Jon Hamilton SCOTT SIMON, HOST: And it has been a banner year in brain science. We've learned that lifestyle changes really can keep your brain young and that electrical pulses can help with rheumatoid arthritis, and that LSD can relieve anxiety and depression. Scientists even managed to replicate a human brain network that carries pain signals. NPR science correspondent Jon Hamilton joins us. Jon, thanks so much for being with us. JON HAMILTON, BYLINE: Hi, Scott. SIMON: Well, let's start with that brain network. What does it do? HAMILTON: Well, it recreates the pathway that carries brain signals from, say, your fingertip to the part of the brain that says, you know, ouch, that hurts. And that pathway has several sort of relay stations along the way. So a team at Stanford decided to recreate those stations using brain organoids, which are these pea-sized clumps of human brain cells that can mimic different types of brain tissue. In this case, the scientists used four different organoids representing the four types of nerve cells that relay pain signals. And when they put these organoids together in a dish, they spontaneously wired up to form the entire pain pathway. SIMON: That sounds extraordinary, but I have to ask - can you tell if the organoids in a dish felt anything? HAMILTON: You can, and the way you can tell is with red hot chile peppers. The scientists took the organoid that was acting like a nerve ending, and they exposed it to chemicals like the ones in hot chile peppers, you know, that burn your mouth. Here is Dr. Sergiu Pasca explaining what happened. SERGIU PASCA: We discovered that if you start adding some of these compounds that are inducing inflammatory responses of pain, then you start seeing that information traveling. The neurons that sends these signals get activated. And they transmit that information to the next station and the next station, all the way to the cortex. HAMILTON: There's good reason for this research, too. It's part of an effort to help people with chronic pain. SIMON: Let's move on to the whole question of trying to keep your brain young. Like, can you really do that? HAMILTON: Why, yes, you can. At least according to a really big study funded by the Alzheimer's Association. This study involved about 2,000 people in their 60s and 70s, and they were all pretty sedentary, at least at the beginning. Half of these people spent two years getting aerobic exercise at the gym, eating a Mediterranean diet, watching their blood pressure and taking part in this really demanding cognitive training program. The other people - they were just told to eat better and exercise more. At the end of the study, the people in the hardcore program did better on tests of thinking and memory. And their scores were actually as good as those from people a year or two younger than they were. © 2025 npr

Keyword: Miscellaneous; Development of the Brain
Link ID: 30063 - Posted: 12.31.2025

By Lauren Schenkman In pursuit of the brain’s secrets, neuroscientist Paul-Antoine Libourel has traveled to the ends of the earth. But during the COVID-19 lockdown in 2020, he worked closer to home—in his own darkened garage in Lyon, filming a sleeping chameleon. Libourel, a researcher at the Center for Functional and Evolutionary Ecology in Montpelier, had heard that chameleons lose their ability to camouflage during sleep. But as the hours passed in his garage, he observed something extraordinary: The chameleon’s skin fluctuated from bright to dark to bright again every few minutes. This strobing skin display, Libourel and his colleagues have since discovered, reflects an inner rhythm. The chameleon’s brain activity alternates between waves of higher and lower amplitude, synchronized with increased and decreased eye movements, plus changes in the animal’s heart rate and breathing rate. Six other species of lizard, including bearded dragons—along with rats, mice, pigeons and humans—show the same “infraslow fluctuations” in EEG activity during non-REM sleep, according to a study Libourel’s team published today in Nature Neuroscience. Because reptiles and mammals diverged about 320 million years ago, the findings mean these cycles “are a central thing, maybe a core building block of sleep,” says study investigator Antoine Bergel, research director at the Centre National de la Recherche Scientifique. They also raise the question of why these rhythms are so conserved, Bergel and Libourel say, and hint at how sleep has evolved. The sleep field, which tends to focus on mice and humans, needed this type of comparative study, says Philippe Mourrain, associate professor of psychiatry and behavioral sciences at Stanford University, who studies sleep in zebrafish but was not involved in the new work. “It’s a tour de force to do science on nonconventional species.” © 2025 Simons Foundation

Keyword: Sleep
Link ID: 30062 - Posted: 12.31.2025

By Ivan Amato The standard sperm-meets-egg story posits that sperm cells are hardly more than bundles of shrink-wrapped DNA with tails. Their mission is simple: Deliver a father’s genes into a mother’s egg for sexual reproduction. Just about all other aspects of a developing embryo, including its cellular and environmental components, have nothing to do with dad. Those all come from mom. But nearly two decades of studies from multiple independent labs threaten to rewrite that story. They suggest that dad’s gametes shuttle more than DNA: Within a sperm’s minuscule head are stowaway molecules, which enter the egg and convey information about the father’s fitness, such as diet, exercise habits and stress levels, to his offspring. These non-DNA transfers may influence genomic activity that boots up during and after fertilization, exerting some control over the embryo’s development and influencing the adult they will become. The findings, so far largely described in mouse models, could end up changing the way we think about heredity. They suggest “that what we do in this life affects the next generation,” said Qi Chen (opens a new tab), a reproductive and developmental biologist at the University of Utah Medical School who is among the pioneers of this research. In other words: What a father eats, drinks, inhales, is stressed by or otherwise experiences in the weeks and months before he conceives a child might be encoded in molecules, packaged into his sperm cells and transmitted to his future kid. The researchers have largely zeroed in on RNA molecules, those short-lived copies of DNA that reflect genetic activity at a given time. It’s a tantalizing notion. But the mechanistic details — how experience is encoded, how it’s transferred from sperm to egg, and whether and how it affects a developing embryo — are not easy to unpack, especially given the challenges of conducting research in human subjects. For this reason, and because of the potentially textbook-rewriting implications of the findings, researchers, including those spearheading the work, are cautious about overselling their results. © 2025 Simons Foundation

Keyword: Epigenetics; Development of the Brain
Link ID: 30061 - Posted: 12.31.2025

By Susan Dominus After years of a marriage that had little sex in it, Greg Carter had largely accepted that his wife no longer had any interest. The last thing he expected was that right around the time that they both were nearing 50, his wife would have a complete change of heart. “She was pouncing on me,” he said. His wife had recently started taking testosterone to manage her menopausal symptoms — at a dose so high that it brought her testosterone levels higher than is typical even for women in their 20s. The difference in her desire was almost immediate. “I had the experience of feeling like a teenage boy,” she told me. The shift vastly improved Greg’s own happiness, so much so that he sometimes felt pangs of regret about the years they spent together without a sex life. “I realized, later in life, all that we had missed out on,” he says. Earlier this year, I published an article on how women are increasingly — with widely varying results — seeking out testosterone to help them with energy or their sex lives. Some women who take testosterone at relatively low doses approved by major medical societies feel little change in their bodies, while others see an increase in their desire. Women who take high doses — doses that exceed levels approved by major medical societies — often report sharp upticks in their interest in sex. Franny’s doctor prescribed her testosterone (along with estrogen and progesterone) in what’s known as a pellet, a small medical product the size of a grain of rice that is inserted beneath the skin. Often those pellets, which release hormones over the course of several months, provide doses of testosterone that bring their levels much higher than those that women would have naturally — which was true in Franny’s case. “I feel like I want it sometimes more than my husband,” Franny told me when I was reporting my original article. There was a hint of nervousness in her tone of voice — that dynamic was a shift from their norm and one that made me realize it wasn’t just Franny’s life that had changed, but also Greg’s. And that made me wonder what it would be like to be the partner of someone who was undergoing such a radical shift. © 2025 The New York Times Company

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 30060 - Posted: 12.31.2025

Jon Hamilton Scientists are updating their view of how drugs like Adderall and Ritalin help children with attention deficit hyperactivity disorder stay on task. The latest evidence is a study of thousands of brain scans of adolescents that confirms earlier hints that stimulant drugs have little direct impact on brain networks that control attention. Instead, the drugs appear to activate networks involved in alertness and the anticipation of pleasure, scientists report in the journal Cell. "We think it's a combination of both arousal and reward, that kind of one-two punch, that really helps kids with ADHD when they take this medication," says Dr. Benjamin Kay, a pediatric neurologist at Washington University School of Medicine in St. Louis and the study's lead author. The results, along with those of smaller studies, support a "mindset shift about what stimulants are doing for people," says Peter Manza, a neuroscientist at the University of Maryland who was not involved in the research. The new research analyzed data from the Adolescent Brain Cognitive Development Study, a federally funded effort that includes brain scans of nearly 12,000 children. About 4% of these kids had ADHD when they entered the study, and nearly half of those were on a prescription stimulant. About 3.5 million children in the U.S. take an ADHD medication, and the number is rising. © 2025 npr

Keyword: ADHD; Learning & Memory
Link ID: 30059 - Posted: 12.31.2025

Andrew Gregory Health editor Scientists have discovered two new subtypes of multiple sclerosis with the aid of artificial intelligence, paving the way for personalised treatments and better outcomes for patients. Millions of people have the disease globally – but treatments are mostly selected on the basis of symptoms, and may not be effective because they don’t target the underlying biology of the patient. Now, scientists have detected two new biological strands of MS using AI, a simple blood test and MRI scans. Experts said the “exciting” breakthrough could revolutionise treatment of the disease worldwide. In research involving 600 patients, led by University College London (UCL) and Queen Square Analytics, researchers looked at blood levels of a special protein called serum neurofilament light chain (sNfL). The protein can help indicate levels of nerve cell damage and signal how active the disease is. The sNfL results and scans of the patients’ brains were interpreted by a machine learning model, called SuStaIn. The results, published in medical journal Brain, revealed two distinct types of MS: early sNfL and late sNfL. In the first subtype, patients had high levels of sNfL early on in the disease, with visible damage in a part of the brain called the corpus callosum. They also developed brain lesions quickly. This type appears to be more aggressive and active, scientists said. In the second subtype, patients showed brain shrinkage in areas like the limbic cortex and deep grey matter before sNfL levels went up. This type seems to be slower, with overt damage occurring later. Researchers say the breakthrough will enable doctors to more precisely understand which patients are at higher risk of different complications, paving the way for more personalised care. © 2025 Guardian News & Media Limited

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 30058 - Posted: 12.31.2025

Amelia Hill One in 10 people in the UK aged 70 and older could have Alzheimer’s-like changes in their brain, according to the clearest, real-world picture of how common the disease’s brain changes are in ordinary, older people. The detection of the proteins linked with the disease is not a diagnosis. But the findings indicate that more than 1 million over-70s would meet Nice’s clinical criteria for anti-amyloid therapy – a stark contrast to the 70,000 people the NHS has estimated could be eligible if funding were available. Experts, including those from Alzheimer’s Research UK, have said the findings from the first-ever population-based research into the disease have huge potential for early and accurate diagnosis. “High-quality studies like this are crucial to enhancing our understanding of how blood tests for Alzheimer’s could be used in clinical practice,” said David Thomas, the head of policy and public affairs at Alzheimer’s Research UK. “We need to generate more evidence so we can use these tests in the NHS.” The lead author of the research, conducted by King’s College London, Stavanger University hospital and the University of Gothenburg, said the findings could be a “gamechanger in the understanding of the disease”. The findings also challenge some long-held assumptions about dementia, including the idea that it is mainly a disease that mainly affects women. Dag Aarsland, a professor of old age psychiatry at the Institute of Psychiatry, Psychology and Neuroscience at King’s College London and the study’s lead author, said: “In an ageing global population, the assessment and treatment of dementia presents a significant challenge. Our study used a simple blood test to establish changes that contribute to cognitive impairment in those with dementia.” © 2025 Guardian News & Media Limited

Keyword: Alzheimers; Development of the Brain
Link ID: 30057 - Posted: 12.20.2025

By Bethany Brookshir Women of reproductive age are more likely than other people to report gut problems like irritable bowel syndrome (IBS), and can feel dismissed by doctors, as clinicians often put the pain down to diet, stress or hormones. It was never just “in their heads.” A complex interplay between an important hormone, chemical signals, rare populations of gut cells and the output of gut bacteria could explain why, researchers report December 18 in Science. While the findings are in mice, they suggest new opportunities for treatment. Gut pain is a visceral experience — literally, pain in the viscera, from nerves that spread throughout the torso and abdomen. “It can be bloating, it can be a sharp pain or it can be just sort of a constant, dull pain,” says David Julius, a neurophysiologist at University of California, San Francisco. About 10 percent of the global population — mostly women —suffers symptoms of IBS, which can occur with diarrhea, constipation or a mix between the two. “What makes this so bad is that these women are feeling this pain, they go into the physician … and they were just ignored,” says Holly Ingraham, a physiologist also at the University of California, San Francisco. Ingraham and Julius knew that the hormone estrogen played a role in this type of pain, which can fluctuate with the menstrual cycle and pregnancy. In a 2023 paper, they showed that female mice are more sensitive to this visceral pain than males. Without estrogen, that extra sensitivity disappeared. The researchers immediately went looking for cells that might sense estrogen in the gut. To affect a given organ, its cells must have proteins called receptors that recognize estrogen and set off signals in response. © Society for Science & the Public 2000–2025

Keyword: Pain & Touch; Sexual Behavior
Link ID: 30056 - Posted: 12.20.2025

By Calli McMurray For the past two and a half years, a team of five labs in the San Francisco Bay Area have endeavored to nail down how psilocybin affects the way mice behave. Psilocybin and other psychedelic drugs have been shown to improve anxiety and depression symptoms in people, but results in mouse studies are less consistent. Those inconsistencies spell trouble for researchers trying to unpack the drug’s mechanism, because if behavioral changes in mice don’t mirror those in humans, the underlying biological changes might be irrelevant, says team member Boris Heifets, associate professor of anesthesiology, perioperative and pain medicine at Stanford University. So, to establish a behavioral ground truth, the five labs gave about 200 mice the same dose of psilocybin and measured how the drug affected the animals’ performance on a range of simple behavioral assays, including the elevated plus maze and open field, tail suspension and forced swim tests, while taking the drug as well as 24 hours later. While on psilocybin, the mice showed a temporary increase in anxiety-like behaviors, including spending less time than usual exploring new objects and open areas, the team reported in April. But, unlike in people, the drug had no lasting effects once it wore off. The issue, some behavioral neuroscientists argue, is not replication between labs—it’s the assays themselves. “I love the idea of these multisite experiments in animal models, but the models—the behavioral models—still have to be the right ones,” says Jennifer Mitchell, professor of neurology and psychiatry and behavioral sciences at the University of California, San Francisco. “The tests themselves—I’m not sure how much they tell us about what a psychedelic is actually doing.” © 2025 Simons Foundation

Keyword: Depression; Drug Abuse
Link ID: 30055 - Posted: 12.20.2025

By Allison Parshall The human brain has 86 billion neurons connected by roughly 100 trillion synapses, making it one of the most complex objects in the known universe. Each year neuroscientists make fascinating, important and downright strange discoveries about how this resilient structure works, and 2025 didn’t disappoint. Here are 10 of the most fascinating brain discoveries of this year for your own brain to noodle on. Brain scans of thousands of people revealed that the human brain has five distinct eras, with turning points in the way it is organized occurring at age nine, 32, 66 and 83. Across each of these stages—for example, the “adolescent” period between age nine and 32—people’s brains tend to experience the same types of changes. You don’t remember being a newborn or even a toddler. Adults’ earliest memories tend to start around preschool and no earlier. But recent research suggests that your brain was making memories back then; you just don’t have access to them now. A study of the infant hippocampus, a deep-brain structure crucial for memory formation, found that it can store memories once babies are around one year old—though it’s not clear why we can’t recall them once we grow up. Untangling Alzheimer’s Researchers also discovered another oddity of newborn babies’ brain: they have very high levels of a protein that, in adults, indicates Alzheimer’s disease. Tau proteins help to stabilize brain cells’ structure, but they can undergo chemical changes that lead them to become tangled up, a process linked to Alzheimer’s. The fact that healthy newborn brains have high levels of these proteins, which later decrease, suggests that these detrimental changes in adults could be avoided or reversed. Fluorescence light micrograph of neural progenitor cells. Astrocytes have been stained orange and neural progenitor cells green. Cell nuclei are blue © 2025 SCIENTIFIC AMERICAN,

Keyword: Brain imaging; Learning & Memory
Link ID: 30054 - Posted: 12.20.2025

By Jan Hoffman Around 2 a.m., Joseph felt the withdrawal coming on, sudden and hard. He fell to the floor convulsing, vomiting ferociously. The delirium and hallucinations were starting. He shook awake his friend, who had let him in earlier to shower, wash his clothes and grab some sleep. “Do you have a few dollars?” he pleaded. “I have to get right.” The friend, a community outreach worker who had been trying for years to get him into treatment, looked up at him standing over her raving and unfocused. “Either leave or let me call an ambulance,” she demanded. At 34, Joseph (who, with his friend, recounted the evening in interviews with The New York Times) had been through opioid withdrawals many times — on Philadelphia streets, in jail, in rehab. But he had never experienced anything as terrifyingly all-consuming as this. A new drug has been saturating the fentanyl supply in Philadelphia and moving to other cities throughout the East and Midwestern United States: medetomidine, a powerful veterinary sedative that causes almost instantaneous blackouts and, if not used every few hours, brings on life-threatening withdrawal symptoms. It has created a new type of drug crisis — one that is occasioned not by overdosing on the drug, but by withdrawing from it. Since the middle of last year, Philadelphia’s hospitals have been strained by patients coming in with what doctors have identified as medetomidine withdrawal. Although the heart rate slows drastically right after use, in withdrawal the opposite occurs: The heart rate and blood pressure become catastrophically high. Patients experience tremors and unstoppable vomiting. Many require intensive care. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 30053 - Posted: 12.17.2025

By Mattha Busby Bruce Damer had the audience under his Gandalf spell. He was giving a keynote speech in a grand hall at Breaking Convention, a psychedelic-consciousness conference in Exeter, England, in April 2025. Tall and slender, very much bearded, and sporting two large gold hoop earrings, one on either side, Damer looked exactly like you would expect a sexagenarian psychedelic professor to look. A boyishly enthusiastic speaker, he said a psychedelic trip had transported him through time to face a deep trauma. Nautilus Members enjoy an ad-free experience. Log in or Join now . “If you believe in a ‘mother ayahuasca’ or a healing force, I was allowed to experience my conception and birth and be in my mother’s belly,” Damer said. His birth mother had given him up because she and his father were too poor to raise him. Ayahuasca had released him from the pain. “Being in the belly, I could feel her love, and it healed,” he said. “As a result of the clarity and the opening of the blockage that had been this sort of knot in my belly, my whole system opened wide,” Damer continued. “And I thought for a moment, I could potentially travel through time to a place where I’ve been working on the question of how life began, the birth of us all.” In psychedelic science, a field dominated by scientists who are loath to be pigeon-holed as too woo-woo, Damer, 63, has become a cult figure by wearing his woo on his sleeve. His adoptive mother described him as “in his own world” when his new parents brought him home. And he has been his own thinker ever since. His science cred is sound: a Ph.D. in computer science from University College Dublin in Ireland, former relationships with Xerox and NASA, and papers published in journals like Astrobiology. Currently he is a research associate in the Department of Biomedical Engineering at the University of California, Santa Cruz. © 2025 NautilusNext Inc.,

Keyword: Depression; Drug Abuse
Link ID: 30052 - Posted: 12.17.2025

By Alex Kwan Despite decades of basic research, many neurological and psychiatric conditions lack effective treatments, or at least treatments that work for everyone. For that reason, when I talk with colleagues about the value of research, I often hear the same negative refrain: “Basic neuroscience has not produced new drugs.” Their argument carries some weight; many of today’s medications trace their origins to long-standing human use or to chance discoveries. The opium poppy, used for thousands of years to ease pain, paved the way for morphine and other opioids that are widely used as analgesics. Ketamine was designed as an anesthetic but was later unexpectedly revealed to be an antidepressant at low doses. Yet this narrative is incomplete. It overlooks a growing list of medications—including zuranolone for postpartum depression, suzetrigine for pain, and the gepants class of migraine medicines—that exist only because of insights from basic research. These drugs were not stumbled upon or borrowed from traditional remedies. They were born out of a long arc of studies in the lab. These success stories matter, because they demonstrate that neuroscience research can deliver new medicines. Acknowledging and publicizing such successes is especially important now, as public funding for basic research in the United States faces growing cuts and restrictions. The development of zuranolone stemmed from an observation about allopregnanolone, a steroid our bodies naturally produce. It has little interaction with steroid receptors and instead acts on GABA receptors in the brain, making neurons less excitable. In the late 1990s, researchers reported that allopregnanolone levels in the rat brain rise dramatically during pregnancy, reaching concentrations of up to three times higher than normal. Just before giving birth, however, the level drops precipitously. © 2025 Simons Foundation

Keyword: Depression; Pain & Touch
Link ID: 30051 - Posted: 12.17.2025

David Shariatmadari In 1973, an American psychologist called David Rosenhan published the results of a bold experiment. He’d arranged for eight “pseudo-patients” to attend appointments at psychiatric institutions, where they complained to doctors about hearing voices that said “empty”, “hollow” and “thud”. All were admitted, diagnosed with either schizophrenia or manic-depressive psychosis. They immediately stopped displaying any “symptoms” and started saying they felt fine. The first got out after seven days; the last after 52. Told of these findings, psychiatrists at a major teaching hospital found it hard to believe that they’d make the same mistake, so Rosenhan devised another experiment: over the next three months, he informed them, one or more pseudopatients would go undercover and, at the end, staff would be asked to decide who had been faking it. Of 193 patients admitted, 20% were deemed suspicious. It was then that Rosenhan revealed this had been a ruse as well: no pseudopatients had been sent to the hospital at all. Not only had doctors failed to spot sane people in their midst; they couldn’t reliably recognise the actually insane. Rosenhan’s gambit seized the public imagination. Were the men in white suits just quacks? Was mental illness even real? Two years later, the film One Flew Over the Cuckoo’s Nest added to the sense of reputational meltdown, and the psychiatric establishment responded with a major tightening up of diagnostic criteria, squeezing disparate symptoms into even tighter boxes. A freewheeling challenge to psychiatry ended up provoking a kind of counter-reformation, making the profession more medicalised than it had been for decades. The whole affair is a neat example of the ideological switchbacks Edward Bullmore maps in his fascinating, personally inflected history of psychiatric ideas. It is all the more mind-boggling – pun intended – when you find out Rosenhan’s paper was largely made up. Research by journalist Susannah Cahalan in 2019 concluded that most of the pseudopatients were invented; one colleague remembered the psychologist as a “bullshitter”. © 2025 Guardian News & Media Limited

Keyword: Schizophrenia
Link ID: 30050 - Posted: 12.17.2025

Lynne Peeples Near the end of his first series of chess matches against IBM’s Deep Blue computer in 1996, the Russian grandmaster Garry Kasparov lamented what he saw as an unfair disadvantage: “I’m really tired. These games took a lot of energy. But if I play a normal human match, my opponent would also be exhausted.” Why thinking hard makes us feel tired Whereas machine intelligence can keep running as long as it has a power supply, a human brain will become fatigued — and you don’t have to be a chess grandmaster to understand the feeling. Anyone can end up drained after a long day of work, at school or juggling the countless decisions of daily life. This mental exhaustion can sap motivation, dull focus and erode judgement. It can raise the odds of careless mistakes. Especially when combined with sleep loss or circadian disruption, cognitive fatigue can also contribute to deadly medical errors and road traffic accidents. It was partly Kasparov’s weary comments that inspired Mathias Pessiglione, a cognitive neuroscientist and research director at the Paris Brain Institute, to study the tired brain. He wanted to know: “Why is this cognitive system prone to fatigue?” Researchers and clinicians have long struggled to define, measure and treat cognitive fatigue — relying mostly on self-reports of how tired someone says they feel. Now, however, scientists from across disciplines are enlisting innovative experimental approaches and biological markers to probe the metabolic roots and consequences of cognitive fatigue. The efforts are getting a boost in attention and funding in large part because of long COVID, which afflicts roughly 6 in every 100 people after infection with the coronavirus SARS-CoV-2, says Vikram Chib, a biomedical engineer at Johns Hopkins University in Baltimore, Maryland. “The primary symptom of long COVID is fatigue,” says Chib. “I think that has opened a lot of people’s eyes.” © 2025 Springer Nature Limited

Keyword: Neuroimmunology; Attention
Link ID: 30049 - Posted: 12.13.2025

By Sara Talpos It’s been more than a decade since scientists first started publishing papers on neural organoids, the small clusters of cells grown in labs and designed to mimic various parts of the human brain. Since then, organoids have been used to study everything from bipolar disorder and Alzheimer’s disease, to tumors and parasitic infections. Because these new tools have the potential to reduce the use of animals in research — a goal of the current Trump administration — the field’s future may be more financially secure than other areas of scientific research. In September, for example, the federal government announced an $87 million investment into organoid research broadly. Matthew Owen brings a unique perspective to this emerging field. As a philosopher of mind, he focuses on trying to understand both what the mind is and how it relates to the body and the brain. He draws on the work of historical philosophers and applies some of their ideas to modern-day science. In 2020, as a visiting scholar in a neuroscience lab at McGill University, he was introduced to researchers working with organoids. Owen, who also does research in bioethics, wanted to help them address a perhaps unsettling question: Could these miniature cell clusters ever develop consciousness? Some experts believe that organoid consciousness is not likely to happen anytime in the near future, if at all. Still, certain experiments are prompting the question. In 2022, for example, researchers, including Brett Kagan of the Australian start-up Cortical Labs, published a paper explaining how they had taught their lab-grown brain cells to play a ping-pong-like video game. (Because the cells were placed in a single layer, the structures were not technically organoids, though they are expected to have similar capabilities.) In the process, the authors wrote, the tiny cell clusters displayed “sentience.” Undark recently spoke with Owen about this particular experiment and about his own writing on organoids.

Keyword: Consciousness; Development of the Brain
Link ID: 30048 - Posted: 12.13.2025

By Christina Caron When Marjorie Isaacson first started taking medication for depression in her late 20s, she considered it lifesaving. At the time, she had been dealing with a rocky marriage and struggling to eat. The drug, she found, helped her gain equilibrium. “I was really grateful just to be able to function,” she said. But recently, Ms. Isaacson, 69, has been considering whether she wants to stay on antidepressants for the rest of her life. Specifically, Ms. Isaacson wonders about the long-term effects of her medication, a serotonin-norepinephrine reuptake inhibitor that is known to raise blood pressure. And she feels unsettled by the emerging backlash against psychiatric drugs that has condemned their side effects and difficult withdrawal symptoms. “As the years have passed, things have changed from ‘Take it and see how it goes, no need now to be concerned’ to ‘Well, it’s turning out things might be kinda complicated,’” she said. “That is worrisome.” Antidepressants are among the most prescribed and easily accessible drugs in the United States, and many people take them for years. But even though modern-day antidepressants have been around for decades — the Food and Drug Administration approved Prozac for depression treatment in 1987 — there is very little information about long-term use. The F.D.A. approved the drugs based on trials that lasted, at most, a few months, and randomized controlled trials of antidepressants have typically spanned only two years or less. Current clinical guidelines do not specify the optimal amount of time they should be taken for. The lack of data can make it hard for people to know when — or whether — to quit. So we asked psychiatrists: How long should someone stay on antidepressants? © 2025 The New York Times Company

Keyword: Depression
Link ID: 30047 - Posted: 12.13.2025

By Kelly Servick In the past 20 years, mice with glowing cables sprouting from their heads have become a staple of neuroscience. They reflect the rise of optogenetics, in which neurons are engineered to contain light-sensitive proteins called opsins, allowing pulses of light to turn them on or off. The method has powered thousands of basic experiments into the brain circuits that drive behavior and underlie disease. As this research tool matured, hopes arose for using it as a treatment, too. Compared with the electrical or magnetic brain stimulation approaches already in use, optogenetics offers a way to more precisely target and manipulate the exact cell types underlying brain disorders. So far only one optogenetic application—addressing certain kinds of vision loss by introducing opsins into cells in the eye—has made it into human trials. But its promising early results, along with the discovery of more sensitive and sophisticated opsins, are inspiring researchers to look beyond the eye, developing treatments that would act on peripheral nerves or deep in the brain. Initial tests of these strategies in animal models of epilepsy, amyotrophic lateral sclerosis (ALS), and other neurological disorders have been encouraging, researchers reported last month at the annual meeting of the Society for Neuroscience (SfN) in San Diego. One company is hoping to launch a human trial for an optogenetic pain treatment by 2027. “We definitely don’t want to oversell the idea of using optogenetics [on human brains] any time soon, but we also are firmly convinced that this is now the right moment to be thinking about this seriously,” University of Geneva neurologist and neuroscientist Christian Lüscher told an SfN session he chaired, in which participants presented a newly published road map for bringing optogenetics to the clinic. Still, the presenters acknowledged major remaining challenges, including possible risks of inserting genes for opsins—many of which are derived from algae or other microbes—into a person’s nerves or brain cells. © 2025 American Association for the Advancement of Science.

Keyword: Pain & Touch; Epilepsy
Link ID: 30046 - Posted: 12.13.2025

By Jan Hoffman To treat their pain, anxiety and sleep problems, millions of Americans turn to cannabis, which is now legal in 40 states for medical use. But a new review of 15 years of research concludes that the evidence of its benefits is often weak or inconclusive, and that nearly 30 percent of medical cannabis patients meet criteria for cannabis use disorder. “The evidence does not support the use of cannabis or cannabinoids at this point for most of the indications that folks are using it for,” said Dr. Michael Hsu, an addiction psychiatrist and clinical instructor at the University of California, Los Angeles, and the lead author of the review, which was published last month in the medical journal JAMA. (Cannabis refers to the entire plant; cannabinoids are its many compounds.) The analysis arrives amid a surging acceptance and normalization of cannabis products, a $32 billion industry. For the review, addiction experts at academic medical centers across the country studied more than 2,500 clinical trials, guidelines and surveys conducted mostly in the United States and Canada. They found a wide gulf between the health purposes for which the public seeks out cannabis and what gold-standard science shows about its effectiveness. The researchers distinguished between medical cannabis, sold at dispensaries, and pharmaceutical-grade cannabinoids — the handful of medicines approved by the Food and Drug Administration with formulations containing either low-grade THC, a psychoactive compound, or CBD, a nonintoxicating compound. Those medicines, including Marinol, Syndros and Cesamet, are available by prescription at conventional pharmacies and have had good results in easing chemotherapy-related nausea, stimulating the appetite of patients with debilitating illnesses like H.I.V./AIDS, and easing some pediatric seizure disorders. © 2025 The New York Times Company

Keyword: Drug Abuse; Pain & Touch
Link ID: 30045 - Posted: 12.13.2025

By Claudia López Lloreda A new commentary calls into question a 2024 paper that described a universal pattern of cortical brain oscillations. But that team has provided a more expansive analysis in response and stands by its original conclusions. Both articles were published today in “Matters Arising” in Nature Neuroscience. Ultimately, the back-and-forth suggests that a frequency “motif” may exist, but it may not be as general as the original study proposed, says Aitor Morales-Gregorio, a postdoctoral researcher at Charles University, who was not involved with any of the work. “The [2024] conclusions are way too optimistic about how general and how universal this principle might be.” The 2024 study identified a brain-wave motif in 14 cortical areas in macaques: Alpha and beta rhythms predominated in the deeper layers, whereas gamma bands appeared in the more superficial layers. Because this motif also showed up in marmosets and humans, the researchers speculated that it may be a universal mechanism for cortical computation in primates. “Results typically come with a level of variability, of noise, of uncertainty,” says 2024 study investigator Diego Mendoza-Halliday, assistant professor of neuroscience at the University of Pittsburgh. But this pattern “was just there the whole time, at all times, in many, many of the recordings.” The team leveraged the findings to create an algorithm that detects Layer 4 of the cortex. But the pattern is “by no means universal,” according to the new commentary, which found the motif in about 60 percent of the recordings in an independent monkey dataset. Further, the algorithm trained to identify Layer 4 of the cortex is unreliable, the commentary shows. © 2025 Simons Foundation

Keyword: Attention
Link ID: 30044 - Posted: 12.13.2025