Emma Bryce Sperm whales produce a specific pattern of clicking noises when they hear the noise of boats, researchers have found. The pattern is so distinct that the scientists who identified it said they can now use it to predict when ships are nearby. Researchers from Project Ceti (the Cetacean Translation Initiative), a non-profit research organisation working to decode sperm whale communication, spent four years tuning in on the calls of 15 sperm whales off the coast of Dominica. They discovered specific differences in sperm whale “codas”, the discrete and distinctive patterns of clicks that this species utters to communicate when those whales encountered shipping. Individual click sequences became shorter, and one type became more prominent than another. Their findings are published in the journal Ecological Informatics. “This research begs the question: are whales talking about the ships, or is it an impact on their voices because the ships are around?,” said David Gruber, the founder and chief executive of Project Ceti. “And then if we’re able to discern what they’re saying about the ships, how might that impact policy and laws?” Under normal conditions, recordings from one of the whales, named “Atwood”, picked up one type of coda comprising five clicks in a 1-1-3 pattern (two clicks preceding three quicker ones), which, Gruber explained, is unique to this specific clan of sperm whales off the Caribbean coast of Dominica. With the background hum of a ship, Atwood issued the same 1-1-3 click rhythm but noticeably faster, with the whale reducing the intervals between each click. The association was so strong that “in general, from their vocalisations alone, we can predict whether ships are around,” said Gašper Beguš, linguistics lead at Project Ceti. © 2026 Guardian News & Media Limited

Keyword: Animal Communication; Evolution
Link ID: 30338 - Posted: 07.22.2026

By K. R. Callaway You (probably) won’t find a monkey in a geometry class, but it looks like our fellow primates can swing the basics. Just like people, monkeys seem to grasp the abstract qualities of geometric shapes, such as whether they are symmetrical, have parallel sides or contain right angles, according to a new study published on Monday in Proceedings of the National Academy of Sciences. This ability allows the monkeys — and us — to understand when two shapes are the same, even when they’ve been rotated or resized. This finding challenges a long-held notion that humans’ geometric abilities are part of what makes our brains one of a kind. “Our hypothesis was that humans are not that unique,” in possessing this mathematical understanding, said Jialin Li, a cognitive neuroscientist at Carnegie Mellon University and the lead author of the study. In their experiment, Ms. Li and her colleagues decided to give monkeys (a total of eight rhesus macaques and olive baboons), preschoolers and adult humans with different education levels the same geometric task. That way, if humans truly had an innate advantage, it would show up when comparing the young children and the monkeys. And if the advantage was learned, it might show up when comparing the humans who had different levels of schooling. It was a challenge to find a task simple enough that even preschool-aged children and monkeys could reasonably complete it, but the team eventually decided to have all the study participants do a matching task. All were shown a shape with a specific size and geometric form on a screen. Then they were asked to pick that same shape out of a group of others. “By manipulating the similarity of the shapes, we were able to look at what kinds of rules they’re using,” said Jessica Cantlon, a cognitive neuroscientist at Carnegie Mellon University whose lab conducted the study. © 2026 The New York Times Company

Keyword: Vision; Learning & Memory
Link ID: 30337 - Posted: 07.22.2026

Lynne Peeples Every heartbeat is choreographed not just by the brain but also by a mysterious nervous system embedded in the heart itself. Now, scientists studying mice have started to unravel how this complex system works to keep the heart beating steadily even at times of extreme stress — findings that challenge the classic view that all cardiac neurons are alike. “The key is to keep the heart functional no matter what happens. Because if the pump function stops, you will die,” says Rui Chang, a neuroscientist at Yale University School of Medicine in New Haven, Connecticut, and co-author of the new paper. The findings, published today in Cell1, could inform better treatments for heart disease. Like the gut’s widely recognized ‘second brain’, the heart contains a mini-brain of its own — known, more formally, as the intrinsic cardiac nervous system. This network of neurons is embedded in the fat pad surrounding the heart. The system’s neurons exchange messages with the brain and with each other, and are the final players in a long chain of neurons that controls cardiac function. But because intrinsic cardiac neurons are exceedingly rare, making up only about 0.01% of the cells in a piece of heart tissue, their precise roles have been hard to pin down, says Chang. Damage from a heart attack comes from brain signals, mouse study suggests To fill that gap, his team genetically engineered mice to label all of the animals’ cardiac neurons. The scientists sequenced genes isolated from these neurons and identified markers for two neuronal subtypes. They then used techniques such as high-resolution imaging to identify the genetically distinct subtypes’ core functions and to map their locations. © 2026 Springer Nature Limited

Keyword: Emotions
Link ID: 30336 - Posted: 07.22.2026

BY Christie Wilcox Goats spend a lot of time bashing their heads into things. Winning a headbutting contest shows other members of the herd who’s boss—but bumping heads is also a way to play or explore new objects, so it’s often assumed goats must be protected against head injury by the shape of their skull and strong neck muscles. A new study challenges that assumption. Researchers have found early signs of neurodegeneration in headbutting goats at just 1 year old, they report in a preprint posted to bioRxiv this month. The findings, they say, suggest goats could be a useful animal model for studying the link between head injuries and neurodegeneration seen in humans. “I think the overall conclusions are pretty convincing,” says Ramon Diaz-Arrastia, a neurologist at the University of Pennsylvania who was not involved with the work. Traditionally, researchers have used rats and mice as animal models for studying brain injuries, and the field has become a “rodent monoculture,” he says. But rodent and human brains are very different, which could be partly to blame for the poor translation of preclinical findings to human trials, so it’s “really interesting to see this work in goats.” Nicole Ackermans, a neuroscientist at the University of Alabama, first identified signs of neurodegeneration in wild headbutting animals in 2022, finding that the brains of dead muskoxen contained an abnormal version of the protein tau. In humans, these tangled tau proteins are associated with neurodegenerative diseases such as Alzheimer’s, and can form after head injuries. “I thought, ‘OK, this is something really interesting to look at for modeling brain damage,’” she says. But tracking how damage accumulates over time in wild animals is not feasible. That’s where the goats came in. The team acquired three 6-month-old male goats—Alvin, Simon, and Theo—from farms and moved them to a nearby agricultural college where cameras recorded them for 6 months to track their headbutts. Each month, the researchers collected samples of blood, saliva, and brain fluid to look for biomarkers of brain injury and, at the start and end of the study, scanned the animals’ brains using positron emission tomography–MRI to spot any structural damage. © 2026 American Association for the Advancement of Science.

Keyword: Brain Injury/Concussion; Aggression
Link ID: 30335 - Posted: 07.22.2026

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

Ian Sample Science editor A man who was paralysed from the chest down in a swimming accident six years ago has been able to feed himself and drink from a cup thanks to a brain implant that bypasses his spinal cord injury. Keith Thomas of Massapequa, New York, could not lift his arms off his wheelchair when he agreed to trial the technology in 2021, but after surgery to implant electrodes in his brain and many months of training, he was able to move the limbs again. Researchers fitted Thomas with a brain-computer interface that not only helped him move his arms and hands, but also sent signals back to his brain to recreate the sensation of touch. He has since been able to feel his sister’s hand and the fur on his pet dog. Remarkably, the technology appears to have partly rewired Thomas’s nervous system, helping to restore some hand functions and sensations that remain even when the system is switched off. “For me this is an incredible moment,” said Prof Chad Bouton, whose team developed the technology at the Feinstein Institutes for Medical Research, the research arm of the New York healthcare provider Northwell Health. “For years, we have been wanting to really tackle the restoration of movement and the sense of touch and bring those together and we’ve also wanted to create lasting effects,” Bouton added. “I think we’re going to continue to see progress and I think it’ll be applicable to the millions of folks around the world who really need this technology.” Thomas was 42 when he broke his neck diving into a swimming pool in July 2020. He blacked out and regained consciousness to see a helicopter on the front lawn. He was immediately taken to hospital. “The next day I couldn’t even move,” he said. The following October, he joined a three-year clinical trial of what the researchers called a “double neural bypass”. It uses electrodes implanted into Thomas’s brain to detect when he wants to move his arms. The signals are then routed to his arms and hands to move them. © 2026 Guardian News & Media Limited

Keyword: Robotics
Link ID: 30331 - Posted: 07.18.2026

By Rachel Nuwer It was 9 a.m. on a Thursday, and Martin Picard was watching his blood flow from an IV in his arm through a hole in the wall. He was sitting on a twin bed in a claustrophobic chamber less than a shoulder’s width from a stainless steel sink and porcelain toilet. Every hour over 24 hours, including while he slept, a nurse channeled blood from his arm to a research team next door; at each time point, if he was awake, he also provided a saliva sample and filled out a survey about his mood. The room looked like a cell, or perhaps a very cramped hotel room, but in fact it was a metabolic research chamber, one of only 50 of its kind in the world. Its conspicuously small size prevented Picard from burning extra energy beyond the bare minimum needed to keep him alive. Napping during the day was prohibited, as was eating anything but the strictly scheduled meals tailored to his caloric needs. Bedtime was at 11 p.m. sharp. Before lights-out, Picard put on a device to monitor his vitals and brain activity while he slept. Though there wasn’t much to do — mostly he sat in bed reading or working on his laptop — excitement was the primary emotion Picard felt that day in July 2021. That’s because he was the first volunteer in an experiment run by the Mitochondrial Psychobiology Lab (opens a new tab), which he directs at Columbia University Irving Medical Center in New York. By studying how much energy is required to sustain baseline existence, his lab aims to explore what he considers an overlooked factor in health and disease, from the level of molecules all the way up to the mind: mitochondria. Most middle school students learn that mitochondria are the powerhouses of the cell. These organelles make adenosine triphosphate (ATP), the energy currency of life, through a cascade of chemical reactions that breaks down glucose and fat from food. But mitochondria are much more than energy factories. Studies over the past decade have shown that they process all sorts of molecules, including neurotransmitters, hormones, and metabolites, which means they directly impact what we experience as mood, stress, sexual arousal, and the need to sleep. This makes them “the consilience point for many known processes demonstrated to underlie consciousness,” Picard said. © 2026 Simons Foundation

Keyword: Consciousness; Evolution
Link ID: 30330 - 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

Laura Russo A surprisingly large number and diversity of bee species – 74 out of 96 tested – have magnetic properties, according to research my colleagues and I recently published in the journal Science Advances. Some animals are able to use iron-based magnetic compounds such as magnetite to detect and navigate via the Earth’s magnetic field – a sense called magnetoreception. We considered magnetism in the insects we tested to be a proxy for which species might be magnetoreceptive. For decades, biologists have known that social, cavity-nesting honeybees exhibit magnetoreception. Most researchers assumed that this internal compass was tied to living in a colony; honeybees communicate the location of floral resources to other colony members through a dance that indicates direction relative to the position of the Sun and the geomagnetic field. Our study had two goals: to compare magnetism between bee species that live in groups versus on their own, and to track down the evolutionary origin of magnetoreception in bees. To test magnetic responses, we collected bee specimens from across the bee family Apidae, which includes social species such as honeybees along with solitary species such as chimney bees. We ground dried dead bees into a powder, then measured how magnetic this powder was in a magnetometer. To our surprise, we found that the magnetic response was strong in both bees that live in groups and those that live alone. This result forced us to reject our initial hypothesis that magnetism was necessary only for social bee species. - © 2010–2026, The Conversation US, Inc.

Keyword: Animal Migration
Link ID: 30328 - Posted: 07.18.2026

By Alissa de Chassey A hallmark of deep sleep—slow-wave brain activity that arises when cortical neurons cycle on and off synchronously between 0.5 and 4 Hertz—may drive some of sleep’s restorative functions, according to a new study published last month in Nature Neuroscience. “We provided direct evidence that these on and off patterns are what really matter,” says study investigator Chiara Cirelli, professor of psychiatry at the University of Wisconsin School of Medicine. As slow waves travel across the cortex during deep sleep, the excitatory synaptic strength that accrued during waking hours gradually returns to a baseline, a process that helps to consolidate memories, according to the synaptic homeostasis hypothesis of sleep that Cirelli and her husband, neuroscientist Giulio Tononi, proposed more than two decades ago. Computational models and studies of anesthetized animals support the idea, but the field has lacked evidence from non-anesthetized animals. “Anesthesia and sleep may share some features, but definitely overall they are not the same thing,” Cirelli says. She and her colleagues used optogenetics to induce sleep-like on/off firing patterns in select regions of the cortex in awake mice. “The idea was to induce these patterns in awake mice, and see whether this is enough to get sleep benefits,” Cirelli says. As expected, the animals showed a decreased need for sleep; reduced neuronal synchrony and synaptic strength during sleep; and improved memory consolidation afterward. © 2026 Simons Foundation

Keyword: Sleep
Link ID: 30327 - Posted: 07.18.2026

By Natalie Wolchover When I was first learning to write, my letters and words ran from right to left, reversed as if in a mirror. Being left-handed, I was imitating the hand strokes of my right-handed teachers instead of reversing their strokes to replicate the letters. I gradually got the hang of writing in the correct direction, but it still feels natural for me to mirror-write. I have a mirror-written childhood diary. Leonardo da Vinci, another lefty, did that too. Being left-handed is mostly no big deal. It is annoying how ink smudges under my hand. And I did once have to jump out of the way of a circular saw that I was holding backward; indeed, left-handers have more accidents while operating machinery. That aside, overall, I enjoy being left-handed. It grants entry into a smug little club, whose members — 10% of the human population — carry the secret knowledge that we are overrepresented among U.S. presidents, famous artists and musicians, and top athletes. But our difference hasn’t always been welcome. My 91-year-old Texan grandmother remembers starting out left-handed (she, too, has examples of mirror-writing from early childhood) before being forced to switch, a common practice in much of the world until about the 1970s. The deep-seated disdain for left hands runs through our very language. “Left” comes from Old English lyft, meaning weak, foolish, worthless, or useless, while “right” means correct or proper. In other languages, the word for “left” can also mean awkward, unlucky, clumsy, suspicious, or sinister. In philosophy, “qualia” refers to the subjective qualities of our experience: what it’s like for Alice to see blue or for Bob to feel delighted. Qualia are “the ways things seem to us,” as the late philosopher Daniel Dennett put it. In these essays, our columnists follow their curiosity, and explore important but not necessarily answerable scientific questions. © 2026 Simons Foundation

Keyword: Laterality; Language
Link ID: 30326 - Posted: 07.15.2026

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 Jake Currie Humans are social animals, so seeing a fellow human face triggers a cascade of activity in our brains. Information about the age, gender, familiarity, emotional state, and more get processed within milliseconds. Now, new research published in the journal Developmental Cognitive Neuroscience suggests how our brains respond to faces in our youth could impact our social lives later on. ​​“Faces contain a lot of social information, and perceptually or cognitively humans process that information really, really quickly,” study author Myles N. Arrington said in a statement. “That makes it great for neuroscience, because as soon as you show a face to a person it doesn’t take long for their brain to respond.” Arrington and his fellow neuroscientists at the University of California, Davis studied brain activity of almost 6,000 children between the ages of 8 and 11 from the Adolescent Brain Cognitive Development Study. The kids were shown pictures of faces displaying positive, negative, and neutral emotions (which contain loads of social information) and places (which contain none) while their brain activity was monitored on an fMRI machine. Combining the fMRI results with two-year follow-ups, they found that increased activity in the amygdala—the brain’s fight-or-flight center—in response to faces was correlated with changes in their social lives. Interestingly, boys and girls with heightened amygdala activity had much different results later in life. Girls with more active amygdalas tended to have more involvement with peers two years down the road, while boys showed less involvement. According to the researchers, this could be due to differences in how the two genders are socialized. For example, “boys may be socialized to withhold intimacy and distance themselves from their peers,” the team wrote. It’s possible that this socialization can impact how their developing young minds process the social information contained in faces. © Copyright 2026

Keyword: Emotions; Sexual Behavior
Link ID: 30324 - 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

by Avery Hurt In 1950, researchers Hector Chevigny and Sydell Braverman set out to, as they put it, “demolish old fables about the emotional life of the blind” and demonstrate that the mental health issues of the blind are no different from those experienced by the sighted. But they did discover one big — and very surprising — difference: There have been no reported cases of schizophrenia in people blind from birth (or who became blind very shortly after birth). At the time, there was limited patient data available, so it wasn’t clear if this astonishing finding would hold up. But in the almost 80 years since, more national databases of mental illness have been maintained, and still no cases have been found, according to a study in Frontiers in Psychology. Is it just a coincidence? Or does never having been able to see somehow offer protection from schizophrenia? And if it does, how would that even work? Schizophrenia is a neurodevelopmental disorder that interferes with the way people interpret reality, Philip Corlett, a neuroscientist at Yale University who studies psychosis and delusional thinking, told Discover. Schizophrenia can cause symptoms such as hallucinations, disorganized speech and thinking, and in some cases, a lack of motivation or engagement with the world. However, the most familiar characteristic of the illness is what Corlett described as “departures from consensus reality,” or, put another way, believing things that most people in your culture don’t believe. Though the causes and mechanisms of schizophrenia are not yet well understood, one increasingly accepted theory is that the illness results from errors in prediction. To understand that, we need to take a look at how the healthy brain processes information. © 2026 Discover Magazine Inc

Keyword: Schizophrenia; Attention
Link ID: 30320 - 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