Lynne Peeples In 2021, dermatologist David Ozog was on holiday with his family in the Bahamas, when his 18-year-old son had a massive stroke. The teenager was airlifted to Florida, and then to Chicago for surgery. As his son was lying partially paralysed in a hospital bed, Ozog got a call from a colleague who had an unconventional suggestion. The colleague, a dermatologist at Harvard Medical School in Boston, Massachusetts, told Ozog about research he was conducting with the US Department of Defense. Early results hinted that red and near-infrared light applied to the head might protect neural tissue after brain injury. He urged Ozog to consider trying it on his son. Ozog stayed up until 4 a.m. that night reading scientific papers and, ultimately, ordering several panels made of red and near-infrared light-emitting diodes (LEDs). “I started sneaking them into the hospital,” says Ozog, who works at Henry Ford Health in Grand Rapids, Michigan. Today, his son is walking and back in university. Ozog cannot prove that light therapy made a difference, but he thinks that it helped. He has since become a convert to an idea that, at the time, was considered fringe. “I thought the same thing,” he says, “How could shining this thing on you possibly have any biologic effect?” But what was at the margins of medicine just a few years ago is now edging towards the mainstream. Red-light devices are increasingly appearing in dermatology offices, wellness centres, locker rooms and homes. According to some projections, the global market will surpass US$1 billion by 2030, propelled by a surge of companies promising benefits for everything from ageing skin to attention deficit hyperactivity disorder (ADHD) — claims echoed widely across social media. Experts warn that there is considerable hype about red-light therapy. But a growing body of legitimate science has been exploring the benefits for several conditions. Clinical studies have reported improvements in peripheral neuropathy1, retinal degeneration2 and certain neurological disorders3. For some indications, expert groups now recommend red-light regimens1. Researchers are also uncovering how red and near-infrared light might exert these effects. Mitochondria — the power plants of the cell — are emerging as a central piece of the puzzle. © 2026 Springer Nature Limited

Keyword: Stroke; Parkinsons
Link ID: 30182 - Posted: 03.28.2026

By Angie Voyles Askham The idea that some neural representations can “drift,” or change over time, even in the seeming absence of learning, is broadly accepted. But characterizing the phenomenon across the brain has proved challenging. “The interesting part is what exactly seems to be stable and what exactly seems to be drifting. That’s not an easy question,” says Tobias Rose, a group leader at the University of Bonn Medical Center, who presented findings on drift in the mouse primary visual cortex earlier this month at the Computational and Systems Neuroscience (COSYNE) annual meeting. Other new research adds nuance to the discussion: Neurons that code for head direction in the mouse post-subiculum show little drift, retaining their tuning for multiple weeks, according to a study published last month in Nature. And they differ from hippocampal place cells, which are also part of the spatial navigation system but have highly variable responses, as reported in previous research. The new findings raise questions about how stable and flexible representations interact in the brain, given that signals from the post-subiculum ultimately feed into the hippocampus, says Rose, who was not involved in the work. “It’s a rather important study,” he says. The relative stability of head direction cell tuning does not invalidate previous reports of drift elsewhere in the brain, says Adrien Peyrache, associate professor at the Montreal Neurological Institute, who led the head direction study. Instead, it may be that these invariant responses act as a “rigid backbone” onto which more flexible sensory and cognitive responses can be mapped, he says. “I find it reassuring.” Still, the low drift reported in the new work may be partially due to the study’s methods, which eliminated cells that lost their response from one day to the next, says Timothy O’Leary, professor of information engineering and neuroscience at the University of Cambridge, who was not involved in the work. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30181 - Posted: 03.28.2026

Gemma Conroy Scientists have created the first atlas of specific key patterns of brain ‘chatter’ and determined how these patterns change over the entire human lifespan1. The comprehensive guide draws on brain scans from almost 3,600 people, ranging from infants to centenarians. It maps a property called functional connectivity, which describes the level of coordination between separate brain regions. The data suggest that in young adults, particular patterns of this connectivity are linked to cognitive performance. Such a guide could be useful for understanding when developmental issues and neurodegenerative conditions emerge, says Jakob Seidlitz, a neuroscientist at the University of Pennsylvania in Philadelphia, who was not involved in the research. “This is an important contribution to the field,” he adds. The findings were published today in Nature. The brain is a noisy place. Sometimes two brain regions that are far apart are active at the same time, suggesting that they work together to support the same function. Such regions are said to be functionally connected, even though they do not necessarily sit close to each other in the brain. To understand how this functional connectivity is organized, brain areas are plotted along a scale, or axis, on the basis of their connectivity patterns with the rest of the brain, says study co-author Patrick Taylor, a computer scientist at the University of North Carolina at Chapel Hill who focuses on neuroscience. There are three main functional axes. The sensory-to-association axis, for example, allows researchers to describe brain regions that lie along a continuum from those that focus mainly on processing sensory information to those that are engaged in sophisticated processes such as integrating sensory information into complex thought. The brain regions at each point along the axis have similar patterns of connectivity. © 2026 Springer Nature Limited

Keyword: Development of the Brain
Link ID: 30180 - Posted: 03.28.2026

By Michael S. Rosenwald Robert Trivers, a visionary, eccentric and volatile evolutionary biologist who explored the genetic reasons humans cooperate, compete and deceive each other, drawing comparisons to Charles Darwin in a career filled with intellectual highs and behavioral lows, died on March 12, in Mount Vernon, N.Y. He was 83. His death, at his daughter Natasha Trivers Howard’s home, was confirmed by his family. No cause was given. Professor Trivers was a rebellious figure in academia who joined the Black Panthers, clashed with colleagues and spoke in support of the convicted sex offender Jeffrey Epstein, from whom he accepted research money. He was often stoned and nearly always armed with a knife for self-defense. “Robert Trivers was unlike any other academic I have known,” David A. Haig, an evolutionary biologist at Harvard, wrote in a remembrance of Professor Trivers for the journal Evolution and Human Behavior. “In another life, he might have been a hoodlum.” Raised by a diplomat and a poet, and educated at Phillips Academy in Andover, Mass., and Harvard University, Professor Trivers thrived on challenging scientific orthodoxies, calling the field of psychology a “set of competing guesses.” (He also scorned physics, noting that its utility was “connected primarily to warfare.”) In the early 1970s, as a graduate student at Harvard and later as an untenured professor there, he published a series of papers applying Darwin’s theory of natural selection to social behavior, arguing that science had failed to connect evolution to an understanding of everyday life. © 2026 The New York Times Company

Keyword: Evolution
Link ID: 30179 - Posted: 03.28.2026

By Andrew Jacobs Over the past two years, Australia, a country long known for its strict drug laws, has been allowing psychiatrists to treat post-traumatic stress disorder with MDMA, the chemical compound better known as Ecstasy or molly. The early results have been striking, researchers say, with more than half of patients who received MDMA along with psychotherapy reporting significant relief from PTSD. Just as notably, Australian drug regulators have not recorded any serious adverse events among the nearly 200 patients who have been through the program, which includes up to three dosing sessions with MDMA, a synthetic stimulant that promotes empathy, emotional connection and feelings of euphoria. That data point is especially relevant given the contentious debate in the United States over the safety of MDMA — one that in 2024 helped sink the prospects for MDMA therapy at the Food and Drug Administration. “Compared to conventional treatments, the outcomes we’re seeing to date with MDMA-assisted therapy have been extraordinary,” said Dr. Ranil Gunewardene, a psychiatrist in Sydney who has treated more than 40 patients since the Australian regulators created a legal pathway for the drug. But Australia’s experiment with psychedelic medicine also highlights the limitations and constraints that the nascent field is likely to face as it gains wider attention from regulators and practitioners. Because Australia is the first country to legalize and regulate MDMA therapy, researchers have been especially eager for real-world data about a drug that has been pejoratively associated with rave culture. © 2026 The New York Times Company

Keyword: Stress; Drug Abuse
Link ID: 30177 - Posted: 03.25.2026

By Jennie Erin Smith Can a “friendly” rivalry between two artificial intelligence (AI) agents help reveal how the brain supports consciousness? That’s the suggestion coma researcher Martin Monti and his colleagues at the University of California, Los Angeles make in a paper published today in Nature Neuroscience. One of their two AI models generated realistic imitations of electrical patterns seen in conscious and unconscious brain states, from wakefulness to deep comas. Its counterpart had to identify these states. The results largely support established ideas about how the brain behaves during comas, vegetative states, and other disorders of consciousness. But they also suggest roles for a brain structure and a pattern of cell signaling not previously known to be involved in such disorders—predictions the scientists were able to test. Monti spoke with Science about how the paper’s two models, which he calls the “black box” and the “glass brain,” could reveal new ways to restore consciousness after brain injury. This interview has been edited for clarity and lengt Q: You built two AI models, with one designed to interrogate the other. Can you explain how they talk to each other? A: So here’s the game: We have two friends. One—let’s call it the black box—knows how to tell consciousness from unconsciousness. It’s been trained on 680,000 snippets of EEG [electroencephalography] data from animals and people in different states of consciousness. The other—think of it as a glass brain—is a real, biologically plausible simulation of the human brain. We tell it, “Your job is to move all of your knobs, every single parameter you’ve got, to trick the other guy—the black box—to think that you’re creating a real EEG of a conscious or unconscious state.” Now, we ask the glass brain, “Which brain parameters made the box think the EEG was unconscious?” © 2026 American Association for the Advancement of Science.

Keyword: Consciousness; Robotics
Link ID: 30176 - Posted: 03.25.2026

By Sarah Scoles When George W. Maschke applied to work for the FBI in 1994, he had already held a security clearance for over 11 years. The government had deemed him trustworthy through his career in the Army. But soon, a machine and a man would not come to the same conclusion. His application to be a special agent had passed initial muster. And so, in the spring of 1995, according to his account, he found himself sitting across from an FBI polygraph examiner, answering questions about his life and loyalties. He told the truth, he said in an interview with Undark. But in a blog post on his website, he recalled the examiner told him that the polygraph machine — which measured some of Maschke’s physiological responses — indicated that he was being deceptive about keeping classified information secret, and about his contacts with foreign intelligence agencies. After a failed polygraph exam in which he says he told the truth, George Maschke eventually co-founded the advocacy website AntiPolygraph.org. “My entire career prospects were basically shattered,” said Maschke. “How could I have told the truth and failed the polygraph?” He wanted an answer. And so soon after his failed exam, he said he went to the research library to try to learn more about what had transpired between his body, that machine, and the measuring man. Further spurred by another negative polygraph experience, the resulting deep dive on polygraphs and examination methods eventually led him to co-found the advocacy website AntiPolygraph.org. “When I had my polygraph experience, I had no one to talk to,” said Maschke, who went on to work as a legal translator in the Netherlands. He hoped his public-facing website meant others wouldn’t have that experience.

Keyword: Stress
Link ID: 30175 - Posted: 03.25.2026

By Holly Barker Astrocytes—but not neurons—in the amygdala encode anxiety-like states in mice, according to a paper published today in Neuron. The findings suggest that the cells—which are altered in people with some neuropsychiatric conditions, including autism—contribute to mental health difficulties documented in such groups. “In a very sophisticated way, the [study] shows that astrocytes are these core computational cells for highly complicated behaviors,” says Michael Wheeler, assistant professor of neurology at Harvard University, who did not contribute to the new work. “Astrocytes are understanding and signaling computations in these circuits.” Violent movies and other stressful stimuli activate the amygdala, human imaging studies have shown. And in mice, neurons in the basolateral amygdala are active when the animals are placed in exposed environments, which they find aversive, previous research has found. But that neuronal activity appears to mark shifts between defensive and exploratory behaviors rather than tracking anxiety-related ones, according to a later study. The new findings suggest that astrocytes not only help neurons to regulate anxiety—as previous studies have shown—but “instruct local neurons from the top down,” says study investigator Ciaran Murphy-Royal, associate professor of neuroscience at the University of Montreal. The cells’ activity appears to function as a “safety signal,” that relays danger to other brain regions, he says. Murphy-Royal and his colleagues used calcium imaging to measure astrocytic activity in the mouse basolateral amygdala. Calcium release tracked with freezing, hesitancy and other behaviors reminiscent of anxiety as mice investigated various environments, the team found. In the elevated plus maze, for example, astrocyte activity rose when the rodents explored an open arm of the maze and surged whenever mice peeked over the edge of the suspended setup. © 2026 Simons Foundation

Keyword: Emotions; Glia
Link ID: 30174 - Posted: 03.25.2026

by Pam Belluck Tango is the national dance of Argentina, known for its passion, precision and heart. In a hospital in Buenos Aires, it has another purpose: as a therapy for patients with Parkinson’s disease. Once a week, about a dozen patients come to Ramos Mejía Hospital to dance — a session that uses the movements of tango to help address issues of balance, stiffness and coordination. The goal is to give them approaches to movement that they can use in their daily lives, as well as a social and emotional boost from moving to music. The program began about 15 years ago, inspired by a patient who had danced tango since childhood and found it offered strategies that improved her mobility and gait problems, said Dr. Nélida Garretto, a neurologist who helped spearhead the sessions. Dr. Tomoko Arakaki, another neurologist leading the program, said Parkinson’s patients can struggle with the stop-and-start motions of walking and can benefit from practicing the “slow, short steps” and pauses of tango. Dr. Garretto said that because tango involves “multitasking with motor stimuli, visual stimuli and auditory stimuli,” it can help patients execute the series of small movements in everyday activities. First, warm-up exercises, usually in a circle, “try to tune everyone in, to prepare the body, to awaken the body,” said Manuel Firmani, a professional tango dancer leading the workshops. Some are done standing, some seated, depending on “the state people are in,” he said. After exercises focusing on posture, balance and other skills, dancing begins. Each patient is paired with a partner who doesn’t have Parkinson’s, often friends, relatives or volunteers. © 2026 The New York Times Company

Keyword: Parkinsons
Link ID: 30173 - Posted: 03.25.2026

Sleeping for 11 minutes more each night, doing 4.5 additional minutes of brisk walking and eating an extra 50g or so of vegetables each day can significantly reduce a person’s risk of heart attack, a study has found. Academics found these small changes could help people avoid major cardiovascular events, including heart attacks and strokes, by about 10%. Small behaviour changes were more “achievable and sustainable”, the research team said. The study, published in the European Journal of Preventive Cardiology, was conducted by experts from Australia, Chile and Brazil who examined data on more than 53,000 middle-aged UK adults taking part in the Biobank study. Researchers looked at sleep habits and levels of exercise through data from wearable technology such as smartwatches. People also self-reported on their dietary habits. The researchers found that 2,034 major cardiovascular events occurred during an eight-year follow-up period. They were able to identify the “optimal” way people could avoid these incidents, including a good diet, eight to nine hours sleep each night and a minimum of 42 minutes of moderate-to-vigorous physical activity each day. Combining these measures leads to a 57% lower risk of heart attacks and strokes. They also found the “clinically relevant” combination of behaviours that could reduce people’s risk, including more sleep, better diet and more moderate-to-vigorous activity. According to the NHS website, moderate activity can include brisk walking, dancing, pushing a lawn mower, water aerobics and riding a bike. Vigorous activity includes running, swimming, skipping and aerobics. Dr Nicholas Koemel, the study’s lead author and a research fellow at the University of Sydney, said: “We show that combining small changes in a few areas of our lives can have a surprisingly large positive impact on our cardiovascular health. “This is very encouraging news because making a few small, combined changes is likely more achievable and sustainable for most people when compared with attempting major changes in a single behaviour. © 2026 Guardian News & Media Limited

Keyword: Sleep
Link ID: 30172 - Posted: 03.25.2026

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