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

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