By Catherine Offord Scientists have plenty of ideas about why aging impairs memory. Reductions in blood flow in the brain, shrinking brain volume, and malfunctioning neural repair systems have all been blamed. Now, new research in mice points to another possible culprit: microbes in the gut. In a study published today in Nature, scientists show how a bacterium that is particularly common in older animals can drive memory loss. This microbe makes compounds that impair signaling along neurons connecting the gut with the brain, dampening activity in brain regions associated with learning and memory, the team found. “This is a tour de force,” says Haijiang Cai, a neuroscientist at the University of Arizona who studies gut-brain communication and was not involved in the work. “They define the pathway all the way from aging and bacteria … to cognitive function—it’s really impressive.” However, he and others emphasize it remains to be seen whether a similar mechanism exists in humans—and if so, how important it is compared with other drivers of cognitive decline. Research on the so-called gut-brain axis has exploded in recent decades. Multiple studies have identified differences in microbiome composition between healthy people and those with cognitive disorders such as Alzheimer’s disease. This kind of research can’t establish cause and effect, though, and the literature is rife with conflicting results. Some groups have used animal experiments to probe the microbe-memory link. In the new study, Stanford University researchers Christoph Thaiss and Maayan Levy tinkered with the microbiomes of young mice—either by housing them with older animals or feeding them these animals’ poop—and then gave them memory tests. For example, one such test rates animals higher if they spend more time exploring new objects than those they’ve seen before. © 2026 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 30162 - Posted: 03.14.2026

By Catherine Offord Scientists have plenty of ideas about why aging impairs memory. Reductions in blood flow in the brain, shrinking brain volume, and malfunctioning neural repair systems have all been blamed. Now, new research in mice points to another possible culprit: microbes in the gut. In a study published today in Nature, scientists show how a bacterium that is particularly common in older animals can drive memory loss. This microbe makes compounds that impair signaling along neurons connecting the gut with the brain, dampening activity in brain regions associated with learning and memory, the team found. “This is a tour de force,” says Haijiang Cai, a neuroscientist at the University of Arizona who studies gut-brain communication and was not involved in the work. “They define the pathway all the way from aging and bacteria … to cognitive function—it’s really impressive.” However, he and others emphasize it remains to be seen whether a similar mechanism exists in humans—and if so, how important it is compared with other drivers of cognitive decline. Research on the so-called gut-brain axis has exploded in recent decades. Multiple studies have identified differences in microbiome composition between healthy people and those with cognitive disorders such as Alzheimer’s disease. This kind of research can’t establish cause and effect, though, and the literature is rife with conflicting results. Some groups have used animal experiments to probe the microbe-memory link. In the new study, Stanford University researchers Christoph Thaiss and Maayan Levy tinkered with the microbiomes of young mice—either by housing them with older animals or feeding them these animals’ poop—and then gave them memory tests. For example, one such test rates animals higher if they spend more time exploring new objects than those they’ve seen before. © 2026 American Association for the Advancement of Science.

Keyword: Learning & Memory; Obesity
Link ID: 30161 - Posted: 03.14.2026

Denis Campbell Weight loss drugs could help people avoid getting addicted to alcohol, tobacco and drugs such as cannabis and cocaine, a study has found. They could also reduce the risk of people already addicted to illicit substances having an overdose, ending up in hospital or dying, according to research published in the British Medical Journal. Glucagon-like peptide-1 receptor agonists used to treat type 2 diabetes and obesity, such as Mounjaro and Ozempic, are thought to work by influencing the brain’s reward pathways in order to cut cravings. They help people feel fuller by mimicking the natural substance released after eating. The US study analysed 606,434 US veterans with type 2 diabetes, who were monitored for up to three years. It found that GLP-1s reduced the risk of alcohol-related disorders in those with no history of substance use by 18% and of using cannabis (14%), cocaine (20%), nicotine (20%) and opioids (25%), compared with those on other sodium-glucose cotransporter-2 drugs also used to treat diabetes. Weight loss drugs also reduce the risk of people already using substances from overdosing (39%), needing emergency help in A&E (31%) or dying (50%). “This study adds to emerging research exploring whether GLP-1 medicines may influence brain pathways involved in reward and addiction”, said Prof Claire Anderson, the president of the Royal Pharmaceutical Society, which represents 35,500 UK pharmacists. She added: “As this was an observational study, it is important to be clear that it does not show these medicines prevent or treat addiction. Further research, including clinical trials, will be needed to understand whether GLP-1 medicines have a direct effect.” © 2026 Guardian News & Media Limited

Keyword: Drug Abuse; Obesity
Link ID: 30150 - Posted: 03.07.2026

By Hannah Thomasy In 1774, British physician-scientist Charles Blagden received an unusual invitation from a fellow physician: to spend time in a small room that was hotter, he wrote, “than it was formerly thought any living creature could bear.” Many people may have been appalled by this offer, but Blagden was delighted by the opportunity for self-experimentation. He marveled as his own temperature remained at 98 degrees Fahrenheit (approximately 37 degrees Celsius), even as the temperature of the room approached 200°F (about 93°C). Today, this ability to maintain a stable body temperature — called homeothermy — is known to exist among myriad species of mammals and birds. But there are also some notable exceptions. The body temperature of the fat-tailed dwarf lemur, for example, can fluctuate by nearly 45°F (25°C) over a single day. In fact, a growing body of research suggests that many more animals than scientists once appreciated employ this flexible approach — heterothermy — varying their body temperature for minutes, hours or weeks at a time. This may help the animals to persist through all sorts of dangers. “Because we’re homeotherms, we assume all mammals work the way we do,” says Danielle Levesque, a mammalian ecophysiologist at the University of Maine. But in recent years, as improvements in technology allowed researchers to more easily track small animals and their metabolisms in the wild, “we’re starting to find a lot more weirdness,” she says. The most extreme — and well-known — form of heterothermy is classic hibernation, which has been most extensively studied in critters who use it to save energy and so survive the long, cold winters of the Northern Hemisphere. These animals enter long periods of what scientists call deep torpor, when metabolism slows to a crawl and body temperature can drop to just above freezing.

Keyword: Evolution
Link ID: 30137 - Posted: 02.25.2026

By Emma Gometz Caribou, large deer that are native to the northernmost parts of the world (and sometimes called reindeer), are the only deer whose females grow antlers. In a study published today, researchers observed behavior that might explain why: female caribou appear to gnaw on shed antlers as a kind of postbirthing supplement. Caribou migrate huge distances every year between the places where they graze during the winter and the grounds where they calve in the spring. They can walk thousands of miles per year and likely have the longest terrestrial migration of any animal. Caribou mothers complete these extremely long migrations with antlers on their head and a calf in their womb. The period is very nutritionally demanding for them but culminates with a reserve stock of supplements when they need it the most. The researchers behind the new study figured this out when they observed bite marks in more than 80 percent of the 1,500 caribou antlers that littered the part of the Arctic National Wildlife Refuge in northeastern Alaska where the deer give birth. “[Caribou] are just really going after the antlers. They are highly selective,” says study co-author Joshua Miller, a paleoecologist at the University of Cincinnati. Female caribou shed their antlers just days before giving birth. Miller and co-author Madison Gaetano, a conservation paleobiologist, say that the findings suggest that female caribou are essentially banking nutrients in the form of antlers before they give birth and then gnawing on their freshly shed antlers to get a boost of protein, calcium and phosphorus they need to make up for having less time to graze as they nurse their calves. © 2025 SCIENTIFIC AMERICAN,

Keyword: Sexual Behavior
Link ID: 30136 - Posted: 02.25.2026

By Delthia Ricks Susan E. Leeman, who helped reshape scientific understanding of how the brain sends chemical signals throughout the body, did not hesitate to leave the laboratory when her research demanded it — even if it meant visiting slaughterhouses. In the late 1960s, while running a small lab at Brandeis University, she was trying to isolate a stress hormone and needed large quantities of the bovine hypothalamus, a cow’s version of the structure found deep in all mammalian brains. When supplies ran short at a local meatpacker in Boston, Dr. Leeman traveled to Chicago, home at the time to the sprawling Union Stock Yards, to secure fresh tissue. What ultimately emerged was not the hormone that she sought but an elusive chemical called Substance P. Discovered decades earlier but never fully understood, it was finally identified by Dr. Leeman in 1970 as a neuropeptide, released by cells in the brain or spinal cord in response to pain. Three years later, she identified another neuropeptide. The two discoveries established her as a leading figure in neuroendocrinology. Dr. Leeman died on Jan. 20 in Manhattan, at the home of her daughter Eve Leeman, where she had been living. She was 95. Her death was confirmed by another daughter, Jennifer Leeman. Although Substance P was identified in 1931 by Ulf von Euler and John Gaddum, researchers working in London, it was Dr. Leeman who discovered that it was a neuropeptide — a tiny, protein-like molecule released by neurons, or nerve cells in the brain and spinal cord, that transmits signals to target tissues. It was the first neuropeptide discovered in what would become a large class known as tachykinins. Dr. Leeman found that Substance P relays pain signals and amplifies the sensation of pain by triggering inflammation. It has since been linked to chronic pain syndromes, arthritis pain and migraines. © 2026 The New York Times Company

Keyword: Pain & Touch
Link ID: 30135 - Posted: 02.25.2026

By Meghan Rosen Ozempic’s key ingredient may act directly on cartilage to repair creaky joints. In mice and people, semaglutide can ease symptoms of the joint disease osteoarthritis and thicken the cartilage pillowed between bones, researchers report February 9 in Cell Metabolism. Thicker cartilage suggests the tissue is being rebuilt, says Di Chen, a physician and biologist at Shenzhen University of Advanced Technology in China. “That’s a good thing,” he says. “That’s the key thing.” More cartilage means more cushion, which means less bone-on-bone grinding and less pain. Osteoarthritis is the most common form of arthritis, affecting more than 500 million people worldwide. The disease can affect the hands, knees, hips and other joints, causing severe pain as cartilage wears away and tissues inflame. There’s no cure, and no medications that prevent it from becoming worse. Doctors can only help patients try to manage pain, Chen says. Scientists think weight loss can help alleviate symptoms by reducing the load on joints. That’s why semaglutide, the smash weight loss drug in Ozempic and Wegovy, is considered a contender for osteoarthritis treatment. And indeed, in 2024, a clinical trial in people with obesity reported that the drug improved joint pain and function. Doctors assumed those benefits were due to weight loss, Chen says. His team wasn’t so sure. The researchers conducted a similar study in mice with a form of osteoarthritis. One group received semaglutide, the other did not. In the drug-free mice, Chen’s team restricted food intake to match that of the semaglutide group. Both groups shed weight, but only the treated mice saw joint-based benefits. These mice had less pain, less broken-down cartilage and more cartilage growth, the team found. The results suggest that weight loss isn’t driving semaglutide’s benefits. © Society for Science & the Public 2000–2026.

Keyword: Neuroimmunology; Obesity
Link ID: 30129 - Posted: 02.21.2026

Mariana Lenharo Exercise pumps up your muscles — but it might also be pumping up your neurons. According to a study published today in Neuron1, repeated exercise sessions on a treadmill strengthen the wiring in a mouse’s brain, making certain neurons quicker to activate. This ‘rewiring’ was essential for mice in the study to gradually improve their running endurance. The work reveals that the brain — in mice and, presumably, in humans — is actively involved in the development of endurance, the ability to get better at a physical activity with repeated practice, says Nicholas Betley, a neuroscientist at the University of Pennsylvania in Philadelphia, and a co-author of the paper. “You go for a run, and your lungs expand, your heart gets pumping better, your muscles break down and rebuild. All this great stuff happens, and the next time, it gets easier,” Betley says. “I didn’t expect that the brain was coordinating all of that.” Betley and his colleagues were curious about what happens in the brain as people get stronger through exercise. They decided to focus on the ventromedial hypothalamus, a brain region that regulates appetite and blood sugar. The team then zeroed in on a group of neurons in that region that produce a protein called steroidogenic factor 1 (SF1), which is known to play a part in regulating metabolism2. A previous study3 found that the deletion of the gene that codes for SF1 impairs endurance in mice. © 2026 Springer Nature Limited

Keyword: Obesity; Learning & Memory
Link ID: 30120 - Posted: 02.14.2026

Yuki Noguchi At just over 5 foot, 5 inches, Christie Woodard weighs a lean 125 pounds. She's also open about relying on a low-dose GLP-1 to keep her weight there. She says sometimes people question why she's on the drug, "because they look at me and think I'm at healthy weight, or maybe they even think I'm thin." What people don't see is Woodard's previous struggles with obesity, which began in her 30s, and landed her at 260 pounds. She took up running half-marathons, but at that weight, it was painful. "I was not fast," she says. "I had massive issues; I was in physical therapy constantly. I tore my meniscus." Woodard, now 53 and living in Easton, Md., got gastric bypass surgery four years ago and cut her weight in half. Elated, she set a goal of completing half-marathons in all 50 states. Her weight remained stable until last year, when pounds began creeping back, despite adhering to a strict diet and lots of exercise. "I feel it in my knees, and mainly I feel it in my soul," she says. "I feel it in my confidence. It's messing with my head in a big way. I was terrified that I was going to go back to what I was." So her bariatric surgeon, Dr. Betsy Dovec, prescribed a low dose of the drug Zepbound, even though Woodard's body mass index didn't technically classify her as overweight. Dovec says Woodard isn't her only normal-weight patient on GLP-1s. "I prescribe medications for all types of people," she says. Though, she clarifies, she does not give the drugs to people for purely aesthetic reasons, like someone trying to shed a few pounds before an event, for example. © 2026 npr

Keyword: Obesity
Link ID: 30118 - Posted: 02.14.2026

By Molly Glick Not long after upending federal diet guidelines in order to prioritize “real food” on our plates, United States Health and Human Services Secretary Robert F. Kennedy Jr. has offered a new piece of questionable advice. During a tour to promote these dietary recommendations, Kennedy recently claimed that a keto diet can cure schizophrenia—an assertion that experts have quickly thrown cold water on. The ketogenic diet promotes fat-rich meals and low amounts of carbohydrates. While keto eating has skyrocketed in popularity in recent years—it ranked the most Googled diet in the U.S. in 2020—it was initially designed in the early 20th century for patients with epilepsy. More recent studies have confirmed that the diet is effective for certain types of epilepsy because it can control seizures. Meanwhile, we have much less evidence for its impacts on symptoms of schizophrenia. So far, small studies have offered some early evidence that ketogenic diets may help people with the condition. “There is currently no credible evidence that ketogenic diets cure schizophrenia,” Mark Olfson, a psychiatrist at Columbia University, told The New York Times. Kennedy also proclaimed that the diet can essentially cure bipolar disorder, according to studies he recently read. But as with schizophrenia, keto’s impacts on bipolar disorder have only been examined in limited numbers of patients so far. Preliminary findings have also hinted that a keto diet could ease symptoms of depression. It may offer “small antidepressant benefits” for people who don’t respond to medication, according to a recently published JAMA Psychiatry paper. But this work is in the early stages as well and remains far from conclusive. © 2026 NautilusNext Inc.

Keyword: Schizophrenia; Depression
Link ID: 30109 - Posted: 02.07.2026

By Jake Buehler Though fearsome predators, snakes can go weeks or even months without eating. Now, scientists think they may know how they do it. Snakes have lost the genes to produce ghrelin, a key hormone that regulates appetite, digestion, and fat storage, researchers report today in Royal Society Open Biology. Chameleons and a group of desert lizards called toadhead agamas that also have huge spaces between meals have also lost the same genes, hinting that cutting off ghrelin is a key way to excel at fasting, possibly by suppressing appetite and holding onto fat stores. “I give [the researchers] a lot of credit for looking more deeply into the data that was staring us all in the face—myself included,” says Todd Castoe, a genomicist at the University of Texas at Arlington not involved with the study. The hormone is ubiquitous across vertebrates, from fish to mammals. So finding that reptiles have repeatedly ditched it is “pretty remarkable,” he says. When scientists first discovered ghrelin nearly 30 years ago, they thought this “hunger hormone” could be key to fighting obesity in humans. But it hasn’t been that simple. Since then, researchers have found that ghrelin has a complicated role within a network of hormones constantly tweaking hunger and energy stores. And even though ghrelin is commonly found in vertebrates, it’s been unclear how it has evolved across various groups of vertebrates. So in the new study, Rui Resende Pinto, an evolutionary biologist at the University of Porto, and his colleagues focused on reptiles, many of which can go long periods without food. The researchers scanned the genomes of 112 species. In snakes, chameleons, and toadhead agamas, ghrelin genes were either missing or so warped by mutations they could no longer encode the hormone, the team found. The degree of the genes’ erosion also varied considerably between snake families: Some snakes such as boas and pythons had malformed ghrelin genes, but others, such as vipers, cobras, and their relatives, barely had anything left.

Keyword: Obesity; Evolution
Link ID: 30104 - Posted: 02.04.2026

By Diana Kwon edited by Jeanna Bryner By the time Maggie May, an Arkansas resident in her 30s, was admitted to a psychiatric clinic in 2024, she had been struggling for years with atypical anorexia nervosa, an eating disorder that leads to severe food restriction and profound disturbances in body image. (Her name has been changed for privacy.) She had already tried traditional interventions with a psychotherapist and a dietitian, but they had failed to improve her condition. So when May heard about a trial of a new and unconventional therapy, she jumped at the opportunity. The treatment was unusual in that alongside talk therapy, May underwent several sessions in a sensory-deprivation chamber: a dark, soundproof room where she floated in a shallow pool of water heated to match the temperature of her skin and saturated with Epsom salts to make her more buoyant. The goal was to blunt May’s external senses, enabling her to feel from within—focusing on the steady thudding of her heart, the gentle flow of air in and out of her lungs, and other internal bodily signals. The ability to connect with the body’s inner signals is called interoception. Some people are better at it than others, and one’s aptitude for it may change. Life events can also bolster or damage a person’s interoceptive skills. Sahib Khalsa, a psychiatrist and neuroscientist at the University of California, Los Angeles, and his colleagues think a disrupted interoception system might be one of the driving forces behind anorexia nervosa. So they decided to repurpose a decades-old therapy called flotation-REST (for “reduced environmental stimulation therapy”) and launched a trial with it in 2018. They hypothesized that in people with anorexia and some other disorders, an underreliance on internal signals may lead to an overreliance on external ones, such as how one looks in the mirror, that ultimately causes distorted body image, one of the key factors underlying these conditions. “When they’re in the float environment, they experience internal signals more strongly,” Khalsa says. “And having that experience may then confer a different understanding of the brain-body relationship that they have.” © 2025 SCIENTIFIC AMERICAN,

Keyword: Schizophrenia; Anorexia & Bulimia
Link ID: 30067 - Posted: 01.03.2026

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

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

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 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

Mariana Lenharo The obesity drug tirzepatide, sold as Mounjaro or Zepbound, can suppress patterns of brain activity associated with food cravings, a study suggests. Researchers measured the changing electrical signals in the brain of a person with severe obesity who had experienced persistent ‘food noise’ — intrusive, compulsive thoughts about eating — shortly after the individual began taking the medication. The study is the first to use electrodes to directly measure how blockbuster obesity drugs that mimic the hormone GLP-1 affect brain activity in people, and to hint at how they curb extreme food cravings. “It’s a great strategy to try and find a neural signature of food noise, and then try to understand how drugs can manipulate it,” says Amber Alhadeff, a neuroscientist at the Monell Chemical Senses Center in Philadelphia, Pennsylvania. The findings were published today in Nature Medicine1. Casey Halpern, a neurosurgeon-scientist at the University of Pennsylvania in Philadelphia, and his colleagues did not set out to investigate the effects of obesity drugs on the brain. The team’s goal was to test whether a type of deep brain stimulation — a therapy that involves delivering a weak electrical current directly into the brain — can help to reduce compulsive eating in people with obesity for whom treatments such as bariatric surgery haven’t worked. The scientists set up a study in which participants had an electrode implanted into their nucleus accumbens, a region of the brain that is involved in feelings of reward. It also expresses the GLP-1 receptor, notes Christian Hölscher, a neuroscientist at the Henan Academy of Innovations in Medical Science in Zhengzhou, China, “so we know that GLP-1 plays a role in modulating reward here”. This type of electrode, which can both record electrical activity and deliver an electrical current when needed, is already used in people to treat some forms of epilepsy. © 2025 Springer Nature Limited

Keyword: Obesity; Attention
Link ID: 30016 - Posted: 11.19.2025

By Lauren Schenkman The purported autism-microbiome connection is having a moment. It’s the focus of a new $50-million call for proposals from Wellcome Leap—a research initiative of the Wellcome Trust—and a 2024 Netflix documentary portrays fecal microbiota transplants as a promising treatment for autism-related traits. “It seems to have captured the public’s imagination,” says Kevin Mitchell, associate professor of genetics and neuroscience at Trinity College in Dublin. But Mitchell says he has long been skeptical. Eventually, he and some colleagues “collectively got exasperated enough by this that we felt that we had to say something about it,” Mitchell says. Today, they published a comprehensive review in Neuron of more than 30 studies on the autism-microbiome connection, including preclinical experiments in mice, human observational studies and clinical trials. After accounting for statistical, technical and conceptual flaws, the team reached a clear conclusion: “There’s nothing there,” Mitchell says. Research projects that include the keywords “autism” and “microbiome” have netted about $20 million to $25 million in U.S. federal funding annually since 2018, Mitchell’s team found using the funding database NIH RePORTER. It’s worrying that funders assume “there’s a solid foundation of work,” Mitchell says. “It’s just this huge amount of scientific effort and funding going into exploring these ideas.” Mitchell spoke with The Transmitter about the problems he sees with studies that claim to show a microbiome-autism link, and how neuroscientists can read them with an analytical eye. © 2025 Simons Foundation

Keyword: Autism
Link ID: 30015 - Posted: 11.19.2025

By Alex Marshall When a Swiss theater invited people with eating disorders to be involved in a play about Joan of Arc this fall, it caused a furor. Some therapists and parents of girls with anorexia criticized the move as “ethnically reprehensible” and said it could jeopardize performers’ health. So when Janine Rickenbach, who has had anorexia for decades, took the Theater Basel stage last week in the premiere, she knew that some audience members were judging her appearance as much as her performance. Yet during the two-hour show, Rickenbach, 44, appeared unfazed. At one point, wearing a camisole top that revealed her arms and neck, she stared impassively at the audience while delivering a monologue that seemed to address the outcry. “What are you thinking right now?” she said: “Are you thinking, ‘Oh my God…’” Was that “because I look the way I look?” she asked, “Or because I’m standing here on this stage? Because my struggle is visible?” Theater makers have long depicted health struggles onstage, including the realities of living with H.I.V. and cancer, but the debate around this production, titled “Jeanne Dark” and running through May 22, has shown that ethical questions remain about how various conditions are portrayed theatrically — and who gets to shape those depictions. Ulrike Schmidt, a specialist in eating disorders at King’s College, London, said in an email that anybody depicting mental health onstage needed to consider the potential for stigmatization, perpetuating stereotypes or “inappropriate glamorization” © 2025 The New York Times Company

Keyword: Anorexia & Bulimia
Link ID: 30014 - Posted: 11.19.2025