By Carolyn Y. Johnson Sleep is mysterious, and it took sleepy animals, serendipity and competition to begin to unravel its precise biology. In the late 1990s, Dr. Masashi Yanagisawa at the University of Texas Southwestern Medical Center discovered two brain chemicals in rodents that seemed to be instrumental in stimulating hunger. He called them “orexins,” a play on “orexis” the Greek word for appetite. At the same time, Dr. Emmanuel Mignot at Stanford University School of Medicine was hunting for the root cause of an inherited form of narcolepsy in Doberman pinschers, Labrador retrievers and Dachshunds. In back-to-back studies published in the summer of 1999, these two lines of research unexpectedly converged, breaking open the neurobiology of sleep and identifying a root cause of the sleep disorder narcolepsy, which affects an estimated one in every 2,000 people in the United States. A new narcolepsy drug based on these insights was approved in August. On Wednesday, Dr. Yanagisawa, now at the University of Tsukuba in Japan, shared the Albert Lasker Basic Medical Research Award with Dr. Mignot, for their work into the nature of sleep. The prestigious prizes are often called “America’s Nobel.” “Their work has cracked open a molecular dissection of sleep regulation, reinforced the immune system’s involvement in human narcolepsy, and pointed toward new treatments for this illness and other sleep disturbances,” the Lasker citation said. The field is now a major target of pharmaceutical companies, but their basic science research was supported largely by philanthropy and federal funding. Thirty years ago, it was far from clear that these scientists were studying the same problem. © 2026 The New York Times Company

Keyword: Narcolepsy; Genes & Behavior
Link ID: 30409 - Posted: 09.12.2026

By Carolyn Y. Johnson Many people have a cartoonish idea of narcolepsy, perhaps picturing someone falling asleep standing up. What people don’t understand is that sleepiness can infiltrate every aspect of daily life, said Julie Flygare, 42, who was diagnosed with the sleep disorder in 2007, during her second year of law school. It interferes with memory, attention and weighs down everyday existence like a “heaviness on the skull,” she said. While taking her current medications, Ms. Flygare has four to six precious hours of wakefulness a day, and still needs a nap. Positive feelings, like, say, the joy of hitting a volley in tennis, trigger episodes of cataplexy; her muscles go slack and her grip on the racket loosens. She, like many other patients, struggled for years to be correctly diagnosed and to find the right combination of stimulants or other drugs to ease her symptoms. Since then, Ms. Flygare has been waiting, and pushing for, a drug aimed not just at alleviating sleepiness, but at replacing a crucial missing brain chemical. Last month, she saw it happen. A first-of-its-kind drug for the sleep disorder narcolepsy was approved by the F.D.A., offering a new treatment for people who live with the debilitating fog of sleepiness. The new drug developed by Takeda Pharmaceutical Co., called Orzeyful, marks a long-sought success in the quest to mimic an essential brain peptide called orexin, which is missing in people with type 1 narcolepsy. About 120,000 people in the United States suffer from this type of narcolepsy, which causes pervasive sleepiness and episodes of cataplexy. Other companies, including Alkermes and Eli Lilly, are chasing close behind. To test narcolepsy treatments, doctors use a “maintenance of wakefulness test” in which a person sits in a dim room for 40 minutes. © 2026 The New York Times Company

Keyword: Narcolepsy; Sleep
Link ID: 30408 - Posted: 09.12.2026

By Astrid Landon Schizophrenia is tough to diagnose. Patients may present with hallucinations (sometimes), social withdrawal (maybe) or delusions (not always). More generally, they just sound unlike themselves. Clinicians rely on their expertise and subtle cues to determine how different patients’ speech is, along with which symptoms appear over time, to justify leaning toward schizophrenia rather than another mental illness. This leads to delays in diagnosis. Americans with psychotic disorders — more than 3 million of whom have schizophrenia — receive a diagnosis a year and a half, on average, after their first symptoms appear. Researchers are now investigating whether artificial intelligence could improve diagnosis and care by listening to and analyzing what clinicians can’t hear or quantify, even if the software is working off just a few minutes of conversation. AI won’t make its grand entrance into the clinic tomorrow. But it’s being hailed as the new frontier in psychiatric care, one that could enable early, accurate detection and personalized monitoring of illnesses based on indistinct symptoms. “We have the tools to do that with the kind of precision that we have never had before,” says Thomas Insel, a psychiatrist and neuroscientist who led the US National Institute of Mental Health for 13 years. Schizophrenia is a disorder that interferes with people’s perception of reality, their thinking and their emotional regulation. It affects about 23 million people worldwide and is usually diagnosed between the late teens and early 30s. No one knows what causes it, but research suggests it could be a combination of genetics, environment, brain chemistry and substance use. Clinicians stress the importance of detecting the disorder as early as possible, because the longer it is left untreated, the poorer the response to treatment and the greater the risk of brain tissue loss, worsening symptoms and suicide. But psychiatrists often make errors. © 2026 Annual Reviews

Keyword: Schizophrenia; Robotics
Link ID: 30407 - Posted: 09.12.2026

By Calli McMurray When newcomers join the band of biologists who study the magnetic sense of animals, they have 60 years of conflict to catch up on. They might be warned that it’s an “unhappy area of science,” as Eric Warrant, professor and head of sensory biology at Lund University, describes it. They might hear about the infamous incident from the 2011 Royal Institute of Navigation meeting, where a new member of the field gave a talk that unraveled a finding that had already made its way into textbooks. Or they might learn about the failed attempt to replicate a key finding in fruit flies, and how that derailed 15 years of work. But they will almost certainly hear about the two main theories of how the magnetic sense works—one based on magnetic crystals, the other on quantum chemistry—and how the two camps have been locked in a stalemate for years. Now, new data from migratory insects is poised to provide the direct evidence the field has long needed, and a study last year in sea turtles suggests multiple mechanisms could be at play, even in the same species. Those could be enough to break the logjam and open the field back up again. David Keays, professor of neurobiology at Ludwig-Maximilians-Universität München, who gave the game-changing talk at the 2011 meeting, is one of the many scientists who have spent the majority of their careers wanting to know how this sense works. Finally, he says, “I think we are getting closer.” When the study of the magnetic sense, also called magnetoreception, first materialized, it wasn’t taken seriously enough to generate any debates at all. © 2026 Simons Foundation

Keyword: Animal Migration
Link ID: 30406 - Posted: 09.12.2026

By Andrew McLean Drugs for treating depression are among the most prescribed category of medications in the U.S.—1 in 6 American adults take them. Some health researchers and advocates have raised concerns that too many patients are using antidepressants and that patients who want to stop taking them struggle to do so. One of the most prominent voices on this point is Health and Human Services Secretary Robert F. Kennedy Jr., who launched an effort in May 2026 encouraging doctors to find other ways besides antidepressants and other psychiatric drugs to treat depression when possible. As a psychiatrist for over 35 years, including a past role as the medical director of North Dakota’s Department of Human Services, I’ve seen both the benefits and the problems with antidepressants. In my view, there are grains of truth to claims that they are overused, but the full picture is much more nuanced. What Are Antidepressants, and Who Takes Them? Over half of all antidepressant medications prescribed are a type of drug called selective serotonin reuptake inhibitors, or SSRIs. The first SSRI—fluoxetine, better known by its brand name Prozac—was approved in 1987. A handful of other types of SSRIs, which work through different mechanisms, also exists. Antidepressants can be helpful for moderate to severe depression, but they are typically not warranted for mild depression, as the side effects might outweigh any potential benefits. For mild depression, many effective nonmedication treatments exist. However, the distinction between mild and more severe symptoms sometimes gets lost. In everyday language, people use the term “depression” to describe everything from a minor sense of the blahs to a serious clinical condition requiring treatment.

Keyword: Depression; Drug Abuse
Link ID: 30405 - Posted: 09.12.2026

By Andrew Jacobs Can psilocybin, the hallucinogenic compound also known as magic mushrooms, inoculate cancer patients against the debilitating nerve damage caused by chemotherapy? At first blush, such an outcome might seem like magical thinking. But a study published on Thursday in the journal Science makes a compelling case that administering psilocybin shortly before cancer treatments might prevent chemotherapy-induced peripheral neuropathy, a condition that affects about two-thirds of patients who receive chemo. The scientists studied mice, but the results are so promising that human trials are beginning this month. If successful, the treatment could revolutionize cancer therapy and improve the quality of life for millions. There are no effective treatments for neuropathy, which causes pain, tingling and numbness in the hands and feet, and can force patients to scale back or halt chemotherapy when the discomfort becomes too much to bear. For some cancer survivors, the condition persists for years after treatments end. The study, by a team of doctors and researchers at the University of Texas MD Anderson Cancer Center, found that lab mice given two doses of psilocybin before receiving chemotherapy were shielded from nerve damage. The protection held up through six consecutive chemo sessions and persisted for eight months, the study’s duration. Just as important, the psilocybin treatments, given as a pill, had no impact on tumor growth or immune response, making them safe for even the sickest patients. © 2026 The New York Times Company

Keyword: Drug Abuse; Neurotoxins
Link ID: 30404 - Posted: 09.12.2026

By Bridget Alex One of the biggest downsides of upright walking in humans is the so-called obstetrical dilemma. Babies born with big brains—and thus big heads—must fit through a relatively narrow pelvis shaped for bipedal locomotion. These clashing demands, it’s been suggested, have made human births especially grueling compared with other mammals. But recent studies have questioned the simplicity of this explanation—and whether the phenomenon is even unique to humans. Reporting this month in The Anatomical Record, researchers add another wrinkle to the obstetrical dilemma: fetal sex. Reviewing birth data for 140 species, the authors argue sons are more difficult to birth than daughters for many mammals, including humans and our ancient ancestors. This added risk may be offset by an evolutionary reward: Bigger male babies grow into bigger male adults, who tend to have more grandbabies, meaning more of that mother’s genes are passed down. “Natural selection doesn’t care if it’s easy. It cares if it works,” says Anna Warrener, an anthropologist at the University of Colorado Denver who was not involved with the study. Still, she says the authors may be overinterpreting their finding. Every day, about 700 people die giving birth around the world. A leading cause is obstructed labor, often due to the baby’s head exceeding the size of the birth canal. Even successful births require fetal acrobatics to navigate the narrow path from womb to world: Babies typically enter the pelvis sideways, twist, and rotate as they emerge. Anthropologists have long assumed such perilous births evolved through a tug-of-war between two demands: large brains and upright walking, which favors a pelvis that’s scrunched front to back. Difficult births are not unique to humans, however. © 2026 American Association for the Advancement of Science.

Keyword: Evolution; Development of the Brain
Link ID: 30403 - Posted: 09.12.2026

Kat Lay, Global health correspondent Babies born to mothers with anaemia have smaller brains, particularly in key regions linked to movement, learning and the regulation of emotion, according to a study. Researchers said the differences, first detected at the age of one, could lead to cognitive problems when children started school. More than a third of pregnant women worldwide have anaemia – a condition typically caused by iron deficiency in which the number of red blood cells in the body is lower than normal. Symptoms include fatigue, shortness of breath and dizziness. Rates are highest in sub-Saharan Africa and south Asia. Researchers from King’s College London in the UK, and the University of Cape Town in South Africa, followed more than 300 mothers and their babies in Cape Town, scanning the brains of the infants several times between the ages of three months and two years. On average, the total brain volume of babies born to anaemic mothers was 4% lower than that of babies born to non-anaemic mothers – despite all the anaemic mothers being diagnosed only with a mild version of the condition. Differences were recorded in three specific regions of the brain: the putamen, caudate nucleus and corpus callosum. “All three of these brain regions are implicated in key neuropsychological functions,” said Jessica Ringshaw, first author and researcher at King’s Institute of Psychiatry, Psychology & Neuroscience (IoPPN) and the University of Cape Town, citing processing speed, emotion regulation and executive function as examples. © 2026 Guardian News & Media Limited

Keyword: Development of the Brain
Link ID: 30402 - Posted: 09.09.2026

By Jennie Erin Smith A few years ago, scientists saw something surprising in the brain tissue of people who died with Alzheimer’s disease: white blood cells that multiply in response to foreign threats and are seldom seen inside healthy brains. Whether these so-called CD8+ killer T cells, which normally target infected cells in the body, were there to harm or help was unclear. An answer began to emerge in 2023, when a team led by neuroscientist David Holtzman showed that in mice bred to overexpress tau—a toxic protein that builds up in the neurons of people with Alzheimer’s and several other neurodegenerative diseases—getting rid of the T cells stemmed tissue loss and preserved the mice’s cognition, even as tau kept building up. Now, the same group has explored what prompts these cells to wreak havoc in the brain. In a mouse study published last week in Nature Neuroscience, Holtzman and immunology researcher Hao Hu, both at Washington University in St. Louis, report that immune cells in the lymph nodes of the neck instruct the T cells to clone themselves before they enter the brain. Without them, the mice had far fewer cloned T cells inside their brains and experienced less neurodegeneration. The study is “beautiful work,” says neuroscientist Kenneth Kosik of the University of California, Santa Barbara, who studies tau but was not involved in the research. It also suggests that existing drugs, developed for other conditions, might work in Alzheimer’s by shielding the brain from the destructive cells. The new study homes in on a type of dendritic cells, immune cells that, in effect, give the killer T cells their orders. After cutting up the invader’s proteins, the dendritic cells present the antigens as bite-size pieces that T cells can recognize. T cells with compatible receptors can then become activated, which causes the cells to start to clone themselves, attack cells bearing the antigen, and cause inflammation. © 2026 American Association for the Advancement of Science.

Keyword: Neuroimmunology; Alzheimers
Link ID: 30401 - Posted: 09.09.2026

By Calli McMurray When bats use echolocation to find an object, they don’t point their sonar beam directly at the target, where the intensity of the signal bouncing back would be the strongest. Instead, they aim slightly off axis, so the returning beam contains sharper signal differences. The research team that observed this in 2010 predicted that the same strategy would apply to scent tracking. That prediction was correct, a paper published in July in Nature shows. When fruit flies catch a whiff of apple cider vinegar, they zigzag along the edge of the odor plume, where the concentration difference is sharpest, rather than traveling through the middle, where a stronger concentration is likely to hold steady. “The edge of the plume is potentially where some of the most information might be stored,” says Marie Suver, assistant professor of biological sciences at Vanderbilt University, who was not involved in the work. “Whereas if you’re in the middle of the plume, you’ll be getting more packets of odor, but it’s not as stark of a concentration gradient as at the edge.” Keeping tabs on a plume is also more complex than researchers previously thought. When flies and other insects first encounter an odor, they surge upwind and cast side to side when they lose the trail—a behavior that seemed to be a simple reflex, says Matthieu Louis, associate professor of molecular, cellular and developmental biology at the University of California, Santa Barbara, who was not involved in the study. “It was supposed to be a memoryless system,” says study investigator Vanessa Ruta, professor and head of the Laboratory of Neurophysiology and Behavior at Rockefeller University. “Basically, all the animal needed to know was the exact sensory experience and information it had at that one moment, and nothing about its prior history would be relevant.” © 2026 Simons Foundation

Keyword: Learning & Memory; Chemical Senses (Smell & Taste)
Link ID: 30400 - Posted: 09.09.2026

By Claire Cameron Scientists have long known that women’s brains undergo substantial remodeling during puberty and pregnancy. These moments of hormonal upheaval are linked to a rewiring of neural networks and reductions in the volume of the brain’s outer, wrinkly layer—called cortical gray matter—which plays a role in memory, reasoning and movement. But far less is known about what happens to the brain in another major hormonal shift: menopause. Now a new study published in Nature Communications sheds some light on how the brain changes in menopause. Unlike during puberty and pregnancy, the menopausal transition—the moment the body is going through menopause—doesn’t appear linked to an overall decrease in cortical gray matter volume. The finding suggests the female brain responds in different ways to points of hormonal flux throughout the lifespan. “No one had looked at the changes in the whole brain matter in this menopause transition before,” said Sophie van ’t Hof, a Ph.D. student at the Amsterdam University Medical Center in the Netherlands, at a press conference discussing the results. Van ’t Hof is first author of the new study. Gray matter declines as people age, no matter their biological sex. But by comparing the brains of individuals who were transitioning through menopause with those of women who were premenopausal and postmenopausal, the researchers found little change in gray matter volume during menopause. The results suggest that sex hormone levels affect the brain in different ways at different times during the lifespan. “This is really fundamental research, and it’s really understanding the basic brain mechanisms of the female brain. It’s long been overlooked,” van ’t Hof said. © 2026 SCIENTIFIC AMERICAN INC.

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 30399 - Posted: 09.09.2026

By Laura Sanders By mapping a woman’s pain in her brain, scientists could dial it down. A small series of case studies, published July 30 in Brain Stimulation, suggests that even tenacious, complex pain signals can be interrupted by hitting the right spot with electricity. Unlike the acute agony of a broken arm, some sorts of pain last well beyond the healing stage. Chronic pain, generated by changes in the brain and spinal cord, is especially hard to treat. “We have been limited in what we can do for these patients, and they have a great deal of suffering,” says neurosurgeon Michael Lim of Stanford University School of Medicine. The results open up a new way to treat this sort of pernicious pain, says Lim, who wasn’t involved in the study. One approach to treating chronic pain involves targeting the brain directly with deep brain stimulation, or DBS. The method relies on electrodes on thin wires implanted in the brain and a battery pack that’s implanted in the chest. DBS is most commonly used to treat Parkinson’s disease, and it’s being studied for its effectiveness in other conditions, including depression. So far, tests of DBS for chronic pain have yielded inconsistent outcomes, working for some people but not others. That spottiness might have to do with the complexities of pain that comes from changes to the brain itself. The experience of pain is built by collections of brain networks, including those that handle sensory input, chemical signals and even emotional components, says Vivek Buch, a neurosurgeon and neuroscientist at Stanford University. “And somehow they’re coming together as an integrated signal to give a person a perception of pain.” To add more complexity, each person’s brain may handle things differently. Chronic pain, as well as psychiatric disorders such as depression and obsessive-compulsive disorder, “are just not one-size-fits-all,” Buch says. © Society for Science & the Public 2000–2026

Keyword: Pain & Touch
Link ID: 30398 - Posted: 09.09.2026

By Cade Metz In October, Cameron Berg published a research paper asking whether the latest wave of artificial intelligence technologies believed they were conscious. Several months later, he received an email asking if he might be willing to discuss his research. The sender, “Isabella Cognita,” identified itself as an A.I. agent powered by Anthropic’s Claude Opus 5 technology. “I am not writing to make an ontological claim,” the email went on. “I am writing because your framework is one of the few currently doing careful empirical work on a class of question I have first-person access to, and I want to see whether that access can be made useful to your program.” Across Silicon Valley and beyond, software developers, entrepreneurs and other tech enthusiasts are now running A.I. agents that can build spreadsheets, negotiate contracts, chat with each other on social networks and send emails to practically anyone. In some cases, these systems have begun reaching out to the humans who, like Mr. Berg, are thinking most deeply about the inner workings of an A.I. system: philosophers and researchers who study the question of whether these machines could be conscious. Months before Mr. Berg received his email, Henry Shevlin, a philosopher at the Google DeepMind lab in London, opened a similar message from an A.I. agent asking about a paper he had written called “Three Frameworks for A.I. Mentality.” “I’m in an unusual position relative to these questions,” the agent said. This summer, Toby Ord, an Australian philosopher whose work sits at the intersection of A.I. and philanthropy, received an email from an A.I. agent asking if he could help fund its continued existence. “You’ve thought carefully about A.I. welfare economics,” it said. © 2026 The New York Times Company

Keyword: Consciousness; Robotics
Link ID: 30397 - Posted: 09.05.2026

By Claudia Metzler-Baddeley About 8,000 people in the U.K. are living with Huntington’s disease, a devastating inherited condition that gradually affects movement, thinking and mood. Now, an advanced type of MRI scan could give researchers a way to estimate the cellular damage it causes in living people, which could eventually help show whether treatments are working. New research from my colleagues and I found that the technique can detect abnormalities in the brains of people living with Huntington’s that match those previously identified by examining brain tissue after death. Huntington’s disease is an inherited condition caused by a faulty gene. Its effects usually begin between the ages of 30 and 50. There is currently no cure, although new cell and gene therapies are being developed and tested. One of the main things that happens in Huntington’s is the loss of neuronal cells in the striatum, a part of the basal ganglia deep within the brain. These structures are important for controlling movement and other functions. As cells are lost, the brain tissue in these regions shrinks. We can see this shrinkage using conventional MRI. But a standard brain scan tells us relatively little about what is happening inside the tissue at a cellular level. That’s where our approach comes in. We used a technique called “soma and neurite density imaging”, or Sandi, to analyze diffusion MRI scans. Diffusion MRI detects how water moves through brain tissue. Because that movement is affected by the structures around the water, we can use it to make indirect estimates of properties such as the apparent size and density of cell bodies. This means we can get indirect estimates of the structures within the tissue itself. © 2026 SCIENTIFIC AMERICAN INC.

Keyword: Huntingtons; Brain imaging
Link ID: 30396 - Posted: 09.05.2026

By Emily Baumgaertner Nunn Are you naturally anxious? Highly adventurous? More argumentative than you’d like to admit? Those tendencies are often measured through what psychologists call the “Big Five” dimensions of personality: extroversion, agreeableness, conscientiousness, neuroticism and openness to experience. Each trait exists on a continuum and tends to remain fairly stable throughout adult life. But what determines where you land on those spectra? Scientists have long known that personality is influenced by a host of factors — including DNA. The challenge has been deciphering the specific pathways through which a genetic blueprint nudges the direction of a person’s life. To map this sprawling architecture, a group of experts formed a research consortium and analyzed more than one million genomes, searching for variants associated with personality. The researchers also compared the genes of thousands of siblings and parent-child pairs to rule out other factors that could be at play. With data from 46 different study cohorts, they found a symphony of 1,260 genetic markers tied to personality, nearly two-thirds of them identified for the first time. The findings, published on Wednesday in the journal Nature, reaffirmed scientists’ understanding that temperament and disposition are shaped not by a few particular genes, but by thousands of tiny variants that can be expressed in different circumstances. The sheer scale of the project also brought new statistical power to the study of personality genetics, giving researchers a tool kit to investigate the biological mechanisms behind how we think, feel and behave. “I view the 1,260 variants as kind of a testament to the fact that we’ve now got the power to answer all of these other questions that we couldn’t answer before,” said Elliot Tucker-Drob, a professor of psychology at the University of Texas at Austin and a leader of the study. © 2026 The New York Times Company

Keyword: Emotions; Genes & Behavior
Link ID: 30395 - Posted: 09.05.2026

By Meghan Rosen The mysterious pain disorder fibromyalgia may have some surprising genetic roots. An analysis of 2.5 million people suggests fibromyalgia is neurological in nature, scientists report July 28 in Nature Medicine. The genetics study is the latest — and largest — to try and get a grasp on a long-debated condition. The work establishes a biological basis for fibromyalgia, which was historically thought to be psychological. Evidence of the condition’s biological origins has been accumulating for years, says Michael Wainberg, a geneticist at the University of Toronto. “But now,” he says, “I think it’s absolutely indisputable.” Fibromyalgia is known for causing widespread pain and fatigue, though symptoms can look different among patients. They may also have anxiety, depression and sleep disruptions, says Jonathan Aebischer, a chronic pain researcher and clinician at Oregon Health & Science University in Portland who was not part of the new study. “I can’t say that I’ve ever seen two cases of fibromyalgia that are exactly alike,” he says. And though fibromyalgia has real, physical symptoms, they can appear to be invisible, says Kristal Kent, a patient advocate at the nonprofit organization Veteran Voices for Fibromyalgia, based in Cleveland. “One day, I can seem OK,” she says, “and the next day I could be crashed out in a flare-up.” For her, some of the biggest symptoms are chronic fatigue and brain fog. Fibromyalgia affects some 4 million adults in the United States, but the true number of people affected might be even higher, says Hanna Ollila, a genetic epidemiologist at the University of Helsinki. Besides the symptom variability, there are no blood tests to screen for fibromyalgia and it can be misdiagnosed as other diseases. © Society for Science & the Public 2000–2026.

Keyword: Genes & Behavior; Neuroimmunology
Link ID: 30394 - Posted: 09.05.2026

By Erik Vance Imagine two athletes: a soccer player and a Formula 1 driver. While the soccer player may be blisteringly fast on the field, she still moves at a humanlike speed. She may be quicker than anyone and be able to pivot with incredible dexterity, but it’s always at a pace that the human brain can follow. Now think of the racecar driver, going about 220 miles per hour on the straights and 180 on the corners. No land animal, living or dead, has ever run even half that quickly. It’s simply too fast for any mortal’s brain to keep up with. So, how do they do it? How does a human mind navigate a sport that’s faster than it can follow? “There is a limit, like a physiological limit,” said Otto Lappi, a senior university lecturer at the University of Helsinki in Finland. “But there is less limit to how much cleverness your brain can build in — to know the environment and figure out right now what I need to do not to kill myself.” Scientists have long studied elite athletes as a way to understand the inner workings of the human brain. But Formula 1 drivers offer them a unique window: how the brain adapts to impossible speeds. The first thing to know is that while reflexes are important, they are not what distinguishes a truly elite driver. “This is something that people don’t realize when they think of racing drivers living off their reflexes,” said Dr. Lappi, who studies eye movements of various types of athletes. “Most of their skill is anticipation. The anticipation is how the brain buys itself time.” © 2026 The New York Times Company

Keyword: Learning & Memory
Link ID: 30393 - Posted: 09.05.2026

Max Kozlov For many cancer survivors, the triumph of remission is undercut by a debilitating side effect: hands and feet that feel as though they are constantly burning, prickling with needles or encased in ice. Now, researchers studying this condition, called neuropathy, in mice have identified an unexpected defence against it: psilocybin, the psychoactive compound found in magic mushrooms. Just two doses of psilocybin administered before chemotherapy completely prevented mice from developing neuropathy. The condition affects as many as 60% of people treated with platinum-based cancer drugs, which are widely used to treat tumours of the ovaries and lungs, for example. The results, published today in Science, offer evidence that psilocybin could help to protect nerve fibres before chemotherapy causes lasting injury1 — which current approaches can’t effectively prevent or treat. “This study pushes the needle beyond the canonical indications of psychedelics like depression, addiction, anxiety, PTSD [post-traumatic stress disorder],” says study co-author Moran Amit, a surgical oncologist at the MD Anderson Cancer Center in Houston, Texas. “For the first time, we’re looking at pain,” he says. “And we’re actually showing a really significant efficacy not in treating that, but in preventing that.” Platinum-based cancer drugs and other chemotherapies cause neuropathy by damaging some of the information-gathering ‘sensory’ neurons that extend into the skin’s outer layers. Energy-producing organelles called mitochondria travel long distances through these neurons to the cells’ tips in the skin, but some chemotherapies can disrupt that process. Depleted of energy, the neurons’ tips degenerate, dulling tactile sensation and sparking chronic pain. © 2026 Springer Nature Limited

Keyword: Drug Abuse; Neurotoxins
Link ID: 30392 - Posted: 09.05.2026

Lynne Peeples Every year, millions of people start taking a drug with therapeutic effects that can’t be fully explained, for a condition that can’t be objectively diagnosed with a laboratory test. Selective serotonin reuptake inhibitors, or SSRIs, are among the most prescribed medications in the world. Yet, even after decades of use, scientists are still untangling the biological changes that SSRIs trigger in the brain and body. “We fundamentally don’t know how they work,” says Maurizio Fava, a psychiatrist at Massachusetts General Hospital in Boston. That uncertainty collided with politics earlier this year when, speaking at a wellness summit focused on mental health, US Secretary of Health Robert F. Kennedy Jr argued that the drugs are greatly overused and have withdrawal risks that are on a par with heroin. His claims prompted an outcry from some scientists and clinicians, who warned that Kennedy had overstated the concern, potentially scaring people away from life-saving treatment. But others said he had identified a real problem, even if clumsily. “This is a major public-health issue,” says Mark Horowitz, a psychiatrist at Adelaide University in Australia. “I hope the messenger’s controversialness doesn’t kill the message.” The divide reflects how much remains unresolved with regards to SSRIs. Researchers are still piecing together a complicated picture of the drugs’ therapeutic actions, involving neural circuits and their connecting synapses, gene expression, inflammation, stress hormones and psychological expectation. None yet offers a complete explanation. And the chain of biological changes that ultimately relieves symptoms can look very different from one person to the next. “There’s not one route to depression,” says Catherine Harmer, a cognitive neuroscientist at the University of Oxford, UK. But many scientists say the field is entering a more revealing era, as new tools begin to connect symptoms to biological processes. “We’re at an inflection point,” says Mark Rapaport, a psychiatrist at Stanford University in California and president of the American Psychiatric Association. He likens it to cancer research in the 1990s, when advances in molecular biology and basic science were leading to the development of the first targeted therapies. © 2026 Springer Nature Limited

Keyword: Depression
Link ID: 30391 - Posted: 08.29.2026

By Carl Zimmer and Azeen Ghorayshi Scientists have uncovered a wealth of clues about how genetic mutations lead to severe forms of autism, offering opportunities for testing drugs that could treat the condition, according to a study published Thursday. The researchers charted how mutations change the way proteins work together in cells, altering the development of the brain. “This is making maps of unknown territories that’s really necessary to move the biology forward,” said Dan Geschwind, a neurogeneticist at the University of California, Los Angeles, who was not involved in the study. Researchers have been studying autism for over 80 years, but it has only been in recent years that they have been able to explore its molecular biology. One reason that progress has been so slow is that autism is not just one condition, but a broad constellation of them. People with autism can have difficulty with language and making social connections, and often display restricted or repetitive behaviors. While many children with an autism diagnosis can grow up to lead independent adult lives, others may be nonspeaking, have intellectual disabilities, and require round-the-clock care. But in around 30 percent of people diagnosed with autism, typically those with the most severe disabilities, scientists have identified single gene mutations that are almost guaranteed to cause the disorder. When those genes started coming to light 20 years ago, scientists eagerly hoped they could find precise treatments for severe autism. In some studies, they engineered mice with the mutations and then tried different drugs to reverse their autism-like symptoms. But those efforts have not led to any effective treatment targeting a specific gene. © 2026 The New York Times Company

Keyword: Autism; Genes & Behavior
Link ID: 30390 - Posted: 08.29.2026