laboratory for more than 50 years. And the study’s results, published in the Journal of Experimental Psychology: Animal Learning and Cognition, suggest these birds experience variability as the spice of life. To see how rewarded behaviors vary, the researchers gave pigeons a series of five colorful buttons to peck. They could peck any buttons in any order, but as long as they pecked five times, a treat would appear. Based on previous theories of learning, the scientists expected the pigeons might eventually slip into a routine—perhaps choosing to repeat patterns they know work or simply pecking the button nearest to them five times. Instead they continued pecking in a variety of patterns. © 2026 SCIENTIFIC AMERICAN,

Keyword: Learning & Memory; Evolution
Link ID: 30304 - Posted: 07.01.2026

By Michael Howerton Healthy brains may be built through a process of controlled damage and rapid repair. The most dangerous type of DNA damage is a regular feature of healthy early brain development, experiments in mice show. As newborn neurons squeeze through the cramped, narrow spaces of developing brain tissue, they break both strands of their DNA, researchers report June 17 in Nature. The breaks are repaired once neurons reach their destination, usually within a day. It’s a paradox of vulnerability and resilience. Newborn neurons routinely sustain a kind of damage that kills most cells, yet they repair it and emerge intact, the researchers found. The speed of the repair surprised the team. “Somehow neurons can repair [the damage] very quickly without any sign of mutations or bad effect,” says neurobiologist Mineko Kengaku of Kyoto University in Japan. “It seems to be a normal developmental event.” The breaks appear in areas of the genome that aren’t crucial, the team found, which in most cases allows neurons to survive and grow without lasting damage. “It is surprising that, during evolution, the mammalian brain acquires such a clever strategy,” Kengaku says. More research is needed to understand the implications beyond mice, but Kengaku says the effect might even be more pronounced in humans. “During development, neurons have to migrate, and if the brain size is larger, then neurons have to migrate longer distances,” she says. “It is quite likely that neurons in human brains probably generate more DNA damage during development” than neurons in mice brains do. But a flawless break-and-repair cycle is not always guaranteed, Kengaku says. When it fails or is incomplete, the damage could persist. These instances, she says, could help explain some neurological conditions later in life. © Society for Science & the Public 2000–2026.

Keyword: Development of the Brain; Neurogenesis
Link ID: 30302 - Posted: 06.27.2026

By K. R. Callaway In the flatwoods of South Florida, tiny brown birds emerge from the underbrush to sing from the branches of pine trees. To human ears, their songs sound nearly identical, but any given population of these birds — Bachman’s sparrows — uses as many as 120 different song types to communicate. Like human language, birdsong is dynamic. Every avian generation makes choices about which songs to continue singing, which to improve upon and which to drop altogether. A single Bachman’s sparrow might learn only 48 of the songs used by its community, and for decades researchers have been trying to figure out how baby sparrows choose which songs to adopt. Previous studies have focused on social and cultural factors. During their critical song-learning phase of development, young songbirds imitate the adult males in their group who are successful in courtship or have elaborately ornamented plumage. Now, a new study of Bachman’s sparrows reveals another possible part of the equation: the physical environment. Trees, dense shrubs and even wind can scatter or block the transmission of some sound waves, and researchers suspect that young sparrows are less likely to latch onto degraded songs, leading in turn to some songs becoming rarer than others. “The rarer song types don’t propagate quite as well over distance than the common ones do,” said Rindy Anderson, a behavioral ecologist at Florida Atlantic University and an author of the study, which appeared on March 24 in the journal Bioacoustics. All the Bachman’s sparrow song types have a similar form, with a buzzing or whistling note followed by a trill. Some trills are faster or slower than others, and some complex songs contain trills of several frequencies. Researchers recorded a variety of rare and common sparrow songs and then rerecorded them playing in different environments — among dense trees, windy plains and other places that Bachman’s sparrows frequent but that could distort audio signals. Under these conditions, the researchers found that rarer songs did not propagate as well as common songs. © 2026 The New York Times Company

Keyword: Language; Evolution
Link ID: 30300 - Posted: 06.27.2026

By Calli McMurray Kanga the marmoset places her hand on the lever and looks at Dodson, a fellow marmoset working with her on a task. As it becomes apparent that Dodson is ready to pull his own lever, neurons in Kanga’s dorsomedial prefrontal cortex ramp up their firing. The activity reaches its peak as Kanga decides to pull the lever, in sync with her partner. As a reward for their coordinated effort, both marmosets earn a sip of liquid marshmallow fluff. This type of neuronal computation underlies the “evidence accumulation model,” a major theory of how perceptual decisions are made: The brain gathers evidence and executes a decision once the evidence reaches a certain threshold. The marmoset study, which was published last month in Neuron, demonstrates that the model also applies to social decisions. This result wasn’t a given; making a social decision relies on the changing behavior of another animal, and the actions of the decider can influence what the other animal does, says study investigator Monika Jadi, associate professor of psychiatry and neuroscience at Yale University. “It’s a very recurrent system,” she says. Support for the evidence accumulation model has come largely from highly controlled experiments; the fact that the same activity pattern appears in a social and less constrained task “implies that this is a generalizable computation,” says Timothy Hanks, associate professor of neurology at the University of California, Davis, who was not involved in the work. Social, perceptual, foraging and other decisions are “categories we’ve created,” but there may not be anything “acutely different” about them, says Cory Miller, professor of psychology at the University of California, San Diego, who was not involved in the study. “I love this line of work; I think it’s super powerful.” © 2026 Simons Foundation

Keyword: Learning & Memory; Emotions
Link ID: 30297 - Posted: 06.27.2026

By Jackie Rocheleau The cerebellum, the wizened “little brain” nestled in the base of the skull, may help keep us sharp as we age. Regions at the back of the cerebellum that resisted shrinkage with age were tied to better mental functioning, or cognition, even in people in the early stages of Alzheimer’s disease, researchers report June 10 in Nature Neuroscience. Though traditionally thought of as a movement control center, scientists now know the cerebellum is a key player in cognition. Researchers also know that parts of the cerebellum don’t age in unison, but the aging cerebellum is a relatively new area of research. In the new study, the team first analyzed brain scans and cognitive test scores from more than 700 U.S. adults whose data was collected as part of the Human Connectome Project, a brain mapping initiative. The test measured abilities including short-term memory, attention, language and visualizing 3-D objects. A clear trend emerged: The cerebellum tended to be smaller with increasing age, but the bigger the cerebellum, particularly in regions in the rear of the little brain, the higher the score on cognitive tests. The trend held even after adjusting for the different levels of education among participants, Princeton University neuroscientist Frederick d’Oleire Uquillas and colleagues report. The researchers found the same link in more than 35,000 adults in the U.K. Biobank, a biomedical database. The findings point to a larger cerebellum preserving cognition with greater age, says d’Oleire Uquillas. The researchers confirmed that scans of the larger cerebellums showed more brain tissue and connections between nerve cells, a © Society for Science & the Public 2000–2026.

Keyword: Alzheimers
Link ID: 30295 - Posted: 06.24.2026

Zoe Beketova When Adam Douglass began to study the tiny, transparent fish in the Danionella genus about 10 years ago, he had to get his animals from an out-of-state fish shop, where they were sold as an exotic pet breed. “The only information at all about trying to grow them in captivity came from online,” says Douglass, a neurobiologist at the University of Utah. Compared with zebrafish, which by that point had been a model species for biology research for decades, Danionella was little known to scientists. How things have changed. Last week, the Janelia Research Campus, the in-house research arm of the behemoth Howard Hughes Medical Institute (HHMI), announced a 10-year, roughly $1 billion research effort focused on using Danionella as a model for how brain cells and circuits drive complex behaviors in vertebrates. The effort will also draw on cutting-edge artificial intelligence (AI) tools to make sense of all the new data on the fish. “I think this is one of the most exciting opportunities that we’ve faced in the entire history of Janelia,” says neuroscientist Nelson Spruston, Janelia’s vice president and executive director. “There are a lot of structures in the brain and the rest of the body of fish that are identifiably similar to those of humans,” he adds, and there’s a long history of simple model organisms “leading to important insights that eventually result in cures and treatments for devastating diseases.” Danionella’s growing popularity comes from one (literally) clear advantage: Unlike zebrafish, which are transparent only for the first few weeks of their 3- to 4-year lives, Danionella remain so, meaning their brain is still visible—and easier to image—when they reach adulthood and engage in behaviors such as schooling, navigation, and courtship. The fish, only about the size of a grain of rice, never grow scales, develop pigmentation, or form a complete, bony skull. “All of these features that stand in the way of being able to get photons into and out of your skull [for imaging] are not there,” says Douglass, who has watched Danionella become a focus of dozens of labs worldwide

Keyword: Development of the Brain; Brain imaging
Link ID: 30294 - Posted: 06.24.2026

By Kathryn Hulick Emma Lembke joined Instagram at age 12. Soon, she found herself “scrolling mindlessly for hours, addicted to gaining a certain number of likes, a certain number of comments.” She often wanted to stop — but couldn’t. She’s not alone. Most of us these days know the feeling of mindlessly scrolling through low-quality content. We call this sensation “brain rot.” The term can also refer to the content being consumed. Tung Tung Tung Sahur, a personified wooden drum (illustrated above), is one in a slew of silly AI-generated characters deemed “Italian brain rot” because many of them have Italian-sounding names. Trendy among middle schoolers, these absurdist characters show up in memes, videos, Roblox games and more. Brain rot is kind of a joke, but it also really isn’t. A growing number of young people and their parents claim that spending too much time on social media, the spawning ground for brain rot, can mess with mental health. Thousands of cases accusing social media companies of harming young users with addictive features are now making their way through U.S. courts. In May, the U.S. government released a Surgeon General’s warning about the harms of screen use for young people, calling out social media as well as gaming, chatbots and more. “Policy makers and tech companies need to acknowledge the potential for harm and create frameworks to protect children to allow for healthy and joyful use,” states the warning, which includes a disclaimer that the document was edited using the AI tool ChatGPT. But the term “brain rot” evokes something more pernicious. Could browsing through stupid content actually make us stupid? This fear isn’t new. Back in 2009, the former CEO of Google, Eric Schmidt, voiced concerns about how digital media was impacting young people’s intelligence: “I worry that the level of interrupt, the sort of overwhelming rapidity of information … is in fact affecting cognition,” he said in an interview with talk show host Charlie Rose. © Society for Science & the Public 2000–2026

Keyword: Attention; Learning & Memory
Link ID: 30288 - Posted: 06.20.2026