By Ingrid Wickelgren The human brain is a vast network of billions of neurons. By exchanging signals to depress or excite each other, they generate patterns that ripple across the brain up to 1,000 times per second. For more than a century, that dizzyingly complex neuronal code was thought to be the sole arbiter of perception, thought, emotion, and behavior, as well as related health conditions. If you wanted to understand the brain, you turned to the study of neurons: neuroscience. But a recent body of work from several labs, published as a trio of papers in Science in 2025, provides the strongest evidence yet that a narrow focus on neurons is woefully insufficient for understanding how the brain works. The experiments, in mice, zebra fish, and fruit flies, reveal that the large brain cells called astrocytes serve as supervisors. Once viewed as mere support cells for neurons, astrocytes are now thought to help tune brain circuits and thereby control overall brain state or mood — say, our level of alertness, anxiousness, or apathy. Astrocytes, which outnumber neurons in many brain regions, have complex and varied shapes, and sometimes tendrils, that can envelop hundreds of thousands or millions of synapses, the junctions where neurons exchange molecular signals. This anatomical arrangement perfectly positions astrocytes to affect information flow, though whether or how they alter activity at synapses has long been controversial, in part because the mechanisms of potential interactions weren’t fully understood. In revealing how astrocytes temper synaptic conversations, the new studies make astrocytes’ influence impossible to ignore. “We live in the age of connectomics, where everyone loves to say [that] if you understand the connections [between neurons], we can understand how the brain works. That’s not true,” said Marc Freeman (opens a new tab), the director of the Vollum Institute, an independent neuroscience research center at Oregon Health and Science University, who led one of the new studies. “You can get dramatic changes in firing patterns of neurons with zero changes in [neuronal] connectivity.” © 2026 Simons Foundation

Keyword: Glia; Learning & Memory
Link ID: 30103 - Posted: 01.31.2026

By Amy X. Wang Alice, fumbling through Wonderland, comes across a mushroom. One bite of it shrinks her down in size. Chowing on the other side makes her swell up, huge, taller than the treetops. Urgently, Alice sets to work “nibbling first at one and then at the other, and growing sometimes taller and sometimes shorter,” until finally she succeeds in “bringing herself down to her usual height” — whereupon everything feels “quite strange.” Is this Lewis Carroll’s 1865 fantasy tale or … the average body-conscious, improvement-obsessed 2026 Whole Foods shopper? Mushrooms, long venerated in literature as dark transformative forces, have become Goopified. Nowadays, you can chug “adaptogenic mushroom coffee,” slurp “functional mushroom cocoa,” doze off with “mushroom sleep drops” or ingest/imbibe any number of other tinctures in the billion-dollar fungal supplements market that promise to fine-tune, or even totally recalibrate, the self. The latest and hottest items in this booming new retail category are mushroom gummies, gushed over by wellness influencers, spilling out from supermarket shelves right there next to your standard cough drops and protein bars. Fungi have aided medical advances like antibiotics and statins, it’s true, and certain species have shown promising results in fighting Parkinson’s or cancer — but what these pastel gumdrops proffer is a broader, more elliptical “cellular well-being.” The mystique feels intentional on product-makers’ part: Like Carroll’s baffled heroine, maybe you’re meant to be in a bit of thrall to the mysterious, almighty mushroom — lurching through Wonderland, charmed and confused by design. After all, you wonder, what are these ancient, alien creatures, growing in the secret dark? Hippocrates was supposedly using them to cauterize wounds around the 5th century B.C.E. In the Super Mario video games, mushrooms might give you extra lives; in HBO’s “The Last of Us,” they bring about the ruin of human civilization. © 2026 The New York Times Company

Keyword: Attention; Drug Abuse
Link ID: 30102 - Posted: 01.31.2026

By Calli McMurray In 2010, Ardem Patapoutian unmasked a piece of cellular machinery that had long evaded identification: PIEZO channels, pores wrenched open by changes in a cell’s membrane tension to allow ions to flow through, thereby converting mechanical force into electrical activity. The discovery marked a turning point for the field of mechanosensation—a process that can be unwieldy to study, says Arthur Beyder, associate professor of physiology and medicine at the Mayo Clinic, because “it reaches its fingers into everything.” The field needed “something to grab onto,” he says, to untangle these processes from other sensory ones—and PIEZO channels provided the first handhold. The PIEZO discovery garnered much attention, and since then, a flurry of studies have outlined how the channels contribute to touch, itch and proprioception. In 2021, Patapoutian shared the Nobel Prize in Physiology or Medicine for his contributions to this work. Now, a growing cadre of researchers is using these receptors as a tool to explore interoception, or the brain’s sense of what the internal organs are doing. “We’re seeing a resurgence and an expansion of research in this area,” says Miriam Goodman, professor of molecular and cellular physiology at Stanford University. The field, she adds, is in the middle of a “PIEZO-driven renaissance.” Even a body at rest is in constant motion: The heart pumps blood, the lungs expand and contract, the gut squeezes food, and the bladder stretches with urine. Biologists had intuited that mechanical force was a key part of these processes—and also part of how organs communicate with the brain—but for decades they did not have a way to dive into the molecular mechanisms behind them. © 2026 Simons Foundation

Keyword: Pain & Touch
Link ID: 30101 - Posted: 01.31.2026

By Azeen Ghorayshi Health Secretary Robert F. Kennedy Jr. has overhauled a panel that helps the federal government set priorities for autism research and social services, installing several members who have said that vaccines can cause autism despite decades of research that has failed to establish such a link. The panel, the Interagency Autism Coordinating Committee, was established in 2000 and has historically included autistic people, parents, scientists and clinicians, as well as federal employees, who hold public meetings to debate how federal funds should best be allocated to support people with autism. The 21 new public members selected by Mr. Kennedy include many outspoken activists, among them a former employee of a super PAC that supported Mr. Kennedy’s presidential campaign, a doctor who has been sued over dangerous heavy metal treatments for a young child with autism, a political economist who has testified against vaccines before a congressional committee, and parents who have spoken publicly about their belief that their children’s autism was caused by vaccines. The group, which also includes 21 government members across many federal agencies, will advise the federal government on how to prioritize the $2 billion allocated by Congress toward autism research and services over the next five years. Though it’s not yet clear what the committee will do — or what it can do, given that it serves only an advisory function — many longtime autism advocates and researchers said they were alarmed by the fact that the committee seemed stacked to advance Mr. Kennedy’s priorities on vaccines. “The new committee does not represent the autism community,” said Alison Singer, who served on the committee from 2007 to 2019. Ms. Singer, whose 28-year-old daughter has profound autism, is the head of the Autism Science Foundation. “It disproportionately, excruciatingly so, represents an extremely small subset of families who believe vaccines cause autism.” © 2026 The New York Times Company

Keyword: Autism
Link ID: 30100 - Posted: 01.31.2026

By Simon Makin Positive thinking may boost the body’s defenses against disease. Increasing activity in a brain region that controls motivation and expectation, specifically the brain’s reward system, is linked with making more antibodies after receiving a vaccine. The finding suggests these boosts were related to the placebo effect, researchers report January 19 in Nature Medicine. “Placebo is a self-help mechanism, and here we actually harness it,” says Talma Hendler, a neuroscientist at Tel Aviv University. “This suggests we could use the brain to help the body fight illness.” The work is important because it “is first-in-human evidence of a relationship between brain reward systems and immune function,” says Tor Wager, a neuroscientist at Dartmouth College in Hanover, N.H., who was not involved in the study. The study was not designed to test vaccine effectiveness. Larger studies, including more complete immune assessments, will be required to test this association as a medical intervention. Scientists have found many links between the brain and bodily health. Both negative and positive mental states can affect the immune system, and studies in rodents have suggested that the brain’s reward network is involved in these effects. To find out if the same circuitry was at play in humans, Hendler and colleagues trained healthy volunteers to regulate their brain activity using neurofeedback, a technique that uses brain imaging to show users the activity of the area they are trying to boost. The team randomly assigned 85 participants to receive training aimed at increasing activity in either their reward network or a different network, or to receive no training. © Society for Science & the Public 2000–2026.

Keyword: Neuroimmunology
Link ID: 30099 - Posted: 01.31.2026

By Alessio Cozzolino After a heart attack, the heart “talks” to the brain. And that conversation may make recovery worse. Shutting down nerve cells that send messages from injured heart cells to the brain boosted the heart’s ability to pump and decreased scarring, experiments in mice show. Targeting inflammation in a part of the nervous system where those “damage” messages wind up also improved heart function and tissue repair, scientists report January 27 in Cell. “This research is another great example highlighting that we cannot look at one organ and its disease in isolation,” says Wolfram Poller, an interventional cardiologist at Massachusetts General Hospital and Harvard Medical School who was not involved in the study. “And it opens the door to new therapeutic strategies and targets that go beyond the heart.” Someone in the United States has a heart attack about every 40 seconds, according to the U.S. Centers for Disease Control and Prevention. That adds up to about 805,000 people each year. A heart attack is a mechanical problem caused by the obstruction of a coronary artery, usually by a blood clot. If the blockage lasts long enough, the affected cells may start to die. Heart attacks can have long-term effects such as a weakened heart, a reduced ability to pump blood, irregular heart rhythms, and a higher risk of heart failure or another heart attack. Although experts knew from previous research that the nervous and immune systems could amplify inflammation and slow healing, the key players and pathways involved were unknown, says Vineet Augustine, a neurobiologist at the University of California, San Diego. © Society for Science & the Public 2000–2026

Keyword: Neuroimmunology
Link ID: 30098 - Posted: 01.28.2026

By Jackie Flynn Mogensen Everyone who menstruates and lives long enough experiences menopause in one form or another. Yet despite that, research into what happens during this natural cessation of menstruation and why is limited. Scientists know that menopause can cause a myriad of neurological symptoms, from hot flashes to poor sleep to depression. But what is going on in people’s brain during this period is still murky. Now new research offers clues to a link between menopause and changes in the brain’s gray matter, as well as anxiety and depression. Using brain scans from 10,873 people in the U.K., the researchers found that postmenopausal participants showed lower volumes of gray matter in the entorhinal cortex and hippocampus, which are involved in storing and retrieving memories, and in the anterior cingulate, which is involved in emotional regulation. The researchers also looked at whether hormone replacement therapy (HRT), a frontline but still rarely prescribed treatment for symptoms of menopause, might ameliorate some of these changes. Barbara Sahakian, a psychiatry professor at the University of Cambridge and an author of the study, explains that she and her colleagues theorized HRT might influence people’s experiences, tamping down their neurological symptoms, for instance. “That was the hypothesis,” she says, “but it didn’t seem to pan out completely that way.” They found that people who were treated with HRT for menopause showed lower volumes of gray matter in some areas of the brain than those who did not receive HRT. The HRT group also showed higher rates of anxiety and depression—importantly, Sahakian says their work doesn’t find that HRT treatment causes brain changes or menopause symptoms. Previous research suggests HRT prescribed during the run-up to menopause and early postmenopause can reduce anxiety, depending on the kind of HRT and dose, in at least some women. And a subsequent analysis found that participants who were prescribed HRT were more likely to have reported anxiety and depression before HRT treatment, the study explains. © 2025 SCIENTIFIC AMERICAN,

Keyword: Hormones & Behavior; Development of the Brain
Link ID: 30097 - Posted: 01.28.2026

By Joshua P. Johansen Growing up in the 1980s in Santa Cruz, California, where redwood-covered mountains descend to the rocky edge of the Pacific, might sound idyllic. But in the dark wake of the drug-fueled ’70s, the beach town could also be frightening. There was a bully at my high school who once chased me down the street threatening to hurt me. Unsurprisingly, catching sight of him in the hallways or at the skate park filled me with dread. Just walking past his house would trigger a wave of anxiety. Yet if I saw him in class, with teachers present, I felt more at ease. How did my brain know to fear him only in specific circumstances? More broadly, how did I infer emotional significance from the world around me? The fact that I or anyone can make these judgments suggests that emotion arises from an internal model in the brain that supports inference, abstraction and flexible, context-dependent evaluations of threat or safety. These model-based emotion systems helped me infer danger from otherwise innocuous features of the environment, such as the bully’s house, or to downgrade my alarm, as I did when an adult was present. Understanding the neural basis of emotion is a central question in neuroscience, with profound implications for the treatment of anxiety, trauma and mood disorders. Yet the field remains divided over what emotions are and how they should be defined, limiting progress. On one side are neurobiologists focused on the neural underpinnings of simple learned and innate defensive behaviors. On the other are psychological theorists who view emotions as subjective experiences arising from complex conceptual brain models of the world that are unique to humans. This divide fuels persistent arguments over whether emotion should be defined primarily as a conscious state or not. Though subjective feelings are undeniably important, limiting our definitions to conscious phenomena prevents us from studying the underlying mechanisms in nonhuman species. To move forward, we need to identify the conserved neural processes that support higher-order, internal-model-based emotional experiences across species, regardless of whether they rise to consciousness. © 2026 Simons Foundation

Keyword: Emotions; Consciousness
Link ID: 30096 - Posted: 01.28.2026

Jon Hamilton At a press conference in late 2025, federal officials made some big claims about leucovorin, a prescription drug usually reserved for people on cancer chemotherapy. "We're going to change the label to make it available [to children with autism spectrum disorder]," said Dr. Marty Makary, commissioner of the Food and Drug Administration. "Hundreds of thousands of kids, in my opinion, will benefit." The Trump administration has suggested that leucovorin, a drug used in cancer treatment, might have some benefit for children with autism. Many researchers and families aren't so sure. The FDA still hasn't made that label change. Since Makary's remarks, though, more than 25,000 people have joined a Facebook group called Leucovorin for Autism. Most members appear to be parents seeking the drug for their autistic children. Also since the press conference, some doctors have begun writing off-label prescriptions for autistic children, against the advice of medical groups including the American Academy of Pediatrics. The buzz about leucovorin has led to a shortage of the drug. In response, the FDA is temporarily allowing imports of tablets that are made in Spain and sold in Canada, but not approved in the U.S. All of this is part of a familiar cycle for Dr. Paul Offit, who directs the vaccine education center at Children's Hospital of Philadelphia. Offit says he realized years ago that leucovorin's popularity was far ahead of the science. Jason Mazzola walks to work at The Residence at Natick South, an LCB Senior Living community in Natick, MA. August 22, 2024. © 2026 npr

Keyword: Autism
Link ID: 30095 - Posted: 01.28.2026

By Yasemin Saplakoglu On a remote island in the Indian Ocean, six closely watched bats took to the star-draped skies. As they flew across the seven-acre speck of land, devices implanted in their brains pinged data back to a group of sleepy-eyed neuroscientists monitoring them from below. The researchers were working to understand how these flying mammals, who have brains not unlike our own, develop a sense of direction while navigating a new environment. The research, published in Science, reported that the bats used a network of brain cells (opens a new tab) that informed their sense of direction around the island. Their “internal compass” was tuned by neither the Earth’s magnetic field nor the stars in the sky, but rather by landmarks that informed a mental map of the animal’s environment. These first-ever wild experiments in mammalian mapmaking confirm decades of lab results and support one of two competing theories about how an internal neural compass anchors itself to the environment. “Now we’re understanding a basic principle about how the mammalian brain works” under natural, real-world conditions, said the behavioral neuroscientist Paul Dudchenko (opens a new tab), who studies spatial navigation at the University of Stirling in the United Kingdom and was not involved in the study. “It will be a paper people will be talking about for 50 years.” Follow-up experiments that haven’t yet been published show that other cells critical to navigation encode much more information in the wild than they do in the lab, emphasizing the need to test neurobiological theories in the real world. Neuroscientists believe that a similar internal compass, composed of neurons known as “head direction cells,” might also exist in the human brain — though they haven’t yet been located. If they are someday found, the mechanism could shed light on common sensations such as getting “turned around” and quickly reorienting oneself. It might even explain why some of us are so bad at finding our way. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30094 - Posted: 01.24.2026

By Claudia López Lloreda The U.S. Brain Research through Advancing Innovative Neurotechnologies (BRAIN) Initiative is kicking off a new phase. In a road map published in November, it identified four research priorities for the next decade: integrating its databases, informing precision circuit therapies, understanding human neuroscience and advancing NeuroAI. The plan shows a thoughtful effort to “protect a very important initiative,” says J. Anthony Movshon, professor of neural science and psychology at New York University—at a time when its future seems unsettled. The BRAIN Initiative is co-led by the directors of the National Institute of Mental Health and the National Institute for Neurological Disorders and Stroke. But the NIMH has had an acting director since June 2024. Last month, the Trump administration terminated the initiative’s other co-director—Walter Koroshetz—from his role as director of the National Institute for Neurological Disorders and Stroke. And it is not clear whether the initiative will have sufficient funding or support to undertake this decade-long effort, says Joshua Sanes, professor emeritus of molecular and cellular biology at Harvard University and contributing editor for The Transmitter. “My guess is that if things continue politically the way they’re going now, [these goals] would not be accomplished in the United States in the next 10 years.” Even if the BRAIN Initiative receives the amount of funding it is expecting, many neuroscientists are too busy grappling with the fallout of grant cancellations, hiring freezes and the loss of training programs to think about the future, says Eve Marder, university professor of biology at Brandeis University. “I’m talking to all these people who are struggling to keep their labs open.” “You can have all the dreams in the universe,” but these big-picture speculations, which may require vast resources, are hard to reconcile with the erosion and destruction of academic science and training programs for young investigators, she adds. “It is difficult to look at a 10-year horizon, and [it] may be a waste of time and effort when we don’t know what is happening to science funding in the next year.” © 2026 Simons Foundation

Keyword: Brain imaging
Link ID: 30093 - Posted: 01.24.2026

Heidi Ledford For decades, researchers have noted that cancer and Alzheimer’s disease are rarely found in the same person, fuelling speculation that one condition might offer some degree of protection from the other. Now, a study in mice provides a possible molecular solution to the medical mystery: a protein produced by cancer cells seems to infiltrate the brain, where it helps to break apart clumps of misfolded proteins that are often associated with Alzheimer’s disease. The study, which was 15 years in the making, was published on 22 January in Cell1 and could help researchers to design drugs to treat Alzheimer’s disease. “They have a piece of the puzzle,” says Donald Weaver, a neurologist and chemist at the Krembil Research Institute at the University of Toronto in Canada, who was not involved in the study. “It’s not the full picture by any stretch of the imagination. But it’s an interesting piece.” Alzheimer’s mystery Weaver has been interested in that puzzle ever since he began his medical training, when a senior pathologist made an offhand comment: “If you see someone with Alzheimer’s disease, they’ve never had cancer.” The remark stuck with Weaver over the years as he diagnosed thousands of people with Alzheimer’s disease. “I can’t remember a single one that has had cancer,” he says. Epidemiological data do not draw such a clear divide, but a 2020 meta-analysis of data from more than 9.6 million people found that cancer diagnosis was associated with an 11% decreased incidence of Alzheimer’s disease2. It has been a difficult relationship to unpick: researchers must control for a variety of external factors. For example, people might die of cancer before they are old enough to develop symptoms of Alzheimer’s disease, and some cancer treatments can cause cognitive difficulties, which could obscure an Alzheimer’s diagnosis. © 2026 Springer Nature Limited

Keyword: Alzheimers; Stress
Link ID: 30092 - Posted: 01.24.2026

By Laura Sanders The brain’s “little brain” may hold big promise for people with language trouble. Tucked into the base of the brain, the fist-sized cerebellum is most known for its role in movement, posture and coordination. A new study maps the language system in this out-of-the-way place. These results, published January 22 in Neuron, uncover a spot in the cerebellum that shows strong and selective activity for language. The new study is “excellent,” says neurologist and cerebellum researcher Jeremy Schmahmann of Massachusetts General Hospital and Harvard Medical School in Boston. His work and that of others have shown that the cerebellum contributes to language and thinking more generally. The new research scrutinized the cerebellum in detail, “confirming and extending previous observations and contributing to our understanding” of the cerebellum’s activity, he says. Neuroscientist Colton Casto combed through about 15 years of brain scanning data collected by study coauthor Evelina Fedorenko, a cognitive neuroscientist at MIT, and her colleagues. Putting the data all together, the scans of 846 people showed brain activity in four spots in the right side of the cerebellum as people read or listened to a story. Three of these spots were also active when people did other things, such as working out a math problem, or listening to music or watching a movie without words. But one spot was more discerning, says Casto, of MIT and Harvard University. This region didn’t respond to nonverbal movies or math. It also ignored orchestral or jazz music, which, like language, relies on syntax and patterns and sound. Instead, this spot is attuned specifically to words. “You have to be reading or listening to language to fully recruit this region,” Casto says. © Society for Science & the Public 2000–2026.

Keyword: Language
Link ID: 30091 - Posted: 01.24.2026

By Allison Parshall Until half a billion years ago, life on Earth was slow. The seas were home to single-celled microbes and largely stationary soft-bodied creatures. But at the dawn of the Cambrian era, some 540 million years ago, everything exploded. Bodies diversified in all directions, and many organisms developed appendages that let them move quickly around their environment. These ecosystems became competitive places full of predators and prey. And our branch of the tree of life evolved an incredible structure to navigate it all: the brain. We don’t know whether this was the moment when consciousness first arose on Earth. But it might have been when living creatures began to really need something like it to combine a barrage of sensory information into one unified experience that could guide their actions. It’s because of this ability to experience that, eventually, we began to feel pain and pleasure. Eventually, we became guided not just by base needs but by curiosity, emotions and introspection. Over time we became aware of ourselves. This last step is what we have to thank for most of art, science and philosophy—and the millennia-long quest to understand consciousness itself. This state of awareness of ourselves and our environment comes with many mysteries. Why does being awake and alive, being yourself, feel like anything at all, and where does this singular sense of awareness come from in the brain? These questions may have objective answers, but because they are about private, subjective experiences that can’t be directly measured, they exist at the very boundaries of what the scientific method can reveal. Still, in the past 30 years neuroscientists scouring the brain for the so-called neural correlates of consciousness have learned a lot. Their search has revealed constellations of brain networks whose connections help to explain what happens when we lose consciousness. We now have troves of data and working theories, some with mind-bending implications. We have tools to help us detect consciousness in people with brain injuries. But we still don’t have easy answers—researchers can’t even agree on what consciousness is, let alone how best to reveal its secrets. The past few years have seen accusations of pseudoscience, results that challenge leading theories, and the uneasy feeling of a field at a crossroads. © 2025 SCIENTIFIC AMERICAN,

Keyword: Consciousness; Brain imaging
Link ID: 30090 - Posted: 01.21.2026

By Pria Anand I loved literature before I loved medicine, and as a medical student, I often found that my textbooks left me cold, their medical jargon somehow missing the point of profound diseases able to rewrite a person’s life and identity. I was born, I decided, a century too late: I found the stories I craved, not in contemporary textbooks, but in outdated case reports, 18th- and 19-century descriptions of how the diseases I was studying might shape the life of a single patient. These reports were alive with vivid details: how someone’s vision loss affected their golf game or their smoking habit, their work or their love life. They were all tragedies: Each ended with an autopsy, a patient’s brain dissected to discover where, exactly, the problem lay, to inch closer to an understanding of the geography of the soul. To write these case studies, neurologists awaited the deaths and brains of living patients, robbing their subjects of the ability to choose what would become of their own bodies—the ability to write the endings of their own stories—after they had already been sapped of agency by their illnesses. Among these case reports was one from a forbidding state hospital in the north of Moscow: the story of a 19th-century Russian journalist referred to simply as “a learned man.” The journalist suffered a type of alcoholic dementia because of the brandy he often drank to cure his writer’s block and he developed a profound amnesia. He could not remember where he was or why. He could win a game of checkers but would forget that he had even played the minute the game ended. In the place of these lost memories, the journalist’s imagination spun elaborate narratives; he believed he had written an article when in fact he had barely begun to conceive it before he became sick, would describe the prior day’s visit to a far-off place when in actuality he had been too weak to get out of bed, and maintained that some of his possessions—kept in a hospital safe—had been taken from him as part of an elaborate heist. Sacks’ journals suggest he injected his own experiences into the stories of his patients. © 2026 NautilusNext Inc.,

Keyword: Attention; Learning & Memory
Link ID: 30089 - Posted: 01.21.2026

By Erin Garcia de Jesús A deck brush can be a good tool for the right task. Just ask Veronika, the Brown Swiss cow. Veronika uses both ends of a deck brush to scratch various parts of her body, researchers report January 19 in Current Biology. It’s the first reported tool use in a cow, a species that is often “cognitively underestimated,” the researchers say. Cows usually rub against trees, rocks or wooden planks to scratch, but Veronika’s handy tool allows her to reach parts of her body that she couldn’t otherwise, says Antonio Osuna-Mascaró, a cognitive biologist at the Messerli Research Institute of the University of Veterinary Medicine, Vienna. It’s unclear how the cow figured it out, but “somehow Veronika learned to use tools, and she’s doing something that other cows simply can’t.” Veronika, a pet cow that lives in a pasture on a small Austrian farm, picks up the brush by its handle with her tongue and twists her neck to place the brush where she needs it. Setting the brush in front of her in different orientations showed that she uses the hard, bristled end to target most areas, including the tough, thick skin on her back. She also uses the nonbristled end, slowly moving the handle over softer body parts such as her belly button and udder. Veronika uses different parts of a deck brush to reach various parts of her body. She uses the brush end to scratch large areas such as her thigh (top left) and back (top right). She uses the handle to scratch more delicate areas such as her navel flap (bottom left) and anus (bottom right). © Society for Science & the Public 2000–2026.

Keyword: Learning & Memory; Evolution
Link ID: 30088 - Posted: 01.21.2026

By Ellen Barry and Pam Belluck Emily Sliwinski got home from the hospital after giving birth to her first child three years ago, and almost immediately began spiraling. Her thoughts raced; she was unable to sleep; she began hallucinating that her dog was speaking to her. She became obsessed with solving the national shortage of infant formula, covering a corkboard with notes and ideas. About a week later, Ms. Sliwinski, of Greensboro, N.C., went to a hospital emergency room, thinking she would be given medication to help her sleep, she said. She had no history of mental health issues. When doctors decided to commit her for inpatient psychiatric treatment, she became so agitated and fearful that she slapped her mother and her husband. She spent 11 days in the psychiatric hospital, but it didn’t help. “Every day I was trying to figure out where I was and what was happening,” Ms. Sliwinski, 33, recalled. Doctors there did not connect her symptoms to childbirth, she said, and diagnosed her with schizophrenia. It was only when her family got her transferred to a specialized perinatal psychiatric unit at the University of North Carolina at Chapel Hill that doctors zeroed in on the right diagnosis: postpartum psychosis. Ms. Sliwinski’s delayed diagnosis reflects an issue simmering in the highest echelons of American psychiatry. For more than five years, a group of women’s health specialists have been pushing for postpartum psychosis to be listed as a distinct diagnosis in the Diagnostic and Statistical Manual of Mental Disorders, the thousand-page guidebook that influences research funding, medical training and clinical care. But two committees at the apex of the D.S.M. have been split over whether to add it. “Psychiatry’s Bible,” as it is sometimes known, has raised the evidentiary bar for including new diagnoses — only one, prolonged grief syndrome, has been added since 2013. © 2026 The New York Times Company

Keyword: Depression; Hormones & Behavior
Link ID: 30087 - Posted: 01.21.2026

By Kristen French In 1998, neuroscientist Christof Koch bet philosopher David Chalmers that within 25 years, scientists would discover the neural correlates of consciousness. He was certain that we were on the cusp of solving the so-called hard problem: how the physical flesh of the brain gives way to the everyday streams of feelings, sensations, and thoughts that make up our waking experience. Nautilus Members enjoy an ad-free experience. Log in or Join now . That bet didn’t go well for Koch: A couple of years ago, he paid up, delivering a case of fine wine to his opponent on a conference stage in New York City. But many scientists still believe that the scientific keys to the kingdom of consciousness are within reach. Lately, some are focusing their attention on a new technology called transcranial focused ultrasound, in which acoustic waves are transmitted through the skull deep into the interior tissues. These waves can be used to stimulate specific target areas as small as a few millimeters in size and to monitor the changes that result. Now, two researchers from MIT have mapped out specific ways to use the technology to chip away at the hard problem. Because transcranial focused ultrasound offers a powerful and noninvasive way to alter brain activity, it will allow scientists to track cause-and-effect for the first time, they argue. In a new paper, published in Neuroscience and Biobehavioral Reviews, they plot out a series of experiments that will aim to answer how consciousness arises in the brain—and where. “Transcranial focused ultrasound will let you stimulate different parts of the brain in healthy subjects, in ways you just couldn’t before,” Daniel Freeman, an MIT researcher and co-author of the paper, explained in a statement. “This is a tool that’s not just useful for medicine or even basic science, but could also help address the hard problem of consciousness. It can probe where in the brain are the neural circuits that generate a sense of pain, a sense of vision, or even something as complex as human thought.” © 2026 NautilusNext Inc.,

Keyword: Consciousness
Link ID: 30086 - Posted: 01.17.2026

By Azeen Ghorayshi A scientific review of 43 studies on acetaminophen use during pregnancy concluded that there was no evidence that the painkiller increased the risk of autism or other neurodevelopmental disorders. “We found no clinically important increase in the risk of autism, A.D.H.D. or intellectual disability,” Dr. Asma Khalil, a professor of obstetrics and maternal fetal medicine at St. George’s Hospital, University of London, and the lead author of the report, said at a news briefing. The study was published on Friday in the British medical journal The Lancet. Acetaminophen, the active ingredient in Tylenol, remains “the first-line treatment that we would recommend if the pregnant women have pain or fever in pregnancy,” Dr. Khalil said. Studies that have examined a possible link between acetaminophen in pregnancy and a risk of neurodevelopmental disorders have produced conflicting data, with some finding no connection and others finding small increases in risk. The new review comes after President Trump told pregnant women during a news conference in September to “tough it out” and “fight like hell” not to take Tylenol, because he said the painkiller could cause autism in children. The message was delivered as part of a broader campaign by Health Secretary Robert F. Kennedy Jr. to try to identify the causes behind rising autism rates among children in the United States, zeroing in on the unproven risks of acetaminophen and long-discredited theories that vaccines cause autism. Medical groups worldwide, including the American College of Obstetricians and Gynecologists, quickly disputed the president’s statements. They argued that doctors already advised their pregnant patients to use acetaminophen judiciously, and cautioned that untreated fevers during pregnancy could cause health problems for the mother and the baby © 2026 The New York Times Company

Keyword: Autism
Link ID: 30085 - Posted: 01.17.2026

By Angie Voyles Askham More than 200 published studies and at least seven ongoing clinical trials rely on potentially faulty brain network maps, according to a study published today in Nature Neuroscience. The findings cast doubt on a widely used method to generate brain network maps, says František Váša, senior lecturer in machine learning and computational neuroscience at King’s College London, who was not involved in the new study and has not used the approach in his own work. “I think it’s worth revisiting some of the literature critically,” he says. And for those who use the method or plan to, “proceed with caution,” he adds. The creators of the method, called lesion network mapping (LNM), say that the issues raised by the new study are not insurmountable. The study’s “results are often striking and tell an important cautionary point—that lesion network mapping can be prone to false-positive findings or nonspecific findings, and study designs need to be constructed carefully in a way that can account for this,” wrote LNM co-developer Aaron Boes, professor of pediatrics at the University of Iowa’s Carver College of Medicine, in an email to The Transmitter. Boes and his colleagues developed LNM in 2015 to identify the pattern of brain activity disrupted in a given neurological condition, whether obsessive-compulsive disorder, Parkinson’s disease or psychopathy. It spawned a new way to put functional MRI to practical use, offering a clear brain network to target for treatment, says Martijn van den Heuvel, professor of computational neuroimaging and brain systems at Vrije Universiteit Amsterdam and an investigator on the new study. © 2026 Simons Foundation

Keyword: Brain imaging
Link ID: 30084 - Posted: 01.17.2026