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

By Natalia Mesa If a longtime friend suddenly becomes a foe, like Brutus to Caesar or Iago to Othello, the brain must update the person’s feelings about the betrayer without altering memories of who that companion is. The hippocampus may sometimes store both pieces of information, but when it comes to updating feelings, it keeps identity and emotional valence separate, according to a mouse study published today in Science. “We found the neural mechanisms that underlie emotion toward others,” says study investigator Teruhiro Okuyama, professor at the Institute of Quantitative Biosciences at the University of Tokyo: Memory-storing neurons in the hippocampus remain relatively stable, but the strength of their connections to the basolateral amygdala neurons shift, the study shows. Okuyama and his colleagues used chemogenetics to induce aggression in previously docile mice and optogenetics to trace how hippocampal circuits change in the animal’s cagemate. They found that they could both “write and erase social memories” by targeting specific neuron populations. “It’s truly unbelievable how much they did in this paper,” says Robert Malenka, professor of psychiatry and behavioral sciences at Stanford University, who was not involved in the work. “They did a beautiful job of taking three brain areas and defining the connectivity and the cell-type-specific connections that are responsible for the phenomenon they’re studying.” Neurons in the hippocampus store social memories and segregate positive and negative ones, previous work shows. But most past work has studied how negative run-ins with unfamiliar animals affect behavior. © 2026 Simons Foundation

Keyword: Aggression; Sexual Behavior
Link ID: 30318 - Posted: 07.11.2026

By Jake Currie One theory, the social brain hypothesis, says we owe our massive noggins in part to the evolutionary pressure exerted by the demands of large social groups. Because we needed to keep a running tally of friends and foes to navigate thorny hierarchies and shifting alliances, we had to have brains that were up to the task (which is why this theory is also known as the Machiavellian intelligence hypothesis). In many animals, especially mammals, there does seem to be a correlation between social group size and brain size. But there’s at least one big exception to this rule: cephalopods. Cephalopods like octopuses have huge brains but aren’t really known for their gregarious behavior. They tend to live solitary lives, mating without forming pair bonds and reproducing without parenting their young. In fact, their behavior can stray into the downright anti-social—many species are territorial, aggressive, and cannibalistic. Still, they’re incredibly intelligent. Octopuses use tools, solve problems, and even like to play. So if sociality can’t explain big cephalopod brains, what can? In a new paper published in iScience, an international team of researchers proposed a new version of the cultural brain hypothesis. This hypothesis—first advanced by one of the authors of the current study—states that big brains evolved to handle mountains of information that are learned both socially and asocially. In this latest research, the team focuses solely on the asocial pathway to brain evolution. To test their asocial brain hypothesis, the team compiled data on cephalopod brain size as well as ecological, behavioral, and social factors from 79 cephalopod species. They found that several ecological factors seemed to correlate with big cephalopod brains, especially the complexity of their habitats. Cephalopods that lived on the ocean floor and in shallow pools—where cleverness can be rewarded with calorie-rich prey—tended to have larger brains. Sociality, on the other hand, showed no such correlation.

Keyword: Evolution
Link ID: 30317 - Posted: 07.11.2026

By Jim Robbins Imagine a chicken that could speak or a pigeon with a voice rivaling that of the most musical songbirds. Granted, the world probably doesn’t need any gossiping chickens or pigeons breaking out in song. But why some birds learn to create a deep repertoire and others are unable to has long been a research focus of the neurobiologist Erich D. Jarvis. “Vocal learning, just like spoken language itself, is a rare trait,” said Dr. Jarvis, who directs the Neurogenetics of Language laboratory at Rockefeller University in New York. He studies the small group of species capable of speech, focusing on birds and mice, and he has long hoped to genetically engineer an animal that can vocalize in new ways. Introducing manipulated genes into the brain of a bird or a mouse that doesn’t vocalize could create that ability and provide new clues into the origins of speech. It may also one day help in finding treatments for people with speech problems or brain disorders. Dr. Jarvis, 60, didn’t start his career in neuroengineering. He once hoped to become a professional dancer, performing ballet at Manhattan’s renowned High School for the Performing Arts and then studying at the Alvin Ailey dance school. He was a member of the Westchester Ballet Company when he began wondering how the brain was able to create dance movements. His mentor at Rockefeller was Fernando Nottebohm, the researcher who discovered in the early 1980s that songbird brains generate new neurons each spring to enable them to sing. That revolutionary understanding of neurogenesis led to further findings that all brains, including human ones, grow new neurons throughout life. Until then, it had been scientific gospel that people came into the world with a fixed number. From 2002 to 2005, Dr. Jarvis helped lead the Avian Brain Nomenclature Consortium, a project that renamed the regions of the avian brain to show that it was remarkably sophisticated. The research undermined the use of the term “bird brain” as a pejorative. © 2026 The New York Times Company

Keyword: Animal Communication; Language
Link ID: 30316 - Posted: 07.08.2026

By Sandy Ong On a Sunday afternoon in April, the main minibus terminal in Sukabumi, Indonesia, looked sleepy from the outside. But in an open space round the back, hundreds of men were gathered. Amid chatter and cigarette smoke, the air buzzed with excitement, for one of the region’s biggest bird-singing competitions was set to begin, and a motorbike was among the prizes. As the day progressed, dozens of songbirds were brought out for their 10-minute rounds, from tiny garden sunbirds and grey-cheeked bulbuls to larger oriental magpie-robins and orange-headed thrushes. Then the emcee announced the main event — the singing contest among the highly popular, strikingly handsome white-rumped shamas — and a hush fell over the crowd. The shamas’ owners murmured final words of encouragement and stepped away from their cages. Judges swept in with clipboards, assessing each bird for its song, ability to hold a steady tune, volume and showmanship. Soon it was down to a final two birds . . . and then “Baby White” was crowned the winner amid cheers from the crowd. Many men gathered on a patio beneath hanging cages holding songbirds Since the 1970s, songbird competitions have grown in popularity across Indonesia. With goats, motorcycles, watches and money (sometimes worth up to 10 years’ salary) up for grabs, the events are driving hordes of people to keep songbirds as pets. Indonesians have a long-standing culture of keeping birds as pets, and songbirds are especially popular, prized by collectors for their melodious singing and colorful plumage. “I keep songbirds as a hobby, to relieve stress and also gain a bit of money,” explained Harry Gunawan, a 78-year-old businessman and owner of 39 shamas, including the multiple prizewinning Baby White, while waiting for his new motorbike. Gunawan’s shamas are among an estimated 66 million to 84 million caged birds that are kept across Java, the island where 56 percent of Indonesia’s population lives and one in three households owns birds. These include more than 3 million white-rumped shamas and 2 million oriental magpie-robins. Wild birds are believed to be better songsters; hence, many are trapped in forests then crammed into tiny crates, drainpipes and even plastic bottles, destined for pet markets in Jakarta, Surabaya and other big cities. Birds that survive the journey — estimates of mortality rates range from 30 to 80 percent — will spend the rest of their lives confined to cages.

Keyword: Animal Communication; Language
Link ID: 30315 - Posted: 07.08.2026

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 Jeneen Interlandi In the mid-2010s, when they were still postdoctoral fellows at the Massachusetts Institute of Technology, Mathilde Poyet and Mathieu Groussin kept bumping into different sides of the same obstacle. Poyet, an ecologist and a microbiologist, was trying to study rare bacterial species, the kind that had never been grown in a lab before. Groussin, a computational biologist in the same lab, wanted to understand how humans and microbes evolved together over millenniums. Each was focused on microbes that make their homes in and on the human body, what scientists collectively refer to as the human microbiome. But the only samples they could find to work with came from the same small sliver of humanity, namely populations that were wealthy, Western and white. “About 90 percent of all human diversity has been completely left out of the picture,” Groussin told me recently. It was as if someone had shone a bright flashlight on one small segment of a giant canvas and left the rest shrouded in darkness. The bright spot was well defined (imagine the face of a man). But they couldn’t really tell what they were looking at (whether that man was a monk, for example, or a matador) without seeing the rest of the canvas. Scientists refer to this vast, unexplored terrain as biology’s dark matter. Our bodies are home to more bacteria — on our skin, up our noses, in our guts and mouths and around our genitals — than there are stars in the Milky Way. These microbes have evolved not only with us but inside us, and scientists who study them closely say that hardly a biological process or system exists in which they do not play a role. They helped create our digestive systems and our immune systems. They influence the size and shape of our bodies. At least some research suggests that they also affect our brains, moods, personalities and behaviors. And yet, most of them have still not been identified, let alone studied. It was tantalizing to think about what a fuller picture might reveal. In recent years, scientists had linked the gut microbiome to a long list of conditions, including Crohn’s and irritable bowel syndrome, Parkinson’s, dementia and autism, and they were hopeful that a better understanding of those links would lead to treatments, if not cures. They were also sifting through the nearly unfathomable array of molecules that microbes produce, in search of biological treasures: not only potential medications but also compounds capable of breaking down pollutants or repairing damaged ecosystems. © 2026 The New York Times Company

Keyword: Obesity
Link ID: 30312 - Posted: 07.08.2026

Christina Jewett The ads were jarring: a man with a hole in his throat where his larynx, or voice box, had once been. A woman whose teeth and jaw had been removed after oral cancer. Another woman speaking in a robotic voice, which was altered when her larynx was removed: “I wish I’d never seen a cigarette in my entire life.” A black screen followed, saying she died two days later. The Centers for Disease Control and Prevention’s 14-year ad campaign, called Tips From Former Smokers, was highly memorable and, research shows, highly effective in motivating people to quit. Last year, though, as tobacco companies gave millions to political organizations related to the Trump administration, the campaign went dark. There is no definitive evidence linking the donations to the lapse of the ad campaign. But the decision to terminate it was one of several steps the administration has taken to unravel federal government antismoking initiatives that had long had bipartisan support during a time when the administration has delivered significant policy wins to tobacco companies. The C.D.C.’s Office on Smoking and Health, which managed the campaign and worked with states on smoking cessation measures, has been shut down for more than a year, after its staff was laid off as part of the administration’s government downsizing efforts. While hundreds of other federal health employees were eventually rehired, the smoking office staff members have not been. Even after Congress restored the office’s funding late last summer, its employees have remained on paid leave as litigation challenging the firings plays out. In recent weeks, under pressure from Congress, the C.D.C. has given states diminished funding to air ads from the campaign’s archive, but the federal government will not produce new ads or negotiate contracts for them to air nationwide. The ads had prompted millions of smokers to dial state quit lines for help on how to stop smoking. In interviews, people who ran quit lines in several states said that since the ads went off the air, calls have plummeted along with enrollment in programs that offered counseling and nicotine gum and patches. © 2026 The New York Times Company

Keyword: Drug Abuse
Link ID: 30311 - 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 Libby Riddle A bear might seem like the scariest thing you could run into in a national park. But a new study suggests maybe you should be more worried about elk. Out of nearly 3,000 wildlife incidents in Canadian national parks, more than half involved an elk, researchers report July 2 in Frontiers in Conservation Science. But the risk of tangling with a given species also depended on what people were doing, say Holly Landles and conservation biologist Shashank Balakrishna of the University of York in England. Camping out? Be wary of elk grazing near your campsite. Quietly hiking or wildlife watching? Watch out for bears using the same trails. “By identifying situations where a potential conflict scenario is more likely, we can help visitors make informed decisions that improve safety whilst also reducing unnecessary disturbance to wildlife,” says Landles, who conducted this research as an undergraduate at York. Landles and Balakrishna analyzed 2,878 aggressive wildlife incidents from 2010 to 2023 involving five animals: black bears, grizzly bears, elk, coyotes and mule deer. Aggressive behaviors included chasing, attacking or bluffing a charge. The analysis identified which animal–human activity combinations were especially risky. Elk topped the list, involved in 62 percent of all the incidents. One of the riskiest combos was elk and camping — the animals turned up in 84 percent of campground incidents. This may be because Canada’s peak camping season aligns with when the animals mate and give birth — times of heightened aggression for the species. “Elk are herbivorous herd animals that don’t immediately inspire fear like a carnivore does,” Balakrishna says. Visitors may underestimate how aggressive they can be. © Society for Science & the Public 2000–2026.

Keyword: Aggression
Link ID: 30308 - 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 Sarah Thau Hunger pangs build with activity in Agouti-related protein (AgRP) neurons, and when we eat, these cells fall silent, signaling to the body that it’s full. Until recently, researchers thought these neurons responded to calorie intake alone, but a new study shows fructose quiets them less effectively than glucose does, even though both simple monomeric sugars carry the same number of calories. “We were really surprised when we tested these different sugars and found that fructose looks much different than glucose,” says study investigator Amber Alhadeff, a member of the Monell Chemical Senses Center and adjunct assistant professor of neuroscience at the University of Pennsylvania. Fiber photometry recordings of individual AgRP neurons in mice consuming fructose or glucose solutions first tipped the lab off to the fact that fructose is the weaker inhibitor. The same difference surfaced when the team infused the solutions directly into the animals’ guts, controlling for the fact that the mice tended to take more licks of the glucose than fructose. Glucose does not require the vagus nerve to inhibit AgRP neurons, according to previous work from Alhadeff’s group, but fructose does, the new study demonstrates. This study is the first to show “that the brain is responding to these things in different ways, and with a real mechanistic underpinning,” says Martin Myers, professor of diabetes research at the University of Michigan Medical School, who was not involved in the research. “This is an absolutely fabulous lab that is doing things that few, if any, other people in the world can do.” Once the team discovered that fructose acts through the vagus nerve, Alhadeff’s graduate student Aaron McKnight hit the mechanistic ground running. He worked for five years, according to Alhadeff, to show that fructose activates the vagus nerve, releasing a hormone called PYY that signals Y2 receptor-expressing vagal afferent neurons and then inhibits AgRP neurons. Glucose does not lead to increased PYY levels, acting through gut-spinal afferent signaling—a separate peripheral pathway. © 2026 Simons Foundation

Keyword: Obesity
Link ID: 30306 - Posted: 07.01.2026

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 Aimee Cunningham Reassuring evidence on acetaminophen’s safety during pregnancy keeps growing. A large, two-decade study in Hong Kong is the latest to find no link between use of the drug — known as Tylenol in the United States — and a risk of autism or attention-deficit/hyperactivity disorder in children. The lack of an association persisted no matter the trimester the drug was prescribed, the dose or the recommended frequency, researchers report June 29 in JAMA Internal Medicine. Joining several other analyses, including ones conducted in Sweden and Japan, the research adds to the body of evidence reporting no association between acetaminophen use in pregnancy and long-term neurodevelopmental disorders in children. All the studies compared siblings born to mothers who had taken the drug at some point, such that some siblings were exposed to the drug in utero and others weren’t. This approach accounts for the fact that both ADHD and autism are largely influenced by genetics. If acetaminophen were also a factor, researchers would expect a difference between siblings exposed to the drug and those not. None of the studies have found one. For the new study, the researchers pored over electronic health records from 2001 to 2023 for more than 700,000 pairs of mothers and children. Around 43 percent of the kids encountered acetaminophen in utero. The team focused on pairs of siblings that differed in exposure and used their records to follow the children for at least two years for autism diagnoses and at least five for ADHD. The autism analysis included more than 124,000 children, while the ADHD component had more than 97,000. Going a step further, the analysis also looked at the timing and amount of acetaminophen that was prescribed. © Society for Science & the Public 2000–2026.

Keyword: ADHD; Autism
Link ID: 30303 - 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