Nate Scharping Whether or not we have free will is a question philosophers have been debating for millennia. In the early 1980s, there was a brief moment when it appeared the debate may finally have been settled. The potential solution came not from philosophy, but neuroscience. The answer, somewhat depressingly, was that free will didn’t exist. Experiments carried out by the neuroscientist Benjamin Libet appeared to show decisions being made in the brain before people were even aware of them. It was as if science had finally revealed the strings of the puppet master controlling our thoughts and actions. To even casual observers of the history of inquiries into free will, this pronouncement felt premature. Thankfully, they were right. Scientists today are much more sceptical not only of the idea that free will doesn’t exist, but also of the notion that brain scans will ever definitively prove or disprove its existence. But why? Ultimately, the question of free will may be best left to philosophers, but that doesn’t mean it’s a topic neuroscientists should ignore. Experiments into how the human brain makes decisions have led to important insights into neurology and psychology, and have expanded our understanding of the brain’s inner workings. Those experiments include the ones Libet conducted in the 1980s, which, although viewed in a more critical light now, paved the way for decades of innovative research. The experiments were simple. Libet attached volunteers to an electroencephalogram (EEG) machine to monitor their brain activity, then placed a button in front of them and asked them to decide when they wanted to press it. While they were deciding, they had to watch a timer, consisting of a dot moving around the inside of a circle (like a second hand on a clock). Each volunteer had to note the dot’s position when they decided to press the button. With the EEGs, Libet was looking for something called a readiness potential, a build-up of activity in the brain’s motor cortex that precedes a muscle movement. He was hoping to see how a volunteer’s awareness of their decision to move (their noting of the dot’s position) lined up with their readiness potential. © Our Media 2026

Keyword: Consciousness; Attention
Link ID: 30171 - Posted: 03.21.2026

Max Kozlov For decades, scientists have struggled to understand exactly how years of taking hits to the head while playing sports can translate into severe memory loss and dementia later in life. Now, a study1 published today in Science Translational Medicine reveals that the protective shield known as the blood–brain barrier can be damaged and leaky decades after an athlete retires from sport. This persistent leakiness seems to trigger a long-lasting immune response that is closely tied to cognitive decline, the study finds. The work is a “very important study that finds the disruption of the blood–brain barrier many years after head trauma”, says Katerina Akassoglou, a neuroimmunologist at the Gladstone Institutes in San Francisco, California, who was not involved in the research. Part of the difficulty in studying the long-term effects of head trauma is that some neurodegenerative conditions, such as chronic traumatic encephalopathy (CTE), can be diagnosed only by examining neuronal tissue after death, says Matthew Campbell, a specialist in neurovascular genetics at Trinity College Dublin, who co-authored the paper. Campbell and his colleagues wanted to see whether they could spot warning signs in living athletes by looking at the blood–brain barrier, a dense layer of cells lining the blood vessels that supply the brain. This layer usually keeps harmful substances from leaking out of the blood and into brain tissue. To investigate, the researchers scanned the brains of 47 athletes who had retired from playing contact sports with a high risk of concussion and repetitive head impact, such as rugby and boxing. They also examined a control group of non-athletes and athletes who had played non-contact sports. © 2026 Springer Nature Limited

Keyword: Brain Injury/Concussion
Link ID: 30170 - Posted: 03.21.2026

By Marlowe Starling The passage of the sun across the sky — dawn, day, dusk, night — drives the clock of life. Some species wake with the sun and sleep with the moon. Others do the opposite, and a few keep odd hours. These naturally driven, 24-hour biological cycles are known as circadian rhythms, and they do more than cue bedtime: They regulate hormones, metabolism, DNA repair, and more. When life falls out of sync, there can be dire consequences for health, reproduction, and survival. Lacking watches, many species keep time using an internal system — a set of interacting genes and their protein products that effectively keeps track of a 24-hour period — that is calibrated by sunlight. This kind of circadian clock is widespread, found even in single-celled algae, which suggests that biological timekeeping evolved billions of years ago. Across animals, most species have the same genetic system, using genes known as CLOCK, BMAL1, and CRY, or recognizable homologues. This form of biological clock mechanism appears even in ancient lineages, including sponges and some jellyfish. But is this the only way to do it? In a pea-size jelly off the coast of Japan, biologists are examining a different kind of timekeeping. Somewhere over the course of their evolution, the class of hydrozoans — which includes certain kinds of jellyfish, hydras, and colonial siphonophores such as the Portuguese man-of-war — lost the genes that operate circadian clocks in the rest of the animal kingdom. Yet a newly discovered hydrozoan jellyfish species has a mysterious circadian clock that regularly tracks 20-hour periods, suggesting that its mechanism evolved independently. The findings, published (opens a new tab) in PLOS Biology in January 2026, push the limits of what chronobiologists consider “circadian.” © 2026 Simons Foundation

Keyword: Biological Rhythms; Evolution
Link ID: 30169 - Posted: 03.21.2026

By Catherine Offord For most people, Oktoberfest means guzzling liters of beer inside a giant tent. But for one research group in Denmark, it’s a chance to study how our bodies know when we’ve had enough. In a preprint posted on bioRxiv last week, researchers combined a small study of people at Germany’s fall beer festival with mouse experiments, genetic analyses, and blood tests from drunk medical students as well as people with alcohol dependence. Their findings, though preliminary, hint that a hormone commonly associated with morning sickness might also have a role in limiting humans’ alcohol consumption. “I found it fascinating,” says Marlena Fejzo, a women’s health scientist at the University of Southern California who has studied GDF15, the hormone involved. Though the study relies mostly on associations and can’t prove cause and effect, it “lends support” to the idea that GDF15 stops us from overconsuming harmful substances, she adds. GDF15 rises sharply during early pregnancy and is thought to contribute to vomiting and feelings of sickness. Some researchers think it evolved as a protective mechanism: Nausea may help an expectant parent avoid unfamiliar or spoiled food that could harm the fetus. But GDF15 is also present in people who aren’t pregnant and has been linked to appetite suppression. It has even attracted interest from the pharmaceutical industry as a potential antiobesity drug. Matthew Gillum, an endocrinologist at the University of Copenhagen, began to wonder about the hormone’s effect on alcohol intake after collaborating on a study of revelers at the Roskilde music festival. That research measured blood hormone levels in young men who’d spent a week binge drinking and eating junk food and found multiple changes—including a rise in GDF15. © 2026 American Association for the Advancement of Science.

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 30168 - Posted: 03.21.2026

By Jamie Ducharme More than 10 percent of U.S. adults take GLP-1 drugs. But not all of them are taking full doses. Around one in seven users has “microdosed” injections, a recent survey by the health tracking app Evidation found. Some take tiny portions for practical reasons, such as cutting costs. Others have loftier ambitions: They hope to harness the drugs’ powerful effects to achieve better health and longer lives without losing a lot of weight or experiencing side effects such as GI issues and muscle loss. Medications such as Ozempic and Wegovy mimic the body’s GLP-1 hormone, which helps regulate appetite, metabolism and blood sugar. That has made the drugs blockbuster treatments for type 2 diabetes and obesity. But to date, “there is no rigorous scientific data to support microdosing,” says bariatric medicine specialist Katy Williams of the University of Missouri Health Care in Jefferson City. That hasn’t stopped some intrepid biohackers from trying it, though. Companies like AgelessRx, a longevity-focused telehealth clinic, explicitly sell GLP-1 microdoses for this purpose, advertising them as “a powerful new path to promoting long-term wellness.” There is some research to suggest GLP-1s can promote healthy aging by improving overall health. The drugs have been found to reduce inflammation and oxidative stress, lower risks of major cardiovascular problems, lower cancer risk and more. Such findings have prompted scientists to study the drugs as potential treatments for illnesses as diverse as Alzheimer’s disease and arthritis. Some experts have even wondered whether the drugs’ systemic effects might slow cellular aging and prevent age-related chronic conditions, potentially making them the first true longevity drugs to hit the market. © Society for Science & the Public 2000–2026.

Keyword: Obesity
Link ID: 30167 - Posted: 03.21.2026

David Adam When neuroscientists gather in the Spanish city of Seville in May for the annual Dopamine Society meeting, one discussion could be unusually lively. Session 31 will feature a debate between researchers who fundamentally disagree about the role dopamine has in the brain. Dopamine is one of the most extensively studied neurotransmitters, chemicals that convey signals from cell to cell. It’s the one with the highest profile outside neuroscience: often known as the ‘pleasure chemical’, it’s depicted as the hit of reward that people get from recreational drugs or scrolling through social media. That’s a gross simplification of what dopamine does; on that, researchers agree. But beyond that, where once there was a simple model that explained how dopamine works in the brain, now there are challenges that seek to amend the theory — or even to overturn it. This could have implications not only for basic neuroscience, but also for clinicians trying to explain and treat conditions such as attention deficit hyperactivity disorder (ADHD) and addiction. If the model is wrong or needs modification, then so might some of the assumptions about what drives these disorders and the best way to treat them. The classic idea, known as the reward prediction error (RPE) hypothesis, is that bursts of dopamine in the brain link stimuli to rewards, helping to reinforce associations that fulfil a need for an animal or a person. The model has dominated and guided research in the field for decades, offering a mathematical framework to interpret data from animal experiments, and it does a good job of explaining behaviour. This was a valuable rarity for researchers struggling to overlay simple theories onto the intense complexity of the brain. “Dopamine was the one field of neuroscience where we had a computational model that explained what the signal was and what it was computing,” says Mark Humphries, a neuroscientist at the University of Nottingham, UK. People in the field knew that some of the assumptions involved in the RPE model were simplistic. But as a working understanding of part of the brain, it was seen as a major step forwards. © 2026 Springer Nature Limited

Keyword: Learning & Memory; Drug Abuse
Link ID: 30166 - Posted: 03.19.2026

By Jennie Erin Smith In 2017, physicist Nir Grossman made a discovery that promised a versatile new way to manipulate the living brain. Working in mice, he and his collaborators applied two high-frequency electrical currents to the skull. At the spot in the rodents’ brains where the currents collided, the electric field altered neural activity. Other noninvasive methods typically reach no further than the cortex, the brain’s outer layer. The new approach, called temporal interference (TI) stimulation, offered access to deep-brain areas previously only targetable with surgery. Neuroscientists were quick to see TI’s potential for studying the brain and treating its disorders, and they are now testing it in a variety of human trials. Although the studies are still small and many have not been replicated, they hint that TI may have potential to ease epilepsy symptoms, help stroke patients recover movement, boost memory in people with Alzheimer’s disease, and treat psychiatric conditions. Many say TI—which uses two pairs of head-mounted electrodes linked to portable current generators—is nimbler and likely safer than transcranial focused ultrasound, another emerging technology that can modulate deep-brain regions without surgery. And because TI equipment is inexpensive and widely available, it’s been easy for labs to try out. “What [TI] should be is an open-source therapy,” says physicist and epilepsy researcher Adam Williamson of St. Anne’s University Hospital. This year, he and his colleagues showed in a pilot study of people with epilepsy that TI stimulation to the hippocampus, a deep-brain structure that is often the source of hard-to-treat seizures, could both suppress spikes of abnormal brain activity and improve participants’ sleep. His group and another at Duke University are collaborating on a larger clinical trial of the approach. In TI, two high-frequency electrical currents applied to the brain meet or interfere to form a low-frequency focal area, or “envelope,” that can boost or suppress the rate of neurons’ electrical signaling. “It’s a powerful way to entrain neuronal activity,” says Melanie Boly, an epilepsy researcher at the University of Wisconsin–Madison. © 2026 American Association for the Advancement of Science.

Keyword: Brain imaging
Link ID: 30165 - Posted: 03.19.2026

By Claudia López Lloreda As cells age and acquire damage, they stop dividing and enter a comatose-like state. This natural process, called senescence, has several classic hallmarks, including the expression of cell cycle arrest genes and enlarged nuclei, and can spread among neighboring cells. But senescence arises and expands differently across human brain cell types and in response to various stressors, two new studies suggest. “We’re living in the new world of the senescence field,” says Joseph Herdy, investigator at the Salk Institute for Biological Studies, who was not involved with the work. Any cell type, it seems, can senesce under the right conditions, he adds, but each responds in its own way, complicating the picture. Human brain cell lines—neurons, astrocytes, microglia, oligodendrocytes and endothelial cells—present cell-type-specific responses to stressors that trigger senescence, according to one of the new studies, published in Nature Communications in December. And like senescent cells elsewhere in the body, some—though not all—brain cells can release molecules that spread the senescent phenotype to other cells, according to the other study, a preprint posted on bioRxiv last month. These cell-type-specific differences may reflect the various ways cells acquire and enter a state of senescence, says Jalees Rehman, professor of biochemistry and molecular genetics at the University of Illinois, who was not involved with either work. “They might all have some shared universal features, such as no more cell cycle, some degree of inflammation, but maybe the path of how you get there might be different between cell types.” Senescent cells are sparse and difficult to find in the brain, says Markus Riessland, assistant professor of neurobiology and behavior at Stony Brook University and an investigator on both new studies. So to study the cell-type specificity, Riessland and his colleagues decided to induce senescence in different cells in culture. “Otherwise, if you only have one cell, there’s no way you could characterize how the cell goes into senescence and what the difference between the senescent cells are,” he says. © 2026 Simons Foundation

Keyword: Development of the Brain; Alzheimers
Link ID: 30164 - Posted: 03.19.2026

Mariana Lenharo The weight-loss drugs that took the world by storm a few years ago have a drawback for anyone afraid of needles: they must be injected weekly. But scientists have been racing to perfect anti-obesity pills — which are now coming to market. An oral anti-obesity drug called orforglipron is likely to be approved by US regulators by the end of April, pharmaceutical analysts say. In December, a pill version of the obesity drug semaglutide won US regulatory approval. Both drugs belong to the class of therapies called glucagon-like peptide-1 (GLP-1) receptor agonists. Semaglutide, sold as Wegovy, is made by Novo Nordisk in Bagsværd, Denmark; orforglipron is made by Eli Lilly and Company in Indianapolis, Indiana. Clinical-trial results have been positive. After around one year of treatment at the highest dosage, people taking orforglipron lost, on average, about 11% of their body weight1, and those taking semaglutide pills lost almost 14%2. But it’s uncertain whether pills could one day replace the GLP-1 pens that have become a weight-loss staple. Oral drugs face formidable developmental challenges, and several injected drugs cause greater weight loss than does either orforglipron or oral semaglutide: the approved injectable drug Zepbound, for example, leads to weight loss of up to 21% of body weight3. “It’s encouraging, and it’s fantastic to have double-digit weight loss with a pill,” says Daniel Drucker, an endocrinologist at the University of Toronto in Canada. “But so far, rather than replace, I would say they’re going to complement the options that we have.” There’s a good reason why the original GLP-1 receptor agonists, which mimic the natural hormone glucagon-like peptide-1, were sold in injectable form. The drugs are composed of peptides, which are relatively large molecules. Because of their size, digestive enzymes quickly break them down, and the intestinal lining limits their entry into the bloodstream. © 2026 Springer Nature Limited

Keyword: Obesity
Link ID: 30163 - Posted: 03.19.2026

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

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

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

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

By Simon Makin A brain repair kit that helps yaks and other animals naturally cope with low oxygen levels at high altitudes may point to a new way to treat brain diseases such as multiple sclerosis. In mice with brain damage that mimics MS, the kit’s tools lessened signs of damage in young mice exposed to low oxygen and improved symptoms of MS in adult mice, researchers report March 13 in Neuron. Previous research found that animals living on the Tibetan Plateau, such as yaks and antelopes, carry a mutation in a gene called Retsat. Their lowland counterparts lack the mutation, leading scientists to suspect that it helps protect the brain in low-oxygen environments. “People usually think it’s because of better lung capability, but I wondered whether evolutionary adaptation changes the brain,” says Liang Zhang, a neuroscientist at Shanghai Jiao Tong University. In particular, he was intrigued that these animals have normal white matter in their brains. White matter makes up about half the brain; it consists of bundles of nerve fibers that allow different brain regions to communicate. This neural wiring is wrapped in myelin, a fatty substance that ensures nerve fibers conduct signals efficiently. In MS, the immune system attacks myelin, leading to neurological symptoms and problems with balance and coordination. Myelin production requires a lot of energy, which the brain gets from oxygen. Low oxygen levels, known as hypoxia, can therefore disrupt myelination. During gestation, such disruption can lead to conditions such as cerebral palsy in newborns. © Society for Science & the Public 2000–2026.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 30160 - Posted: 03.14.2026

By Viviane Callier The difference between a doting dad and a deadbeat one may come down to a molecular switch in the brain — at least in African striped mice. Boosting activity of a particular gene in part of the brain known for regulating maternal care turned nurturing males into standoffish ones and even, in some cases, into mouse pup killers, researchers report February 18 in Nature. The findings reveal how social context can alter gene activity in the brain and thereby shape male caregiving. Male caregiving is prevalent in fish and amphibians, suggesting that it is a very ancient behavior in vertebrates. Among mammals, however, fewer than 5 percent of species have fathers that stick around to raise their young. Male African striped mice (Rhabdomys pumilio) are one of the exceptions to the rule, though they vary a lot in their nurturing tendencies, making them an ideal species in which to study the factors that influence this behavior. Some look after the young and groom them; others ignore the pups or even attack them. The same male could become aggressive or doting. To understand that behavior, comparative neurobiologist Forrest Rogers and his colleagues observed the mice’s social environment. In laboratory settings, group-housed males tended to be aggressive toward mouse pups when introduced to them. But surprisingly, when these males were moved to be housed alone, they became very paternal. “I thought clearly something must be wrong, because all the work we know of in mice and rats is that if you socially isolate them, they become very anxious and often not the most caring of individuals,” says Rogers, of Princeton University. But the lone African striped male mice didn’t seem anxious at all. © Society for Science & the Public 2000–2026.

Keyword: Sexual Behavior; Aggression
Link ID: 30159 - Posted: 03.14.2026

By Phie Jacobs Talk about an odd couple. At least 100,000 years ago, a female Atlantic molly (Poecilia mexicana) living in the fresh waters near what is now Tampico, Mexico, mated with a male sailfin molly (Poecilia latipinna). The offspring of this cross-species coupling ought to have been sterile, like a mule. But this particular hybrid went on to birth a brood of daughters—all of which were genetic clones of their mother. Scientists have long assumed this reproductive strategy of birthing clones to be an evolutionary dead end among vertebrate animals, with offspring inevitably succumbing to genomic degradation over time. But the Amazon molly (Poecilia formosa), named for the fierce female warriors of Greek mythology, has kept on defying the odds. According to research published today in Nature, it all comes down to a quirk of genetics that helps reverse harmful mutations. “This is a very cool story,” says University of Oklahoma biologist Ingo Schlupp, who provided the study authors with samples but otherwise wasn’t involved in the new work. Researchers who study asexual animals, he explains, have been “scratching our heads” trying to figure out how some species manage to avoid what evolutionary theory predicts to be certain doom. Although asexual reproduction is common in bacteria and plants, it only rarely occurs in vertebrate animals. Often, these “virgin births” involve a process called parthenogenesis, in which an embryo develops from an unfertilized egg cell—no contribution from the other sex required. The Amazon molly, however, is far from celibate. These fish still mate with males from closely related species because they need sperm to kick-start the development of their embryos. But none of the male’s genetic material gets passed on to the next generation. © 2026 American Association for the Advancement of Science.

Keyword: Sexual Behavior; Evolution
Link ID: 30158 - Posted: 03.14.2026

Ian Sample Science editor Scientists have reconstructed short movies from the brain activity of mice that watched videos for a project that aspires to lift the veil on how animals perceive the world. The brief movie clips are grainy and pixellated, but provide a glimpse of how mice processed footage that featured people taking part in various sports from gymnastics to horse riding and wrestling. The work is in its infancy, but as technology advances, scientists hope to eavesdrop on a richer suite of animal perceptions and ultimately gain fresh insights into their experiences and how brains more broadly respond to their surroundings. “The nice thing with humans is you can just ask someone, what did you dream about? What did you see? What are you hallucinating?” said Dr Joel Bauer at the Sainsbury Wellcome Centre at University College London. “But we don’t have that access with animals in the same way.” Central to the work was an artificial intelligence program that won a recent scientific competition to predict how electrical activity in the visual cortex of the mouse brain changes depending on what the animals are seeing. The visual cortex receives raw input from the retina and turns it into a coherent view of the world. To reconstruct what mice were watching, the scientists first used an infrared laser to record how neurons were firing in the visual cortex as the rodents watched 10-second-long movie clips. They then fed blank video data into the AI program and steadily altered the imagery until the AI predicted the same patterns of brain activity as those seen in the mice. Details are published in the journal eLife. Mice have poor eyesight compared with humans, so the reconstructed videos may never be as clear as the originals. But at a rough guess, Bauer suspects scientists could make the footage about seven times sharper than it is at present. © 2026 Guardian News & Media Limited

Keyword: Vision; Brain imaging
Link ID: 30157 - Posted: 03.11.2026

By Robert Draper The hallucinations began the moment I lay back onto the mat and pulled the mask over my eyes. Oh, I instantly thought, this is not at all what I expected. The first images were assembled like a film strip, a sharply focused Technicolor row of strong, grim-faced men who appeared to be some sort of tribal chiefs. Within seconds, a green tint covered their faces, which then dissolved, replaced by images of conflict. Bodies strewed across a battlefield. Starving children. They, too, dissolved. A pile of rocks took shape. From the pile, several long, dark snakes slithered out. This could be unpleasant, I thought. A crackling sensation coursed through my entire body, as if all my neurons were firing — not in any way painful, but also inescapable. I could feel my hands sweating. My ears buzzed, and it wasn’t long before I heard the murmuring voices of people who weren’t there, followed by the sound of puking from people who were. There were 11 of us in the treatment room, in a basement in a cottage that overlooked the Pacific Ocean just south of Tijuana, Mexico, where ibogaine — a Schedule I drug in the United States — is legal. It was the night before Thanksgiving. We all had our reasons for coming to the treatment clinic called Ambio Life Sciences. Several in the group were veterans suffering from PTSD, traumatic brain injury, substance abuse or some combination of those. A sex-crimes detective had been in a terrible car accident and lost much of her short-term memory. A Marine veteran and blueberry farmer in Georgia was quietly drinking his life away. And there was Erin, a Texas-based corporate consultant who had suffered trauma that began in childhood and continued in the workplace. Erin’s mat was next to mine at the far end of the treatment room. Because we were the only two in the group not to throw up during the 10-hour experience, we later referred to ours as the Quiet Corner. The drug is derived from the Tabernanthe iboga plant, found mainly in Gabon in central Africa. The powerful hallucinogen has long been used there in the initiation ritual that is part of the Bwiti spiritual tradition, involving an intense all-night group ceremony of dance and music and fire-keeping that culminates in a trancelike state. © 2026 The New York Times Company

Keyword: Stress; Drug Abuse
Link ID: 30156 - Posted: 03.11.2026

Will Stone The long-running campaign against smoking could find reinforcements from the new wave of research into psychedelics. Though much of the attention around psychedelics has focused on depression and other mental health conditions, researchers believe these substances also hold the potential to transform addiction treatment. A new study makes the strongest case yet for a psychedelic drug's impact on smoking, which remains the leading cause of preventable death in the U.S. The trial, conducted by a team at Johns Hopkins University, compared nicotine patches to the active ingredient in magic mushrooms, known as psilocybin. At the end of six months, those who had taken just one dose of psilocybin had more than six times greater odds of being abstinent from cigarettes than their counterparts who relied on the nicotine substitute. Everyone in the study also underwent cognitive behavioral therapy for smoking cessation over the course of 13 weeks. "I was surprised by the sheer magnitude of the effect," says Matthew Johnson, the study's author and a professor of psychiatry at Johns Hopkins. The findings, published in the medical journal JAMA Network Open on Tuesday, came from a sample of 82 current smokers, who were randomly separated into two groups. Similar to other psychedelic trials, the participants had support from facilitators to make sure they were comfortable and prepared for their trip. They ingested a relatively high dose of pure psilocybin. © 2026 npr

Keyword: Drug Abuse
Link ID: 30155 - Posted: 03.11.2026

By Natalia Mesa Experience kindles most of our learning throughout life, without any explicit instruction or reward. Thanks to this process, called statistical learning, people unconsciously recognize patterns in their surroundings, and infants soak up language. The hippocampus, it turns out, may be essential for this capability, according to a new preprint, beginning to resolve a long-standing debate. Numerous functional MRI studies have suggested that the structure is involved in statistical learning, but lesion studies have produced mixed results. “This is a tour-de-force study,” says Anna Schapiro, associate professor of psychology at the University of Pennsylvania, who was not involved in the work. “It makes me feel more confident that, yes, the hippocampus is involved in statistical learning, but it’s also necessary for that learning across species.” In the study, people and mice learned to respond—by pressing a key or licking a waterspout, respectively—to a particular sound. As they performed this “cover” task, they also heard an irrelevant four-note sequence at random times, interspersed with the other sound. After repeating this cover task 100 times, both people and rodents showed strong pupil dilation, a sign of surprise, whenever the sequence of notes changed slightly, with more similar sequences evoking a smaller response—indicating that they had passively learned the original musical motif and abstract rules about its structure. Neuronal populations in the hippocampus encoded not only the original and altered tone sequences but also how frequently each occurred. Pharmacologically or optogenetically shutting down hippocampal neurons in the mice prevented them from passively learning the auditory pattern and making generalizations about how often it played, but it didn’t disrupt their performance on the cover task. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30154 - Posted: 03.11.2026

By Brianne Kane, Fonda Mwangi, Alex Sugiura, Kylie Murphy, Jeffery DelViscio & Kendra Pierre-Louis In this episode of Science Quickly, journalist Michael Pollan joins Scientific American’s Bri Kane to unpack why consciousness is so hard to define in a discussion that explores what brain science, artificial intelligence experiments and even psychedelics might reveal about how awareness works. Bri Kane: Just to get us going on something really easy I wanted to ask you, Michael Pollan: Are you conscious, do you know if I’m conscious, and are you 100 percent certain that this microphone is not conscious? Michael Pollan: I can’t be sure you’re conscious. I have to infer that from the evidence: that you’re the same species as me, and our species can be conscious, and we have something called philosophy of mind, which is an imaginative faculty that allows us to imagine what other people are thinking. I know I’m conscious, I think. That’s actually the thing we know with the greatest certainty. I mean, [René] Descartes told us that 400 years ago: The only thing we can be sure of is the fact that we exist, and we are conscious. Everything else is an inference. So I’m inferring you’re conscious, and I’m gonna operate on that basis, if it’s okay. And then the microphone, the microphone hasn’t shown me any evidence of consciousness. Kane: So I mean, like you’re saying, there’s only so much evidence to point to for consciousness; some of it is kind of just your gut understanding. And our February cover issue this year was about these 29 different theories of consciousness, which you’ve covered is further evidence that science is really floundering on finding some solid ground on: What is consciousness, and how can we provide evidence to prove this, to tackle this subject with science? But your work seems to really discuss when science and philosophy start rubbing up against each other, which I think is why you get into some really interesting questions in this book. So I wanted to ask you: What theory, out of those 29, do you find yourself leaning towards that seems like the most probable understanding of consciousness? © 2025 SCIENTIFIC AMERICAN,

Keyword: Consciousness
Link ID: 30153 - Posted: 03.07.2026

Rachel Fieldhouse A group of specialized cells play a crucial part in clearing toxic proteins from inside the brain1. But in people with Alzheimer’s disease, these cells malfunction, leading to the build up of tau proteins — a hallmark of the disease. Tanycytes, specialized cells that line the third ventricle of the brain, are unique because they are in direct contact with both the bloodstream and the cerebrospinal fluid (CSF). This means that they can circumvent the blood–brain barrier to allow molecules into and out of the brain. “Tanycytes are highways for the brain,” says Vincent Prévot, a neuroendocrinologist based in Paris at Inserm, the French National Institute of Health and Medical Research. Although it was known that tanycytes transport molecules into the CSF, Prévot and his colleagues are the first to show that tanycytes also transport molecules out of the CSF. In particular, they move tau proteins from the CSF surrounding the brain into the bloodstream. The findings are fascinating, says Amy Brodtmann, a cognitive neurologist and researcher at Monash University in Melbourne, Australia. “No one has looked at these cells before” in relation to Alzheimer’s disease, she adds. The works shows a potential explanation for how abnormal tau proteins accumulate in the brain, she adds. Tau proteins usually help to support the internal structure of cells and make them stronger, including cells in the brain. But in people with Alzheimer’s disease, the protein stops working properly. Brodtmann says tau then becomes “sticky”, forming clumps in the cells and causing them to die. These tau tangles tend to accumulate in regions of the brain that are involved in memory. © 2026 Springer Nature Limited

Keyword: Alzheimers; Glia
Link ID: 30152 - Posted: 03.07.2026