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

By Conor Feehly Every moment of our lives, our bodies are awash in sensory signals. Photons hit our retinas. Waves of compressed air collide with our eardrums. Volatile molecules bind to receptors in our nostrils, and chemicals slather our taste buds. Pressure and heat activate nerve endings in our skin. We are able to navigate this torrent because the brain does an enormous amount of data compression. Through a process known as categorization, the brain turns the messy, noisy, information-rich world into objects, people, concepts, and emotions that we can understand and act on at the level of experience. In neuroscience’s traditional view, categorization happens at the very end of sensory processing. The brain passively receives sensory details, then decodes their features and matches them to stored templates in memory, like a clerk shuffling through a neural filing cabinet. But this approach to categorization struggles to account (opens a new tab) for the extraordinary flexibility in the way we assign labels to features of the world. On a clear day on an open street, a sudden rhythmic patter is a pigeon taking flight, yet when we’re walking down a dimly lit alley at night, the same sound is the shuffle of a stranger’s footsteps. How can the brain categorize similar sets of sensory signals in radically different ways for different situations? Two of the world’s leading neuroscientists have brought an updated understanding of brain function and structure to this question. In the pages of Nature Reviews Neuroscience, Lisa Feldman Barrett (opens a new tab), who studies the psychology and neuroscience of emotion at Northeastern University, and Earl Miller (opens a new tab), who studies how the brain carries out goal-directed behavior at the Massachusetts Institute of Technology, collaborated on a new view of categorization. They describe how the brain constantly reconstructs its categories (opens a new tab) moment to moment based not only on senses and memory, but on the body’s immediate physiological needs. © 2026 Simons Foundation

Keyword: Attention
Link ID: 30389 - Posted: 08.29.2026

By Claudia López Lloreda The proteins encoded by 100 genes involved in autism form an interconnected network consisting of multiple protein complexes that serve different cellular functions, according to a study published today in Science. Autism-associated variants may cause this network to rewire, the study also found. Even though autism is a genetically heterogeneous condition, “when you look at the proteins encoded by the genes, and also the specific mutations and the interfaces of protein interactions, the biology starts to converge,” says Kasper Lage, managing director of the Novo Nordisk Foundation Center at the Broad Institute, who was not involved in the work. Many of the proteins the study considered converge on complexes already associated with autism and that are involved in processes such as neural progenitor proliferation and differentiation and neuronal migration, the researchers found. The idea behind the work was to go beyond the genetic studies, which have linked about 250 genes to autism, says study investigator Belinda Wang, assistant professor of psychiatry at the University of California, San Francisco. “Genes can tell us where autism risk begins, but proteins do a lot of the work inside the cells, and so by studying autism at the protein level, maybe this can give us a more direct view of the underlying biology.” Previous network analyses did not reach this magnitude, Lage says. “When you get to the scale that they’re doing in this paper, you can start to do really interesting secondary analysis and pathway and discovery.” © 2026 Simons Foundation

Keyword: Autism; Genes & Behavior
Link ID: 30388 - Posted: 08.29.2026

By Ailie McWhinnie Whether in a deep burrow under frozen winter ground or aboard a far-future interplanetary spaceship, hibernation has long mesmerized sci-fi enthusiasts and nature lovers alike. But exactly how animals lower their body temperatures and metabolisms to enter this state has remained mysterious. “Very little has been known about these mechanisms, especially the neuronal mechanisms,” says Takeshi Sakurai, a sleep and hibernation researcher at the University of Tsukuba. Now, in a preprint posted on bioRxiv, researchers studying hibernating Syrian hamsters have pinpointed for the first time a brain circuit that regulates an animal’s entry into hibernation. The results reveal a “key, really, in the network” and provide “more solid [evidence] than anything we had before” of an ancient hibernation circuit within the mammalian brain, says Matteo Cerri, a physiologist at the University of Bologna who studies hibernation and was not involved in the work. For those pursuing synthetic hibernation, it’s good news. A dormant hibernation circuit across species could help scientists figure out how to induce hibernation in people therapeutically, or even—in a much more distant goal— to enable long-distance space travel. Whereas many animals rely on their environment for heat, birds and mammals can raise and control their body temperatures. The benefit is a high and fairly constant metabolic rate, but the energetic cost is enormous. When this cost gets too high—in particularly cold or food-scarce times, for instance—some animals cope by hibernating. Hibernating animals enter long, deep bouts of a state called torpor in which their body temperature and metabolism drop, usually broken up by brief awakenings. When faced with similar challenges, other animals can enter shorter, shallower one-off bouts of torpor whose relationship to true hibernation has long been debated. Many birds and mammals do neither. © 2026 American Association for the Advancement of Science.

Keyword: Biological Rhythms
Link ID: 30387 - Posted: 08.29.2026

By John Branch Since the degenerative brain disease known as C.T.E. was first scientifically linked to football about 20 years ago, and as hundreds of former professional football players have been diagnosed with the disease after their deaths, a haunting question has lingered: Just how many N.F.L. players will end up with C.T.E.? New data provides a sobering indication: At least one in four of all the people who have played in the N.F.L. might expect to end up with chronic traumatic encephalopathy, according to a study of hundreds of cases over a recent six-year period. Researchers considered every former N.F.L. player who died from 2016 to 2021. There were 878. Some died in their 20s, some in their 80s, most in between. The study’s main finding was simple math: At least 215 of those 878 former players — 24.5 percent — had C.T.E. The actual prevalence could be far higher. The roughly 25 percent rate does not consider the 643 brains that were not examined. Some of those, maybe many of them, likely had C.T.E. too. C.T.E. is a progressive neurological disease caused by repeated impacts to the head. It can be definitively diagnosed only by examining the brain after death. Studies have shown that the rate of C.T.E. in people who have not sustained repeated impacts to the head is nearly zero. If the new study’s statistics were applied to today’s players — 1,696 on the league’s 32 regular-season rosters, not including more than 500 members of practice squads and those ineligible due to injury — at least 400 of them would be diagnosed with C.T.E. Experts say that the rate of brain disease represents an occupational safety hazard with little comparison in the American workplace. “There are workers who’ve been exposed to high levels of asbestos exposure, which leads to very high rates of lung disease,” said David Michaels, who led the Occupational Safety and Health Administration during the Obama administration and is now a professor at the George Washington School of Public Health. “And certainly, you know, a lifetime working in coal mines leads to very high risk of black lung disease. © 2026 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 30386 - Posted: 08.29.2026

By Melinda Wenner Moyer When Juan Rivera was in college, he noticed that the activities he loved, such as going out with friends, had stopped making him happy. “I would be with my friends but not enjoying it fully and just sort of feeling flat,” he said. On bad days, he could barely get out of bed, much less summon the motivation to leave the house. Mr. Rivera, now 35, discussed his struggles with a psychiatrist. She evaluated him, diagnosed him with depression and prescribed an antidepressant. It didn’t work. Over the next few years, she prescribed several others, but those didn’t help him, either. Mr. Rivera, an immigration attorney in Miami, suffers from what most clinicians would call “treatment-resistant depression.” There is no broadly accepted definition of the condition, and there can be various degrees of treatment resistance, said Dr. Gerard Sanacora, director of the Yale Depression Research Program. But many doctors, he said, consider depression to be treatment-resistant if a person has not experienced at least a 50 percent improvement after trying two different antidepressants in succession, each for four to six weeks. Despite its name, treatment-resistant depression can improve and even be cured, experts say. A number of therapies, often in combination, have been shown to help. Why Depression Can Resist Treatment Various factors may increase the likelihood that a person with depression won’t respond to initial drug treatments, said Dr. Debra Kahn, director of the Advanced Psychiatric Therapeutics Clinic at UC Davis Health. © 2026 The New York Times Company

Keyword: Depression
Link ID: 30385 - Posted: 08.22.2026

BY Christie Wilcox Naegleria fowleri is a harmless pond dweller—unless it ends up in the nose of a human swimmer. Once inside, the amoeba can crawl along nerve fibers in the nasal cavity and through little openings in the skull until it reaches the brain. Once there, it can cause an infection that is almost universally fatal, earning it the frightening moniker the “brain-eating amoeba.” Exactly why N. fowleri, which normally feeds on bacteria, exhibits this behavior has long been unclear. But a study posted last month on the preprint server bioRxiv suggests a possible reason: The parasite loves to seek out tight spaces. This “claustrophilic” behavior may help it find its prey—and explain why it occasionally ends up deep in the human brain. “A lot of the research done on Naegleria is focused on drug discovery and not the fundamental reasons behind pathogenesis,” says Ashley Moseman, an immunologist at Duke University who studies the body’s immune response to N. fowleri but who was not involved with the new work. A better understanding of the pathogen’s basic biology could help pave the way for specific drugs against it, which currently don’t exist. N. fowleri, which lives in warm freshwater and soil around the world, can cause a disease called primary amoebic meningoencephalitis (PAM) that starts with a headache, fever, and nausea, quickly followed by confusion, a stiff neck, seizures, hallucinations, and coma. PAM is exceedingly rare, with fewer than 500 reported cases globally since 1962, but it has a fatality rate of about 95%. Doctors have saved some patients using a combination of drugs, including antifungal medications and miltefosine, which is used primarily to treat a parasitic disease named leishmaniasis. But because PAM is so rare and its early symptoms are similar to those of other diseases, the diagnosis often comes after patients have died. © 2026 American Association for the Advancement of Science.

Keyword: Brain Injury/Concussion
Link ID: 30384 - Posted: 08.22.2026

By Michele Patterson Ford When survivors of trauma recount their experiences, they are often questioned because of how they relay their stories. They may have problems remembering what happened, or their memories may be jumbled or even contradictory. People hearing those stories—attorneys, reporters, healthcare workers or friends—may expect a clearer, linear narrative. Those unaffected by trauma may also be surprised to hear how the person acted in the moment. It’s easy to assume that someone experiencing a traumatic event would have a “fight or flight” response, instinctively fighting off a perpetrator or fleeing the scene—but that might not be the case. Understanding the science of how trauma affects memory and behavior reveals why these responses can actually be expected and are not contradictory. In both my academic and clinical work as a psychologist, I have witnessed the impact trauma has on people’s memories and behaviors, especially when an event in their present life triggers something from their past. Research shows that taking a trauma-informed approach, which prioritizes understanding and curiosity about someone’s experience as opposed to judgment or critical evaluation, increases empathy for survivors’ thoughts, feelings and behaviors. According to the World Health Organization, approximately 70 percent of people worldwide report experiencing a traumatic event in their lifetime. The majority of these people do not develop PTSD, a clinical diagnosis of symptoms, such as having nightmares and flashbacks about the event, avoiding places that are reminders of it, and increased arousal that can make concentration and sleep difficult. Many survivors don’t meet criteria for PTSD but struggle with feeling distressed, depressed or anxious. © 2026 SCIENTIFIC AMERICAN INC.

Keyword: Learning & Memory; Stress
Link ID: 30383 - Posted: 08.22.2026