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

By Claudia López Lloreda For five years, several small batches of cortical organoids grew in an isolated incubator, away from possible contamination and doted upon by a Harvard University research team. The organoids didn’t merely survive, though—they generated diverse neurons and glia and acquired transcriptional and epigenetic features of postnatal brains, all on a human-like schedule, according to a new study published today in Nature. Organoids typically model only pre- and perinatal brains and notoriously lack robust electrical activity, says In-Hyun Park, associate professor of neuroscience and genetics at Yale University, who was not involved with the study. The new work provides an avenue to study postnatal stages of development, he says. However, the long-lived organoids started losing neuronal signals around the one-year mark, which continued as they aged, the team found. “Yes, the organoid was maturing, everything was great, but the neurons were suffering,” says study investigator Paola Arlotta, professor of stem cells and regenerative biology at Harvard. Modifying the culture medium enabled the team to grow a new set of organoids that had more mature excitatory neurons, greater neuronal complexity and enhanced electrical activity. “If you want to move forward with more network activity, mature human neurons, you need to adapt your tissue culture,” says Alysson Muotri, professor of pediatrics and cellular and molecular medicine at the University of California, San Diego, who was not involved with the study. “I think it’s an important message.” © 2026 Simons Foundation

Keyword: Development of the Brain
Link ID: 30382 - Posted: 08.22.2026

Sarah Berg Here is something we have never quite said out loud: for a significant portion of the world’s women, hunger is not a temporary state. It is a cognitive condition. It flows beneath everything: the meeting, the conversation, the stream of thought that almost ran its course before something more insistent pulled it back. For many of us, the state of hunger was present since we were old enough to understand that our bodies were under review. I was 11. I was sitting beside a swimming pool that summer, the one before middle school started, trying to follow a conversation I kept losing. I had decided, with the particular certainty children sometimes develop about the rules of the world they are entering, that I would eat as little as possible before sixth grade. The plan involved a sleeve of SnackWell’s cookies per day: fat-free, engineered to taste like cardboard, manufactured specifically for women and girls who had been told that fat was the enemy and desire was something to be managed rather than answered. The SnackWell’s cookie was itself a cultural artefact, a product designed to help women comply with an instruction they had already internalised. It did not quiet the hunger, because hunger is not a preference. It is biology doing what biology does when a body is not fed, sending signals that push everything else aside. During the day, we swam, lay on the concrete, and talked about the coming year. My attention kept sliding away from the conversation. A thought would begin and dissolve into the same insistent loop: how long until dinner, how little I could manage when it arrived, whether anyone had noticed what my body was doing without my permission. I remember listening to a teammate tell a long story and realising I had not heard most of it. Something louder had taken the space the story needed. © Aeon Media Group Ltd. 2012-2026.

Keyword: Anorexia & Bulimia
Link ID: 30381 - Posted: 08.22.2026

By Aimee Cunningham In 2025, the number of children receiving a drug promoted — but unproven — for autism treatment grew, especially toward the end of the year. A new study suggests the late rise was influenced by a Trump administration announcement. At a White House briefing on September 22, 2025, President Trump touted the drug leucovorin as a potential therapeutic for autism. The week before the announcement, roughly 5 children per 100,000 received leucovorin via a prescription in the United States. The week of the announcement, the pharmacy dispensing rate climbed to roughly 7 children per 100,000. By the end of the year, the rate rose to 8 children per 100,000, researchers reported August 12 in the New England Journal of Medicine. “Our study demonstrates the power of the federal government to influence clinical practice,” says Kao-Ping Chua, a pediatrician and health policy researcher at the University of Michigan Medical School in Ann Arbor. If administration communications and decisions are not based on rigorous scientific evidence, it could lead to harms “including giving people false hope and potentially exposing them to the side effects of ineffective medical treatments.” Leucovorin is a form of the essential vitamin folic acid. The drug is prescribed when the body’s method for breaking down folic acid from food is impaired. The U.S. Food and Drug Administration had approved leucovorin for use with certain genetic disorders and to help reduce the side effects of chemotherapy drugs that disrupt that break down. The American Academy of Pediatrics does not recommend leucovorin for autism because of the lack of evidence surrounding dosing, effectiveness and safety. © Society for Science & the Public 2000–2026.

Keyword: Autism
Link ID: 30380 - Posted: 08.22.2026

By Amanda Heidt Earlier this month, the US Food and Drug Administration approved the first drug designed to treat the root cause of narcolepsy, a condition that affects millions of people by causing extreme sleepiness during the day and wakefulness at night. The success of the drug, called oveporexton and marketed as Orzeyful, is being celebrated by those who struggle with narcolepsy. “It’s the best thing that has ever happened to me,” says Tyler Chapman, who volunteered for one of the clinical trials that contributed to the drug’s approval. But it’s also being watched with anticipation by researchers, who see it as the first in a line of therapies for sleep disorders that are likely to be approved in the coming years. These emerging treatments, known as orexin agonists, are exciting because they promise not just to alleviate symptoms of narcolepsy but also to target the disease’s biological cause — and might even have implications for other neuropsychiatric disorders. With this new strategy against narcolepsy, pharmaceutical companies have jumped at the chance to tap into a market that is projected to top US$6.4 billion annually by the early 2030s. “This is a tremendously exciting time for patients and for clinicians and scientists who have been working towards this for many years,” says Barry Lubarsky, the vice-president of medical affairs at the pharmaceutical company Alkermes, which is based in Dublin and is developing its own narcolepsy treatment. A chance to feel normal For Chapman, a 19-year-old student at the University of Tennessee, Knoxville, the milestone is life changing. Chapman had long struggled with his condition, at times sleeping for 16 hours a day, struggling in school and relying heavily on coffee. When he laughed, it would sometimes trigger his body to collapse, even though he remained fully conscious — a symptom known as cataplexy. Instead of experiencing all that university life has to offer, Chapman says that he rarely went out. © 2026 Springer Nature Limited

Keyword: Narcolepsy; Sleep
Link ID: 30379 - Posted: 08.19.2026

By Jake Buehler This nose grows. During harsh Japanese winters, long-clawed shrews’ snouts temporarily expand. The seasonal swelling is the opposite of the previously known winter pattern in shrews, in which the brain and surrounding cranium shrink. The findings complicate our understanding of an already extreme adaptation for harsh, frigid conditions, researchers report August 19 in Proceedings of the Royal Society B. The temporary dwindling and regrowth of the brain and skull tissue in shrews is part of Dehnel’s phenomenon, first described by Polish zoologist August Dehnel in 1949. The phenomenon involves winter reductions in body size and internal organ mass. It’s thought to be an adaptation for surviving winter. Paring back tissues cuts food energy costs, which is useful when calories are scarce. The new findings add an unexpected wrinkle to our understanding of the phenomenon. Yugo Ikeda, a mammalogist at Toyo University in Tokyo, and his colleagues knew about these “mind-boggling” seasonal shifts. Some other animals like weasels, voles and moles experience similar winter changes. But scientists didn’t know if any shrews outside of Europe also went through these changes. Northeast Asia, for instance, has extreme, snowy winters that might present a challenge to local small mammals. The researchers carefully measured the dimensions of 136 skulls from museum specimens of long-clawed shrews (Sorex unguiculatus), a species native to the region. The shrews were collected between 1948 and 1988 on the Japanese island of Hokkaido. Ikeda and his colleagues took photos of the skulls and used software to measure dozens of physical landmarks across them. The team then compared the skull dimensions with the season in which the shrews were collected. © Society for Science & the Public 2000–2026.

Keyword: Biological Rhythms; Chemical Senses (Smell & Taste)
Link ID: 30378 - Posted: 08.19.2026

By Zoe Beketova Efforts to explain rising rates of myopia, or nearsightedness, in children worldwide have made two things clear: More time spent outdoors seems protective, and more time spent indoors increases risk. A new study in tree shrews now suggests a key to preventing myopia may be the indigo portion of sunlight. Adding this part of the light spectrum to the animals’ environment prevented them from developing myopia, researchers report today in Cell Reports Medicine. The findings have not yet been confirmed in humans, but some researchers are cautiously optimistic that increasing children’s exposure to indigo wavelengths could preserve their developing vision as well. “No one knows why outdoor light is good for kids’ eyes,” says Lisa Ostrin, a vision scientist at the State University of New York College of Optometry, who was not involved in the study. “If it turns out to be [the presence of certain wavelengths], it could be so simple to just add in overhead lights and enhance them with additional short wavelengths.” But she stresses that more research is needed to draw that conclusion. Myopia, or nearsightedness, affects almost 3 billion people worldwide, and this number is projected to climb to almost 5 billion by 2050. The condition occurs when the eyeball grows too long in childhood, instead of developing its typical spherical shape. This causes light to focus in front of the retina, the light-sensing layer of tissue along the back of the eye, instead of directly on it, making the resulting image transmitted to the brain unclear. Human genetics do not change fast enough over time to account for the rising rates, which some have blamed on increased reading or computer screen use. Others have said greater exposure to indoor light, with its more limited spectrum of wavelengths compared with outdoor light, could be the problem. © 2026 American Association for the Advancement of Science.

Keyword: Vision; Development of the Brain
Link ID: 30377 - Posted: 08.19.2026

By Sarah Thau Sound the alarm! Activating a subset of neurons in the medulla promotes anxiety in mice, a study published in Neuron finds. Anxiety is typically thought of as a set of “complex, social, environmental, biological, neurobiological interactions” involving multiple regions across the brain, says Oliver Robinson, professor of neuroscience and mental health at University College London, who was not involved in this work. So he was “surprised that you can have such dramatic effects by just looking at a single cell type.” The role of medullary neurons in anxiety adds to a growing body of work on anxiety circuitry, says study investigator Carlos Fernández-Peña, assistant professor of neurological sciences at the University of Nebraska. “It was already complex. Now let’s add some more.” Two sets of neurons—C1 and A1—in the rostral ventrolateral medulla (RVLM) produce catecholamines that could drive anxiety, but only C1 neurons are activated when mice are stressed, Fernández-Peña says. The challenge, then, was to study only C1 neurons, which are intermingled with A1 neurons, in awake mice to uncover their role in anxiety-like behaviors, he says. He and his colleagues employed two different genetic recombination tools—one called INTRSECT and another called ConVERGD—for the first time, according to study investigator Lindsay Schwarz, associate member of the St. Jude Children’s Research Hospital faculty, who co-developed the latter tool. This pairing enabled them to make transgenic mice in which they could optogenetically modulate only the C1 neurons and not the A1 cells, using careful genetic logic. © 2026 Simons Foundation

Keyword: Emotions
Link ID: 30376 - Posted: 08.19.2026

Emily Mullin Erin McNulty had been missing for weeks when her mother, Linda, sat down on a chair in her living room, exhausted. Linda had put in her usual seven-day workweek at the antiques shop she runs near Burlington, Vermont. She’d spent her free evenings driving around, trying to track down her daughter. Erin, 45 at the time, had been using methamphetamine for years. Her substance use started in high school—first alcohol, then marijuana, and eventually heroin. Erin’s brother used heroin, too. When Linda found out, she started driving her kids to a methadone clinic three hours away in Massachusetts. The methadone helped, but it made Erin feel tired all the time, so she started using cocaine to stay awake. There were stretches of sobriety—she had her daughter during one of them, in 2008. The family took trips to the Great Escape waterpark in New York and Hampton Beach in New Hampshire. There were also several overdoses and attempts at rehab. Eventually, Erin switched to suboxone and stopped using heroin. But when a friend introduced her to meth, Linda says, “Erin was gone.” Linda turned on the TV and was flipping through the channels when a 60 Minutes segment caught her attention. It was early 2024, and the show focused on a procedure that might help people with substance use disorders. Linda immediately thought of her daughter. The procedure involved beaming ultrasound through the skull to treat the brain. Researchers at West Virginia University were testing it on people with Alzheimer’s disease and addiction. The neurosurgeon behind the procedure, Ali Rezai, was a pioneer in the field of deep brain stimulation, which involves cutting into the skull to implant electrodes that can reach neurons deep in the brain. He was excited by the ability of ultrasound—the imaging tool best known for observing fetal development during pregnancy—to reach into the same brain structures without breaking the skin. There would be no drilling into the skull, no poking or prodding the brain’s delicate tissue. The ultrasound could be delivered in 20 minutes, and patients could go home the same day. © 2026 Condé Nast.

Keyword: Drug Abuse; Biomechanics
Link ID: 30375 - Posted: 08.15.2026

By Kristen French When evolutionary anthropologist David Samson was living and working among the Hadza tribe in northern Tanzania, he noticed something puzzling: Their sleep was highly fragmented, short in duration, and low in “efficiency,” or actual time spent sleeping versus time in bed. This broken sleep was partly the consequence of activity and noise well into the night in the camps. People stayed up late telling stories, sharing food, and dancing. Yet, the Hadza uniformly reported high satisfaction with their sleep. It challenged the so-called Paleo sleep hypothesis, the notion that hunter-gatherer sleep must be optimally long and deep, but also ran counter to the medical orthodoxy that unbroken sleep is essential to a good night’s rest. Samson traveled to Tanzania to hang out with the Hadza because he was trying to untangle what he calls the sleep paradox: Sleep is critical to human functioning, and yet, we sleep fewer total hours than any other ape, and are still arguably the most evolutionarily successful of the primates. This riddle sent him climbing into chimpanzee nests high in the trees and exploring the sleeping huts and practices of communities around Africa and Madagascar. The stories he collected, people he met, and research findings he uncovered are vividly described in his new book The Sleepless Ape: The Story of Sleep in Human Evolution. I spoke with Samson about what we really need for a good night’s sleep, why we may be on the cusp of a “sleep enlightenment,” and the origins of what he calls the “lie-down-and-die” model of Western sleep. What is the paradox of human sleep? You can just say, “Oh, here’s where humans are relative to other primates on sleep.” But that misses the deeper evolutionary story. When I was a postdoc at Duke University about a decade ago, new data was emerging showing that even after controlling for brain size, body size, social order, and actual phylogenetic relatedness, humans are weird outliers—we’re the shortest sleeping primates, yet we pack in the most REM sleep relative to this short duration.

Keyword: Sleep; Evolution
Link ID: 30374 - Posted: 08.15.2026

By Siddhant Pusdekar Visual experiences during early life famously shape cortical circuits. Animals deprived of vision in one eye rewire their cortex to favor the other eye, according to Nobel Prize-winning work by Hubel and Wiesel. And animals raised in controlled visual environments—surrounded by vertical stripes or horizontal ones, for example—adjust their cortical neurons’ orientation tuning. This kind of experience-dependent plasticity also occurs in the retina itself, leading to lasting changes in behavior, according to a recent zebrafish study in Neuron. The sensory structure had long been thought to be hardwired. “The field in general doesn’t think that activity has any effect on the retina, and it’s always [acting] downstream,” says Marla Feller, professor of neuroscience at University of California Berkeley, who wasn’t involved in the study. Previous research suggests that waves of spontaneous neuronal activity in the retina that begin prenatally and continue till mice open their eyes help shape visual circuitry. The new work is the first to show that what an animal sees can prompt retinal activity that changes the shape and function of its interneurons, altering downstream processes including behavior, Feller says. Vertebrates share many aspects of wiring in the retina, where layers of interneurons transform the pixel-like input from photoreceptors into distinct information channels encoding features of the visual environment. This commonality includes amacrine cells, which are one of the most diverse kinds of interneurons, says Robert Hindges, professor of developmental neurobiology at King’s College London and an investigator on the new study. © 2026 Simons Foundation

Keyword: Development of the Brain; Vision
Link ID: 30373 - Posted: 08.15.2026

By Jennie Erin Smith In the past decade, as opioids claimed nearly half a million lives across the United States, surgeons, dentists, and other clinicians have pined for pain relievers that work as well as hydrocodone or oxycodone but without the high risk of addiction and overdose. Last year, the U.S. Food and Drug Administration (FDA) approved suzetrigine, the first in a new class of drugs that promised pain relief approaching that of opioid pills without those concerns. Many expected to see even more powerful drugs emerge from this class of agents, known as Nav1.8 inhibitors, which block sodium channels on pain-sensing neurons to quell their activity. But efforts to improve on suzetrigine—which has been shown to offer consistent but moderate effects on acute pain—have not produced stronger relief. Recent research has aimed to explain what seems to be a ceiling to the drugs’ benefits, and to get a better handle on their real-world limits. Nav1.8 inhibitors are a needed advance, pain researchers agree, as federal guidance has sought to curb use of opioid painkillers. “Almost everyone you talk to either has a friend or family member that’s been affected by the opioid crisis,” says independent pharmacologist Paul Desjardins, who designed some of the widely used surgical protocols for testing pain drugs and consults for companies developing Nav1.8 inhibitors. But “the data to this point don’t convince me that any of the sodium channel blockers that I’ve seen are better than ibuprofen or naproxen or acetaminophen when they are combined.” The origin story of the drug class led to high hopes. Starting in the late 1990s, genetic studies of people with rare syndromes marked by chronic or excessive pain flagged mutations that caused peripheral sensory neurons, which relay pain signals to the brain, to become hyperactive. The syndromes were linked to changes in the function of two proteins, Nav1.7 and Nav1.8, that regulate neuronal activity by allowing sodium to flow into the cells. Blocking these channels offered a more precise painkilling strategy compared with drugs such as lidocaine, which blocks sodium channels more broadly and has too many toxic effects to be given systemically. © 2026 American Association for the Advancement of Science.

Keyword: Pain & Touch
Link ID: 30372 - Posted: 08.15.2026