By John Pavlus Even in a world where large language models (LLMs) and AI chatbots are commonplace, it can be hard to fully accept that fluent writing can come from an unthinking machine. That’s because, to many of us, finding the right words is a crucial part of thought — not the outcome of some separate process. But what if our neurobiological reality includes a system that behaves something like an LLM? Long before the rise of ChatGPT, the cognitive neuroscientist Ev Fedorenko (opens a new tab) began studying how language works in the adult human brain. The specialized system she has described, which she calls “the language network,” maps the correspondences between words and their meanings. Her research suggests that, in some ways, we do carry around a biological version of an LLM — that is, a mindless language processor — inside our own brains. “You can think of the language network as a set of pointers,” Fedorenko said. “It’s like a map, and it tells you where in the brain you can find different kinds of meaning. It’s basically a glorified parser that helps us put the pieces together — and then all the thinking and interesting stuff happens outside of [its] boundaries.” Fedorenko has been gathering biological evidence of this language network for the past 15 years in her lab at the Massachusetts Institute of Technology. Unlike a large language model, the human language network doesn’t string words into plausible-sounding patterns with nobody home; instead, it acts as a translator between external perceptions (such as speech, writing and sign language) and representations of meaning encoded in other parts of the brain (including episodic memory and social cognition, which LLMs don’t possess). Nor is the human language network particularly large: If all of its tissue were clumped together, it would be about the size of a strawberry (opens a new tab). But when it is damaged, the effect is profound. An injured language network can result in forms of aphasia (opens a new tab) in which sophisticated cognition remains intact but trapped within a brain unable to express it or distinguish incoming words from others. © 2025 Simons Foundation

Keyword: Language
Link ID: 30043 - Posted: 12.06.2025

By Siddhant Pusdekar A single dose of psilocybin leads to widespread network-specific changes to cortical circuitry in mice, according to a new study published today in Cell. The results help explain how psilocybin can bring about lasting changes in behavior, and they pinpoint “the neurons that are most affected,” says Andrea Gomez, assistant professor of molecular and cellular biology at the University of California, Berkeley, who was not involved in the study. Specifically, the psychedelic strengthens cortical inputs from sensory brain areas and weakens inputs into cortico-cortical recurrent loops. Overall, these network changes suggest that psychedelics reroute information in a way that enhances responses to the outside world and reduces rumination, says study investigator Alex Kwan, professor of biomedical engineering at Cornell University. “This study provides some more mechanistic insight for why the drug may be a good antidepressant.” And the rewiring itself is not static, Kwan adds: “It can be influenced by manipulating neural activity” during psychedelic treatment. With this locus of psychedelic-induced changes identified, researchers can unpack how these neuronal ensembles coordinate “to create particular percepts or particular cognitions,” Gomez says. Kwan’s team focused on the mouse dorsal medial prefrontal cortex (dmPFC), which includes the anterior cingulate cortex—an important hub for the serotonin receptors that psilocybin targets. One dose of psilocybin increases dendritic spine growth in the medial prefrontal cortex of mice, an effect that lasts for at least a month, according to a 2021 study by Kwan’s team. And the treatment reduces the animals’ learned stress-related behaviors, but only if pyramidal tract neurons—one of the major types of excitatory neurons in the dmPFC—are active, Kwan’s group reported in April. © 2025 Simons Foundation

Keyword: Drug Abuse; Depression
Link ID: 30042 - Posted: 12.06.2025

By Emily Anthes In just a few short years, new diabetes and weight loss drugs like Ozempic, Wegovy and Mounjaro have taken the world by storm. In the United States, one in eight adults say they’ve tried one of these medications, which are known as GLP-1 drugs, and that number seems sure to rise as prices fall and new oral formulations hit the market. Fluffy and Fido could be next. On Tuesday, Okava Pharmaceuticals, a biopharmaceutical company based in San Francisco, is set to announce that it has officially begun a pilot study of a GLP-1 drug for cats with obesity. The company is testing a novel approach: Instead of receiving weekly injections of the drugs, as has been common in human patients, the cats will get small, injectable implants, slightly larger than a microchip, that will slowly release the drug for as long as six months. “You insert that capsule under the skin, and then you come back six months later, and the cat has lost the weight,” said Dr. Chen Gilor, a veterinarian at the University of Florida, who is leading the study. “It’s like magic.” Results are expected next summer. If they are promising, they could represent the next frontier for a class of drugs that has upended human medicine, and a potentially transformative treatment option for millions of pets. Some veterinarians have already begun administering human GLP-1 drugs, off label, to diabetic cats, and Okava is not the only company developing a product specifically for companion animals. “I think this is going to be the next big thing,” said Dr. Ernie Ward, a veterinarian and the founder of the Association for Pet Obesity Prevention. Veterinarians, he added, are “on the precipice of a complete new era in obesity medicine.” © 2025 The New York Times Company

Keyword: Obesity
Link ID: 30041 - Posted: 12.06.2025

By Emily Cataneo Imagine having a dream that you are trapped in a room with five rabid tigers. No matter how hard you try, you can’t escape. The tigers are screeching and thrashing and you’re terrified. Now imagine repurposing this dream. Imagine it from the perspective of one of the tigers. Now, you realize that the animals are panicking only because they want to escape. You open the door, inviting them to freedom, and they lie down, docile. Suddenly, the dream has become peaceful and calm, not terrifying and chaotic. BOOK REVIEW — “Nightmare Obscura: A Dream Engineer’s Guide Through the Sleeping Mind,” by Michelle Carr (Henry Holt and Co., 272 pages). Freud might have had a field day with this dream, but thanks in part to psychoanalysis’ fall from grace over the last century, medical professionals no longer put much stock in our minds’ nighttime wanderings as markers of either physical or mental health. That’s what dream scientist Michelle Carr aims to change. Carr, who serves as director of the Dream Engineering Laboratory in the Center for Advanced Research in Sleep Medicine in Montreal, has spent two decades gathering data on people like the tiger dreamer: She’s spent countless nights in labs watching people sleep, probing why we dream, why we have bad dreams, and how studying and even manipulating dreams can improve mental and physical health. In “Nightmare Obscura: A Dream Engineer’s Guide Through the Sleeping Mind,” Carr makes a passionate case for why the answers to these questions matter, deeply, especially for sufferers of trauma and suicidal ideation. What emerges is a passionate case for why dreams and nightmares are not just “random electrophysiological noise produced by the brain during sleep,” as scientists believed for many years, but rather a nightly exercise in “revising the shape of our autobiography.” In other words, Carr argues, our dreamscapes are essential pillars of who we are.

Keyword: Sleep
Link ID: 30040 - Posted: 12.06.2025

Sara Protasi I love napping. I love napping in the summer, when rhythms are more relaxed and the guilt of taking a break less intense (if only slightly). But I also love napping in the winter, when it’s cold outside, and burying myself under a warm blanket makes me feel like I’m hibernating. No matter the season, when lying in bed, I luxuriate in the feeling of my body relaxing, waiting for the moment when odd images start forming somewhere in that space between my closed lids and my corneas – or, most likely, somewhere in my mind. I love drifting into unconsciousness without worrying about the next item on my to-do list. I’m not a sound sleeper or someone who falls asleep easily at night, but napping comes easily and sweetly. I treasure the days in which I can nap. And I treasure even more the nights in which I sleep long and well. Yet our culture prizes efficiency and productivity, often seeing sleep as a waste of time. ‘Tech bros’ boast about regularly working more than 70 hours a week, and aim to reduce their sleep time as much as possible. Elon Musk suggested even more intense work schedules for government workers during his time at the US Department of Government Efficiency (DOGE). His approach resonated with many adherents of the Silicon Valley grind culture, which has sought to ‘hack’ sleep for a long time. As one CEO of a cost-cutting firm told the news site Business Insider this year: ‘While a 120-hour workweek isn’t a practical or sustainable solution for most, the principle behind it resonates. Companies that prioritise efficiency, automation and proactive cost management will always outperform those weighed down by bureaucracy.’ This approach is mirrored in a seemingly contradictory trend in the tech industry: a number of years ago, tech companies such as Apple and Google started introducing nap time for their workers. However, this approach was less a gesture of care than a response to exhaustion and sleep deprivation induced by their grind mentality, providing ‘recharging time’ to boost creativity and sustain the long hours required for work. Workers in less high-paying careers, who need to work multiple jobs, rarely have time to nap, and often have to resort to drugs such as modafinil, a stimulant prescribed for narcolepsy and used, often illegally, by students cramming for exams. This substance has gained the attention of the military. The US defence research agency DARPA has funded pharmaceutical companies and researchers to reduce sleep deprivation, with the long-term ambitious goal of operating without any need for sleep in the field. And the US isn’t alone: militaries worldwide are exploring how to keep their soldiers awake and functioning when sleep is in short supply. © Aeon Media Group Ltd. 2012-2025.

Keyword: Sleep
Link ID: 30039 - Posted: 12.06.2025

Alison Abbott For decades, neuroscientists focused almost exclusively on only half of the cells in the brain. Neurons were the main players, they thought, and everything else was made up of uninteresting support systems. By the 2010s, memory researcher Inbal Goshen was beginning to question that assumption. She was inspired by innovative molecular tools that would allow her to investigate the contributions of another, more mysterious group of cells called astrocytes. What she discovered about their role in learning and memory excited her even more. At the beginning, she felt like an outsider, especially at conferences. She imagined colleagues thinking, “Oh, that’s the weird one who works on astrocytes,” says Goshen, whose laboratory is at the Hebrew University of Jerusalem. A lot of people were sceptical, she says. But not any more. A rush of studies from labs in many subfields are revealing just how important these cells are in shaping our behaviour, mood and memory. Long thought of as support cells, astrocytes are emerging as key players in health and disease. “Neurons and neural circuits are the main computing units of the brain, but it’s now clear just how much astrocytes shape that computation,” says neurobiologist Nicola Allen at the Salk Institute for Biological Studies in La Jolla, California, who has spent her career researching astrocytes and other non-neuronal cells, collectively called glial cells. “Glial meetings are now consistently oversubscribed.” As far back as the nineteenth century, scientists could see with their simple microscopes that mammalian brains included two major types of cell — neurons and glia — in roughly equal numbers. © 2025 Springer Nature Limited

Keyword: Glia
Link ID: 30038 - Posted: 12.03.2025

By Jennie Erin Smith More than a decade ago, when researchers discovered a ghostly network of microscopic channels that push fluid through the brain, they began to wonder whether the brain’s plumbing, as they sometimes refer to it, might be implicated in neurodegenerative diseases such as Alzheimer’s. Now, they are testing a host of ways to improve it. At the Society for Neuroscience (SfN) meeting last month in San Diego, several teams reported early promise for drugs and other measures that improve fluid flow, showing they can remove toxic proteins from animal or human brains and reverse symptoms in mouse models of neurological disease. Plastic surgeons in China, meanwhile, have gone further, conducting experimental surgeries that they say help flush out disease-related proteins in people with Alzheimer’s. The trials have generated excitement but also concern over their bold claims of success. A group of academic surgeons in the United States is planning what they say will be a more rigorous clinical trial, also in Alzheimer’s patients, that could begin recruiting as early as next year. The surgical approach “sounds unbelievable,” says neuroscientist Jeffrey Iliff of the University of Washington. “But I’m not going to say I know it can’t work. Remember, 13 years ago we didn’t know any of this existed.” In 2012, Iliff, with pioneering Danish neuroscientist Maiken Nedergaard and colleagues, described a previously unrecognized set of fluid channels in the brain that they dubbed the glymphatic system. Three years later, other groups revealed a second, related system of fluid transport: a matrix of tiny lymphatic vessels in the meninges, or membranes covering the brain. © 2025 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 30037 - Posted: 12.03.2025

Elie Dolgin Last April, neuroscientist Sue Grigson received an e-mail from a man detailing his years-long struggle to kick addiction — first to opioids, and then to the very medication meant to help him quit. The man had stumbled on research by Grigson, suggesting that certain anti-obesity medications could help to reduce rats’ addiction to drugs such as heroin and fentanyl. He decided to try quitting again, this time while taking semaglutide, the blockbuster GLP-1 drug better known as Ozempic. “That’s when he wrote to me,” says Grigson, who works at Pennsylvania State University College of Medicine in Hershey. “He said that he was drug- and alcohol-free for the first time in his adult life.” Stories like this have been spreading fast in the past few years, through online forums, weight-loss clinics and news headlines. They describe people taking diabetes and weight-loss drugs such as semaglutide (also marketed as Wegovy) and tirzepatide (sold as Mounjaro or Zepbound) who find themselves suddenly able to shake long-standing addictions to cigarettes, alcohol and other drugs. And now, clinical data are starting to back them up. Earlier this year, a team led by Christian Hendershot, a psychologist now at the University of Southern California in Los Angeles, reported in a landmark randomized trial that weekly injections of semaglutide cut alcohol consumption1 — a key demonstration that GLP-1 drugs can alter addictive behaviour in people with a substance-use disorder. More than a dozen randomized clinical studies testing GLP-1 drugs for addiction are now under way worldwide, with some results expected in the next few months. © 2025 Springer Nature Limited

Keyword: Drug Abuse; Obesity
Link ID: 30036 - Posted: 12.03.2025

Jonathan Lambert For centuries, the nature of a fever — and whether it's good or bad — has been hotly contested. In ancient Greece, the physician Hippocrates thought that fever had useful qualities, and could cook an illness out of a patient. Later on, around the 18th century, many physicians regarded fever as a distinct illness, one that could actually cook the patient, and so should be treated. These days, researchers understand that fever is part of the immune system's response to a pathogen, one that's shared by many animal species. And while there's accumulating evidence that fevers can help kick an infection, precisely how they can help remains mysterious. Sponsor Message "There's a cultural knowledge that there's this relationship between temperature and viruses, but at a molecular level, we're quite unsure how temperature might be impacting viruses," says Sam Wilson, a microbiologist at the University of Cambridge. There are two main ideas, he says. The heat of a fever itself could be harming the virus, akin to Hippocrates' hypotheses. Alternatively, the heat is a means to an end, either stoking our immune system to work better, or simply a regrettable, but unavoidable byproduct of fighting off an infection. "The fact that there weren't definitive answers to these questions piqued my interest," says Wilson. That interest led to a study, published Thursday in Science, that suggests — at least in mice — that elevated temperature alone is enough to fight off some viruses. © 2025 npr

Keyword: Neuroimmunology
Link ID: 30035 - Posted: 12.03.2025

Helen Pearson In some parts of the world, record numbers of people are being diagnosed with attention deficit hyperactivity disorder (ADHD). In the United States, for example, government researchers last year reported that more than 11% of children had received an ADHD diagnosis at some point in their lives1 — a sharp increase from 2003, when around 8% of children had (see ‘ADHD among US boys and girls’). But now, top US health officials argue that diagnoses have spiralled out of control. In May, the Make America Healthy Again Commission — led by US health secretary Robert F. Kennedy Jr — said ADHD was part of a “crisis of overdiagnosis and overtreatment” and suggested that ADHD medications did not help children in the long term. One thing that’s clear is that several factors — including improved detection and greater awareness of ADHD — are causing people with symptoms to receive a diagnosis and treatment, whereas they wouldn’t have years earlier. Clinicians say this is especially true for women and girls, whose pattern of symptoms was often missed in the past. Although some specialists are concerned about the risks of overdiagnosis, many are more worried that too many people go undiagnosed and untreated. At the same time, the rise in awareness and diagnoses of ADHD has fuelled a public debate about how it should be viewed and how best to provide support, including when medication is required. The emergence of the neurodiversity movement is challenging the view of ADHD as a disorder that should be ‘treated’, and instead proposes that it’s a difference that should be better understood and supported — with more focus on adapting schools and workplaces, for instance. “I do have a big problem with ‘disorder’,” says Jeff Karp, a biomedical engineer at Brigham and Women’s Hospital in Boston, Massachusetts, who has ADHD. “It’s the school system that’s disordered. It’s not the kids.” But many clinicians and people with ADHD argue that it is associated with difficulties — ranging from academic struggles to an increased chance of injuries and substance misuse — that justify its label as a medical condition, and say that medication is an important and effective part of therapy for many people. © 2025 Springer Nature Limited

Keyword: ADHD
Link ID: 30034 - Posted: 11.29.2025

By Pam Belluck A recently recognized form of dementia is changing the understanding of cognitive decline, improving the ability to diagnose patients and underscoring the need for a wider array of treatments. Patients are increasingly being diagnosed with the condition, known as LATE, and guidelines advising doctors how to identify it were published this year. LATE is now estimated to affect about a third of people 85 and older and 10 percent of those 65 and older, according to those guidelines. Some patients who have been told they have Alzheimer’s may actually have LATE, dementia experts say. “In about one out of every five people that come into our clinic, what previously was thought to maybe be Alzheimer’s disease actually appears to be LATE,” said Dr. Greg Jicha, a neurologist and an associate director of the University of Kentucky’s Sanders-Brown Center on Aging. “It can look like Alzheimer’s clinically — they have a memory problem,” Dr. Jicha said. “It looks like a duck, walks like a duck, but then it doesn’t quack, it snorts instead. ” On its own, LATE, shorthand for Limbic-predominant age-related TDP-43 encephalopathy, is usually less severe than Alzheimer’s and unfolds more slowly, said Dr. Pete Nelson, an associate director of the Sanders-Brown Center, who helped galvanize efforts to identify the disorder. That can be reassuring to patients and their families. But there is no specific treatment for LATE. Also, many older people have more than one type of dementia pathology, and when LATE occurs in conjunction with Alzheimer’s, it exacerbates symptoms and speeds decline, he said. © 2025 The New York Times Company

Keyword: Alzheimers
Link ID: 30033 - Posted: 11.29.2025

By Catherine Offord Researchers have tested a proof-of-concept device that enabled people who had lost their normal sense of smell to detect the presence of certain odors. Rather than exploiting the smell pathway, in which nasal cells send signals along olfactory nerves to the brain, the technology makes use of a less known nerve highway in the nose that transmits other sensations, including the kick of wasabi and the coolness of mint. “It’s an interesting study,” says Zara Patel, a rhinologist at Stanford Medicine who was not involved in the work, published today in Science Advances. “This is not recovering a sense of smell, this is activating a different system.” But she and others caution it remains to be seen how beneficial this kind of technology could be for people with smell loss, or anosmia. Humans have about 400 different olfactory receptors that are thought to enable the nose to detect billions of odors. But people can lose some or all of their sense of smell for a variety of reasons, including head trauma and viral infections such as COVID-19. People with long-term anosmia describe a significantly reduced quality of life and are at higher risk of mental health disorders, notes Halina Stanley, a research scientist at CNRS, the French national research agency, and co-author on the new paper. “The idea that if you lose your sense of smell, this isn’t as bad as losing another sense, I think is actually quite wrong.” Research by another team in 2018 found that electrodes placed in the sinuses near the olfactory bulb, the brain region that processes odor signals, could stimulate perception of smell, with people reporting onion or fruity scents, for example. Scientists are now working to develop implants that could more directly and specifically stimulate the olfactory bulb—akin to cochlear implants, which replace lost hearing by detecting sounds and stimulating the auditory nerve. However, such technology would be complex and invasive, and, at present, is a long way from becoming a therapy. © 2025 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Robotics
Link ID: 30032 - Posted: 11.29.2025

By Trip Gabriel Paul Ekman, a psychologist who linked thousands of facial expressions to the emotions they often subconsciously conveyed, and who used his research to advise F.B.I. interrogators and screeners for the Transportation Security Administration as well as Hollywood animators, died on Nov. 17 at his home in San Francisco. He was 91. His daughter, Eve Ekman, confirmed the death. Dr. Ekman sought to add scientific exactitude to the human impulse to interpret how others feel through their facial expressions. He recorded 18 types of smiles, for example, distinguishing between a forced smile and a spontaneous one; a genuine smile, he discovered, crinkles the orbicularis oculi muscle — that is, it creates crow’s feet around the eyes. Sometimes described as the world’s most famous face reader, Dr. Ekman was ranked No. 15 in 2015 by the American Psychological Association in its list of 200 eminent psychologists of the modern era. He was influential in reshaping the way facial expressions were understood — as the product of evolution rather than environment — and his findings crossed over to popular culture. The Fox TV drama “Lie to Me,” which ran for three seasons starting in 2009, featured a psychologist modeled on Dr. Ekman (played by Tim Roth) who assists criminal investigations by decoding the hidden meanings of facial expressions and body language. The show was developed by the producer Brian Grazer, who was inspired by a lengthy profile of Dr. Ekman by Malcolm Gladwell in The New Yorker in 2002. “The idea that you could tell a liar by some scientific test and know what they’re feeling just by looking at them was staggering to me,” the show’s writer, Samuel Baum, told The New York Times in 2009. As a young research psychologist in the late 1960s, Dr. Ekman changed the scientific consensus on facial expressions. In the postwar era, the conventional wisdom of eminent anthropologists like Margaret Mead was that human facial expressions were learned and that they varied across cultures. © 2025 The New York Times Company

Keyword: Emotions; Evolution
Link ID: 30031 - Posted: 11.29.2025

By Carl Zimmer Last year, Ardem Patapoutian got a tattoo. An artist drew a tangled ribbon on his right arm, the diagram of a protein called Piezo. Dr. Patapoutian, a neuroscientist at Scripps Research in San Diego discovered Piezo in 2010, and in 2021 he won a Nobel Prize for the work. Three years later, he decided to memorialize the protein in ink. Piezo, Dr. Patapoutian had found, allows nerve endings in the skin to sense pressure, helping to create the sense of touch. “It was surreal to feel the needle as it was etching the Piezo protein that I was using to feel it,” he recalled. Dr. Patapoutian is no longer studying how Piezo informs us about the outside world. Instead, he has turned inward, to examine the flow of signals that travel from within the body to the brain. His research is part of a major new effort to map this sixth, internal sense, which is known as interoception. Scientists are discovering that interoception supplies the brain with a remarkably rich picture of what is happening throughout the body — a picture that is mostly hidden from our consciousness. This inner sense shapes our emotions, our behavior, our decisions, and even the way we feel sick with a cold. And a growing amount of research suggests that many psychiatric conditions, ranging from anxiety disorders to depression, might be caused in part by errors in our perception of our internal environment. Someday it may become possible to treat those conditions by retuning a person’s internal sense. But first, Dr. Patapoutian said, scientists need a firm understanding of how interoception works. “We’ve taken our body for granted,” he said. Everyone has a basic awareness of interoception, whether it’s a feeling of your heart racing, your bladder filling or a flock of butterflies fluttering in your stomach. And neuroscientists have long recognized interoception as one function of the nervous system. Dr. Charles Sherrington, a Nobel Prize-winning neuroscientist, first proposed the existence of “intero-ceptors,” in 1906. © 2025 The New York Times Company

Keyword: Obesity; Stress
Link ID: 30030 - Posted: 11.26.2025

By Caroline Hopkins Legaspi In a study published Monday in JAMA Neurology, researchers linked obstructive sleep apnea, a condition that causes temporary pauses in breathing during sleep, with Parkinson’s disease. Parkinson’s disease is a progressive nervous system disorder that causes tremors, stiffness, and difficulty speaking, moving and swallowing. It is the second-most common neurodegenerative disease in the United States, after Alzheimer’s disease, with 90,000 people diagnosed each year. There is no cure for Parkinson’s disease, said Dr. Lee Neilson, a neurologist at Oregon Health & Science University who led the study. But the researchers did find that treating sleep apnea with a continuous positive airway pressure (or CPAP) machine was associated with a reduced likelihood of developing Parkinson’s. So identifying those at highest risk for the neurological condition — and intervening early, Dr. Neilson said, “might make the biggest impact.” The researchers analyzed medical records from more than 11 million U.S. veterans treated through the Department of Veterans Affairs between 1999 and 2022. The group was predominantly male with an average age of 60, representing those at highest risk for sleep apnea, experts said. The researchers found that about 14 percent of the participants had been diagnosed with sleep apnea between 1999 and 2022, according to their medical records. When the researchers looked at their health six years after those diagnoses, they found that the veterans with sleep apnea were nearly twice as likely to have developed Parkinson’s disease compared with those who had not been diagnosed with sleep apnea. This held even after controlling for other factors that could influence the development of sleep apnea or Parkinson’s disease, including high body mass index and conditions like diabetes, high blood pressure, traumatic brain injuries and depression. © 2025 The New York Times Company

Keyword: Sleep; Parkinsons
Link ID: 30029 - Posted: 11.26.2025

By Angie Voyles Askham Rats, like people, jump at the chance to repeat a task that rewards them handsomely, but they are less eager when the reward is paltry: They learn from past experience and update their behavior accordingly. That learning is shaped by the hormone estradiol, according to a new study. And when estradiol levels peak during the estrus cycle, female rats adapt their behavior in response to reward size more quickly than they do during other phases—and faster than males overall. The female rats also have a larger release of dopamine in response to an unexpected reward, along with reduced expression of dopamine transporters in a reward center of their brain after the hormone peaks, the new work shows. “It’s giving mechanistic insight into how estrogen modulates reinforcement learning—all the way down to the molecular mechanism,” says Ilana Witten, professor of neuroscience at Princeton University and Howard Hughes Medical Institute investigator, who was not involved in the study. The team behind the new work used a task that measures how much an animal values an anticipated reward: Thirsty rats poke their nose into a central port and then listen for a tone that indicates how much water one of two side ports will dispense. The animals choose to either hold out at the cued location for the reward or to abandon the trial and start a new one by poking their nose into the other side. Rats learn to initiate their next trial more quickly when the experiment is doling out large rewards and to hold off on initiating new trials when rewards are small, previous work from the group has shown. “It takes a lot of energy to initiate a trial, so if there are small rewards, it’s not as motivating,” says study investigator Carla Golden, a postdoctoral researcher in Christine Constantinople’s lab at New York University. © 2025 Simons Foundation

Keyword: Hormones & Behavior; Attention
Link ID: 30028 - Posted: 11.26.2025

Hannah Devlin Science correspondent Scientists have identified five major “epochs” of human brain development in one of the most comprehensive studies to date of how neural wiring changes from infancy to old age. The study, based on the brain scans of nearly 4,000 people aged under one to 90, mapped neural connections and how they evolve during our lives. This revealed five broad phases, split up by four pivotal “turning points” in which brain organisation moves on to a different trajectory, at around the ages of nine, 32, 66 and 83 years. “Looking back, many of us feel our lives have been characterised by different phases. It turns out that brains also go through these eras,” said Prof Duncan Astle, a researcher in neuroinformatics at Cambridge University and senior author of the study. “Understanding that the brain’s structural journey is not a question of steady progression, but rather one of a few major turning points, will help us identify when and how its wiring is vulnerable to disruption.” The childhood period of development was found to occur between birth until the age of nine, when it transitions to the adolescent phase – an era that lasts up to the age of 32, on average. In a person’s early 30s the brain’s neural wiring shifts into adult mode – the longest era, lasting more than three decades. A third turning point around the age of 66 marks the start of an “early ageing” phase of brain architecture. Finally, the “late ageing” brain takes shape at around 83 years old. The scientists quantified brain organisation using 12 different measures, including the efficiency of the wiring, how compartmentalised it is and whether the brain relies heavily on central hubs or has a more diffuse connectivity network. From infancy through childhood, our brains are defined by “network consolidation”, as the wealth of synapses – the connectors between neurons – in a baby’s brain are whittled down, with the more active ones surviving. During this period, the study found, the efficiency of the brain’s wiring decreases. © 2025 Guardian News & Media Limited

Keyword: Development of the Brain; Brain imaging
Link ID: 30027 - Posted: 11.26.2025

By Gina Kolata Hopes were high. In retrospect, perhaps too high. On Monday, Novo Nordisk announced that two large studies failed to find any effect of the drug semaglutide on cognition and functioning in people with mild cognitive impairment — an early stage of Alzheimer’s — or with dementia. The participants were randomly assigned to take a pill of semaglutide, the compound at the heart of the weight-loss injections Ozempic and Wegovy, or a placebo for two years. “Today we announced that our efforts to slow down the progression of Alzheimer’s disease has come to an end,” said Maziar Mike Doustdar, chief executive at Novo Nordisk, in a video posted on LinkedIn. He added, “Based on the indicative data points we had, this is not the outcome we had hoped for.” The studies, involving 1,855 people in one trial and 1,953 in the other, seemed to stem an initial phase of optimism. The drugs appeared miraculous in their treatment of obesity, diabetes, heart disease and kidney disease. Alzheimer’s and other brain illnesses looked like the next frontier. But there had been other recent warnings, in two smaller studies of brain diseases. One, done by researchers in Britain, asked if a similar drug could help with Parkinson’s disease. That drug had no effect. Another study found that semaglutide did not help with cognitive impairment in people with major depression, a severe form of the disease. The company will present more detailed results from its Alzheimer’s study at a conference on Dec. 3, and another in March of 2026. Novo Nordisk’s stock was down nearly 6 percent on Monday, deepening a monthslong slump for the once-surging company. “We always knew there would be a low likelihood of success, but it was important to determine if semaglutide could take on one of medicine’s most challenging frontiers,” Mr. Doustdar said. © 2025 The New York Times Company

Keyword: Alzheimers; Obesity
Link ID: 30026 - Posted: 11.26.2025

By Meghan Rosen Taking just a few thousand steps daily could potentially stave off Alzheimer’s disease. People with the disease tend to experience debilitating cognitive challenges, like memory loss and difficulty communicating, that worsen over time. But physical activity may slow that steady downward march. In an observational study of people at risk for Alzheimer’s, researchers linked walking between 3,000 and 5,000 steps per day to a three-year delay in cognitive decline, compared with sedentary individuals. For people who walked between 5,000 and 7,500 steps per day, the reprieve appeared to last even longer — seven years, Harvard Medical School behavioral neurologist Jasmeer Chhatwal and his colleagues report November 3 in Nature Medicine. The association still needs to be tested in a clinical trial, Chhatwal says, but his team’s results hint at something important. Quality of life for people with Alzheimer’s and their families often plummets in the later stages of the disease. “If the disease can be delayed,” he says, “that can have a very big impact on people’s lives.” Previous studies have reported links between physical activity and delayed Alzheimer’s progression, says Deborah Barnes, an epidemiologist who studies dementia at the University of California, San Francisco, and who was not part of the research team. But the new study pinpoints the step count where people begin to see benefits. It also “helps to explain how,” she says. Chhatwal’s team reported a connection between exercise and less accumulation of certain Alzheimer’s proteins in the brain. It’s a mechanism that illustrates how physical activity probably works to slow Alzheimer’s progression, Barnes says. © Society for Science & the Public 2000–2025

Keyword: Alzheimers
Link ID: 30025 - Posted: 11.26.2025

Davide Castelvecchi Pigeons can sense Earth’s magnetic field by detecting tiny electrical currents in their inner ears, researchers suggest. Such an inner compass could help to explain how certain animals can achieve astonishing feats of long-distance navigation. The team performed advanced brain mapping as well single-cell RNA sequencing of pigeon inner-ear cells. Both lines of evidence point to the inner ear as the birds’ ‘magnetoreception’ organ. The results appeared in the Science on 20 November 1. “This is probably the clearest demonstration of the neural pathways responsible for magnetic processing in any animal,” says Eric Warrant, a sensory biology researcher at the University of Lund in Sweden. Studies have suggested that various animals, including turtles, trout and robins, can sense the direction and strength of magnetic fields, although the evidence has sometimes been contested — and the mechanisms have remained controversial. Bird-brained navigation Two leading hypotheses have led the research into how birds sense magnetic fields. One is a quantum-physics effect in retina cells where birds ‘see’ magnetic fields. Another is that microscopic iron oxide particles in the beak could act as tiny compass needles. However, it’s largely unknown where magnetic information is sensed in animals’ brains and how sensory neurons confer sensitivity to electromagnetic changes. In 2011, researchers found hints that magnetic fields triggered pigeons’ vestibular system, the organ that enables vertebrates to sense accelerations (including gravity) and helps them to stay balanced2. The structure is made of three fluid-filled loops which are mutually perpendicular, so they can communicate to the brain the direction of an acceleration by breaking it down into three ‘x, y, z’ components. © 2025 Springer Nature Limited

Keyword: Animal Migration; Hearing
Link ID: 30024 - Posted: 11.22.2025