By Matt Richtel A 27-year-old woman began an experiment on herself early one morning in December 2024. Her laboratory was her childhood bedroom, tucked into a second-floor corner of a pale yellow house in the Boston suburbs. On a bookshelf behind her sat a small stuffed sloth and some favorite books, including “Siddhartha” by Hermann Hesse. Her parents were asleep in the room next door. Her name is Rebecca, but she goes by Becks. Sitting at her desk in a gray T-shirt, she opened a small plastic bag filled with white powder. The bag was stamped “SR-17018,” and “NOT FOR HUMAN CONSUMPTION.” She extracted some powder with a red microscooper, poured it onto a digital scale and carefully weighed out 25 milligrams. She gathered this into a blue and white pill capsule and sealed it, and then swallowed the capsule with water. It was 4:27 a.m. “It’s my turn to be a guinea pig,” Becks wrote in the online diary she was keeping of her experience. In sharing her story with The New York Times, she asked that her last name not be used so potential employers don’t discover her drug history. Becks had joined the vanguard of a dangerous, highly speculative do-it-yourself approach to getting sober. For a decade, on and off, she had been addicted to various drugs, most recently kratom, an opiate-like substance, which cleared her head and covered up her pain but required constant dosing. She feared the call of fentanyl, which she’d tried a few times. “Every morning, I woke drenched in sweat from overnight withdrawals. It was a grim existence,” she wrote of her kratom use. She tried various methods to get sober, including three short inpatient detox stays and one monthlong rehabilitation treatment. She had periods of sobriety but couldn’t sustain it. © 2026 The New York Times Company

Keyword: Drug Abuse; Depression
Link ID: 30241 - Posted: 05.09.2026

By Rachel Nuwer Despite billions of dollars spent on potential drug treatments for cocaine addiction, none have proved effective—and cocaine use is increasing in the United States and around the world. But one class of possible remedy has remained untested: psychedelics, which have shown promise for treating post-traumatic stress disorder, depression, anxiety, alcohol use disorder, smoking, and more. Now, the results of a pioneering randomized trial—more than a decade in the making—reveal a single dose of psilocybin, the psychedelic component of magic mushrooms, brought significant relief for people addicted to cocaine. The study of 40 people, described today in JAMA Network Open, showed that 180 days after treatment, 30% of the psilocybin group was completely abstaining from cocaine, versus none of the placebo group—and those who continued using the drug did so less frequently. “This is significantly better than any medication ever tested to treat cocaine use disorder,” says Stephen Ross, a professor of psychiatry at New York University who was not involved in the work. He called results “remarkable,” and the magnitude of the effects “highly substantial.” The study, funded by the University of Alabama at Birmingham (UAB) and the nonprofit Heffter Research Institute, was also notable for its participant pool. Of the 40 people who took part, more than 80% were Black and 65% earned less than $20,000 a year. “Although the study was small, one strength is that most participants had lower than average income and education, which are associated with barriers to addiction treatment,” says Nora Volkow, director of the National Institute on Drug Abuse, who was not involved in the trial. More research will be needed to replicate the findings, she says, but the study provides evidence “that psilocybin has promise for treating addiction to cocaine and potentially other illicit stimulants.” © 2026 American Association for the Advancement of Science.

Keyword: Drug Abuse
Link ID: 30240 - Posted: 05.09.2026

By Helena Kudiabor Microglia, known for scavenging debris and attacking pathogens, may also help regulate the hypothalamic-pituitary-gonadal axis, a new study shows. The findings, published in March in Science, suggest that microglia interact with and influence the function of hypothalamic neurons that release gonadotropin-releasing hormone (GnRH), which stimulates the pituitary to produce the hormones that spark ovulation and spermatogenesis. “One of the biggest surprises was the role of microglia in controlling the GnRH neurons, because this is a link that hadn’t been seen before,” says study investigator Alejandro Collado-Solé, a postdoctoral researcher in Eva González-Suárez’s group at the Spanish National Cancer Research Center. Microglia express a protein called RANK that is crucial to their effects on the hypothalamic-pituitary-gonadal axis. Knocking out RANK in mice reduces microglia’s interactions with GnRH neurons, lowers sex hormone levels and renders some of the animals infertile, the new study found. “The fact that these specific interactions in such a small region of the brain can have such profound effects on fertility—a very fundamental aspect of the survival of a species—was quite unexpected,” says Annie Ciernia, assistant professor of biochemistry and molecular biology at the University of British Columbia, who was not involved in the research. Microglia have been widely studied for their role in brain development, but the new study is the first to explore how these cells support the reproductive system. © 2026 Simons Foundation

Keyword: Development of the Brain; Glia
Link ID: 30239 - Posted: 05.09.2026

By Alonso Daboub Brain cells that help make us human are also uniquely vulnerable to multiple sclerosis. A newfound cellular repair kit can’t keep up with the disease’s damage, leading to the cell death that’s a hallmark of progressive MS, researchers report April 1 in two papers in Nature. The discovery uncovers an important and underexplored mechanism behind how the condition progressively shrinks the brain. By better understanding how MS kills brain cells, scientists can design treatments aimed at preventing cognitive decline, says David Rowitch, a developmental neuroscientist at the University of Cambridge. Each year, 10,000 people in the United States are diagnosed with MS. The body’s immune system attacks neurons in the brain, causing inflammation and unpredictable flare-ups of muscle weakness, tingling and pain. Research has primarily focused on the way the disease causes nerve fibers to lose myelin, the fatty insulation that helps them send messages. But in a second, progressive phase, neurons in the brain begin to die. Patients experience sharper declines in their cognitive ability, leading to difficulties in memory and reasoning as their brains shrink. “There’s no treatment really for that part,” says Steve Fancy, a neuroscientist at the University of California, San Francisco Previous research identified a specific group of neurons in the human cortex, the brain’s wrinkly outermost layer, that are particularly vulnerable to degeneration in progressive MS. Called CUX2 neurons, these brain cells help make up two layers of the cortex thought to play an important role in things like cognition and computation. These layers in the brain are “really very important for making us human,” Fancy says. © Society for Science & the Public 2000–2026.

Keyword: Multiple Sclerosis
Link ID: 30238 - Posted: 05.09.2026

Ian Sample Science editor A single dose of psilocybin, the active ingredient in magic mushrooms, can induce anatomical changes in the brain, according to research among people who took the psychedelic compound for the first time. Scientists spotted apparent changes in the brain’s structure which were still apparent a month after healthy volunteers took the drug. If confirmed, they may help explain the therapeutic effects that psychedelics can have on anxiety, depression and addiction, researchers said. Evidence for the changes came from specialised scans that measured the diffusion of water along nerve bundles in the brain. They suggested that some nerve tracts had become denser and more robust after the drug was taken. While the findings are preliminary, the scientists said the opposite was seen in ageing and dementia. “It’s remarkable to see potential anatomical brain changes one month after a single dose of any drug,” said Prof Robin Carhart-Harris, a neurologist at the University of California, San Francisco, and senior author on the study. “We don’t yet know what these changes mean, but we do note that overall, people showed positive psychological changes in this study, including improved wellbeing and mental flexibility.” Scientists have long sought to understand how psychedelics affect the brain and the work has gained fresh impetus in the wake of trials and studies that suggest the compounds could be used to treat a range of mental health disorders. The drugs are thought to help by boosting flexible thinking and allowing people to escape destructive cognitive ruts. © 2026 Guardian News & Media Limited

Keyword: Depression; Brain imaging
Link ID: 30237 - Posted: 05.06.2026

By Jake Currie Psychedelics are getting a renewed boost of interest lately. The FDA recently announced they were fast-tracking research investigating psilocybin, the compound that gives magic mushrooms their magic, as a treatment for depression. Now, new research published in Nature Communications is showing just how powerful a single dose of this psychedelic compound can be. Neuropsychopharmacologists from the University of California, San Francisco recruited 28 physically and mentally healthy people who had never taken psychedelics before and gave them their inaugural magic mushroom trip. But first, they administered a single placebo dose of 1 milligram of the magic mushroom compound. Most of the subjects reported the experience was “no more unusual than an everyday state of consciousness,” which was backed up by EEG readings. After the preview, it was time for the main event. The research team fitted the participants with EEG electrodes and administered a 25-milligram dose of psilocybin. An hour into their trip, the EEGs showed a surge of entropy (or diverse neural activity), indicating they were processing more complex information. The next day all of the subjects (except one) rated the experience as the “single most unusual state of consciousness” they’d experienced in their lives (the lone holdout rated it in the top five). During the following few weeks, the newly minted psychonauts reported experiencing more insight as well as an increased sense of well-being. A full month after their first trip, they performed better on assessments of their cognitive flexibility. “Psilocybin seems to loosen up stereotyped patterns of brain activity and give people the ability to revise entrenched patterns of thought,” study author Taylor Lyons said in a statement. “The fact that these changes track with insight and improved well‑being is especially exciting.” © 2026 Nautilus

Keyword: Drug Abuse; Depression
Link ID: 30236 - Posted: 05.06.2026

By Lauren Schenkman More than 3,000 genes are differently expressed in the cerebral cortex of people with XX versus XY sex chromosomes, according to a single-cell transcriptomics study published last month in Science. The differences could help explain why certain neurodegenerative and neurodevelopmental conditions affect one group more than the other, or vice versa. The results present “a pretty dramatic shift in how we’re thinking about sex differences,” says Tomasz Nowakowski, associate professor of neurological surgery, anatomy and psychiatry, and of behavioral sciences, at the University of California, San Francisco. He was not involved in the new work but uncovered gene expression differences in prenatal developing brains last year. Previous research traced sex differences to subcortical structures, where sex hormone receptors are expressed, but “the cortex is not the part of the brain that you typically think of when you think about sex differences,” he says. “I think it’s a landmark.” Of the thousands of genes flagged in the new study, 133 showed consistent sex differences across all brain cell types in six cortical regions sampled from postmortem brains, donated by 15 men (who all had XY sex chromosomes) and 15 women (who all had XX sex chromosomes), aged 26 to 78 years. Two of these regions—the fusiform gyrus and the inferior lateral temporo-occipital cortex—have more gray-matter volume in men, previous MRI studies suggest; two others, the caudal insula and intraparietal sulcus, have more gray matter in women; and the final two regions, the angular gyrus and the retrosplenial cortex, show no sex bias in gray-matter volume. Intriguingly, 119 of the 133 genes are autosomal, meaning men and women should have, at least in theory, an equal dose. That makes them “ground zero for molecular sex differences in the brain,” says study investigator Armin Raznahan, chief of the Section on Developmental Neurogenomics at the U.S. National Institute of Mental Health. © 2026 Simons Foundation

Keyword: Sexual Behavior; Genes & Behavior
Link ID: 30235 - Posted: 05.06.2026

By Jan Hoffman Since last fall, new and deadly synthetic opioids called orphines have begun appearing in street drugs in the United States. They are far more potent than fentanyl but cannot be detected by standard toxicology tests. Orphines are still much less common than fentanyl, but they are proliferating quickly. As of last month, they have been found in 14 states, mostly in the South and the Midwest. Law enforcement officials and public health officials are trying to assess the gravity and endurance of the threat they pose. Here are answers to some basic questions. What are orphines? They are a class of opioids that was created in the 1960s by Paul Janssen, a Belgian doctor and pharmacologist, whose teams investigated rapid, safe pain relievers for surgery. As part of that effort, they also developed fentanyl. Dr. Janssen and others discovered that orphines had life-threatening side effects such as acute respiratory depression and were highly addictive. Within a few years, the research on them was halted. Researchers characterize orphines as 10 times more powerful than fentanyl, even in quantities no greater than a few sand-size grains. They can be lethal with stunning speed, with victims slumping over abruptly, respiration shutting down, chest walls rigid. Sometimes the classic signature of overdose, “the foam cone” — froth from the nostrils and mouth — does not even have time to bubble up. Still, it is possible for people overdosing on orphines to be revived with naloxone, the opioid reversal medication. But numerous doses may be required, many more than the one or two doses typically needed for fentanyl. © 2026 The New York Times Company

Keyword: Drug Abuse
Link ID: 30234 - Posted: 05.06.2026

Mariana Lenharo Is testosterone the next miracle drug? That seemed to be the consensus of an expert panel convened by the US Food and Drug Administration (FDA) in December. It argued for major changes in policy that would expand access to the hormone for people with a range of conditions. Committee members called testosterone replacement “a cornerstone of preventive health” and “a multibillion-dollar preventive-care opportunity”. Testosterone is already available in the United States for people who have low levels of the hormone owing to a known medical issue, such as testicular damage. But evidence is growing that more men — and women — might benefit from the hormone, which is delivered through injections, patches, subcutaneous implants or gels. (This article uses ‘men’ and ‘women’ to reflect the language used by the panels and studies cited, while recognizing that trans, non-binary and intersex people are also affected by this issue.) The panel’s recommendations intensify a debate that has been brewing about who might benefit from the treatment. Some clinicians say that most men with low testosterone, especially young ones with no medical issue contributing to the problem, don’t need supplemental treatment at all and should be able to raise their testosterone levels by adopting a healthier lifestyle and losing weight. Others argue that men with low testosterone who have symptoms such as low libido, fatigue and irritability could gain from the therapy. More-enthusiastic proponents, including many members of the FDA panel at the December meeting, take a third view: that all cis men should be tested, and those with low testosterone levels should be treated even if they have no symptoms. “You could make a very strong argument that having a normal testosterone level is important for health and prevention of illness,” says Abraham Morgentaler, a urologist at Harvard Medical School in Boston, Massachusetts, who took part in the December panel. © 2026 Springer Nature Limited

Keyword: Hormones & Behavior; Sexual Behavior
Link ID: 30233 - Posted: 05.06.2026

Pien Huang Adults should be getting at least seven hours of sleep each night, according to the American Academy of Sleep Medicine. "Below that, there's clear evidence that you're going to feel lethargic during the day," says James Rowley, a pulmonologist and the program director of the Sleep Medicine Fellowship at Rush University Medical Center, as well as a past president of the AASM board of directors. Rowley also says not getting enough sleep is linked with cardiometabolic disorders like diabetes and obesity, as well as cardiovascular problems. But many in the U.S. are not sleeping enough. A new data brief, published this week by the Centers for Disease Control and Prevention (CDC), finds that 30.5% of U.S. adults surveyed in 2024 are getting less than the recommended amount. The results have not changed much since 2020, when CDC researchers found that just under 30% of U.S. women and men were sleeping less than seven hours a night. Some people are working multiple jobs or shifts that cut into their sleeping time. But others are just doomscrolling, says Rowley, who was not involved in the paper. "Many patients tell me they go to bed with their cellphone, laptop or tablet," he says. "Patients tell me they see one YouTube video and before they know, it's an hour later." Some people are gaming, and others are watching TV late into the night. For many, that time could be better spent sleeping — an activity in which the brain repairs and restores itself. "A lot of people could go to bed earlier if they chose to," Rowley says. © 2026 npr

Keyword: Sleep
Link ID: 30232 - Posted: 05.06.2026

Liam Drew Three hearts; blue blood; no skeleton; arms like tongues. These are just some of the alien features of octopuses, squid and cuttlefish — members of the cephalopod family. The outlandish list continues. Cephalopod skin can taste chemicals, sense light and change colour and texture rapidly. In many species, the sucker-covered arms can even regenerate. These invertebrates have evolved independently from the vertebrate lineage for more than 600 million years. Their last common ancestor was probably a worm-like creature with a rudimentary nervous system and eye-like patches of light-sensitive cells. Despite this evolutionary gulf, vertebrates and these highly specialized molluscs share strange similarities. Their eyes, for example. “It’s eerie how similar they ended up,” says Cristopher Niell, a neuroscientist at the University of Oregon in Eugene. “The convergent evolution of the eye still blows my mind.” Now, one similarity is spurring a boom in cephalopod neuroscience. Around 400 million years ago, cuttlefish, squid and octopuses diverged from the only other living cephalopods — the nautiluses. They then lost their protective shells and evolved brains that are uniquely large among invertebrates. These brains bestow the soft-bodied cephalopods with high intelligence. Cuttlefish, squid and octopuses have excellent memories, use tools and are adept problem-solvers; they have a concept of time and are capable of delayed gratification. Cephalopods are the only non-vertebrate animals that have big, smart brains, says Cliff Ragsdale, a comparative neuroscientist at the University of Chicago in Illinois. And that presents a unique opportunity. Neuroscientists have gained a wealth of knowledge about how vertebrate brains work, but are increasingly looking to cephalopods for insights into ways to build large, high-functioning nervous systems. © 2026 Springer Nature Limited

Keyword: Evolution; Intelligence
Link ID: 30231 - Posted: 05.02.2026

By Meghan Rosen For the first time, doctors have used stem cells to try and repair the spinal cords of human fetuses in the womb. The new technique attempts to heal nerve damage caused by spina bifida, a disabling birth defect. In this condition, the bony tissue of a fetus’s spine doesn’t knit together properly around the spinal cord. That can cause a kaleidoscope of medical issues, including lifelong paralysis and bladder and bowel problems. Traditional fetal surgery to patch up the spine can limit the scope of these problems — but it does not repair nerve damage that has already occurred. Adding living stem cells to the procedure might. At least, that’s the goal of fetal surgeon Diana Farmer’s team. So far, the approach appears to be safe, the researchers reported earlier this year in theLancet. In six fetal patients with severe spina bifida, applying a stem cell–loaded patch to their exposed spinal cords did not cause infection, tumor growth or interfere with healing. That’s important because “no one knew what stem cells would do inside a fetus,” says Farmer, of the University of California, Davis. For now, the vital question — whether the technique mends fetal spinal cords — remains unanswered. That’s because researchers are still performing follow-up assessments of the patients, who are now toddlers. At this stage, it’s too early to say how well the surgery worked, and Farmer is careful not to speculate. “If we could get every kid to not be in a wheelchair,” she says, “that would be fantastic.” But the team won’t know for a few years. Until then, Farmer says, she doesn’t want to give people false hope. In some ways, this study represents “a seismic shift” in the field, says Ramen Chmait, director of Los Angeles Fetal Surgery at the University of Southern California, who was not involved with the work. If the technique pans out, he says, it “could be a huge, important step in modern-day medicine.” © Society for Science & the Public 2000–2026.

Keyword: Development of the Brain; Stem Cells
Link ID: 30230 - Posted: 05.02.2026

By Kate Golembiewski By watching their peers, dolphins learn to capture fish in empty conch shells, then ferry the shells up to the water’s surface in order to eat. Octopuses can master experimental tasks by watching their tankmates in the laboratory. Crows follow the cues of others in their flock to attack specific humans who have harassed fellow crows in the past. Scientists call it “social learning,” and it essentially means monkey see, monkey do, an adage that turns out to apply to many animals beyond just primates. Now, a study of Australia’s sulfur-crested cockatoos shows that the birds employ social learning to understand whether unfamiliar foods are safe to eat. In more forested areas of the cockatoos’ native range in Australia, New Guinea, and Indonesia, these mohawked parrots eat plant roots, seeds, fruits and insect larvae. But the birds have learned to thrive in urban environments. “They’re everywhere in Sydney,” said Julia Penndorf, a behavioral ecologist and lead author of the study in PLOS Biology, who encountered the birds as a postdoctoral researcher at the Australian National University in Canberra. In urban areas, the birds have expanded their diets to include nonnative plants and nuts, including almonds and sunflower seeds people offer to them, and they can be seen prying the lids off garbage bins in order to forage. “The big issue with urban birds is, they kind of eat everything,” Dr. Penndorf, who now works at the University of Exeter, said. This expanded diet is high-risk, high-reward: the birds have more options for food, but there’s always a chance that strange new snacks might be poisonous. © 2026 The New York Times Company

Keyword: Learning & Memory; Evolution
Link ID: 30229 - Posted: 05.02.2026

By Ellen Barry As Health Secretary Robert F. Kennedy Jr. sets out to rein in the use of psychiatric medications, a group of prominent psychiatrists are developing guidance for helping patients to stop taking them, noting that providers sometimes “park” patients on medications that are no longer necessary or effective. The experts, whose first recommendations appeared in JAMA Network Open and the British Journal of Psychiatry, identify structural problems that may lead to overprescribing: There are few clinical trials showing when it is advisable to stop a medication; many providers do not regularly review whether a prescription is still needed; and psychiatry residents receive more training in starting drug prescriptions than stopping them. “We have not really taught our trainees to think about, what is the logical endpoint?” said Dr. Joseph F. Goldberg, a past president of the American Society of Clinical Psychopharmacology, which convened a group of 45 psychiatrists to agree on basic principles for “deprescribing,” as supervised drug tapering is sometimes called. “You’ll see a patient in consultation who has been parked on a medication which seems to be ineffective for years, and you’ll ask, ‘Why are you still on this medicine?’” he said. “We’ve got a bugaboo going about passive re-prescribing, and I hope we’ll see much less of that.” The new recommendations come amid rising pressure from Mr. Kennedy and his allies in the Make America Healthy Again movement, who have long made the case that Americans overuse psychiatric medications. The Department of Health and Human Services will convene expert panels on deprescribing the main class of medication used to treat depression — selective serotonin reuptake inhibitors, or S.S.R.I.s — this summer, with an eye toward developing official guidance. © 2026 The New York Times Company

Keyword: Depression
Link ID: 30228 - Posted: 05.02.2026

By Jennie Erin Smith Seizures are the most dramatic symptom of epilepsy, but they’re not the only type of abnormal brain activity in people with the condition. Brief electrical bursts called interictal epileptiform discharges, or interictal spikes, can occur hundreds or thousands of times a day, usually without a person noticing. Though not as dangerous as seizures, they can cause temporary confusion and contribute to long-term cognitive problems even in those whose seizures are controlled. A new study of highly detailed recordings from human brains reveals these spikes occur in a choreographed sequence of events that is consistent and predictable. The research, published today in Nature Neuroscience, also shows spikes recruit some of the same neurons involved in speech perception, pulling them briefly off their jobs. The new findings are “impactful,” says Jennifer Gelinas, a neurologist and epilepsy researcher at the University of California (UC), Irvine who was not involved with the study. The work, she says, opens the door to a new generation of brain stimulation technologies that might anticipate and abort spikes before they can cause harm. Named for the distinct peaks they form on electroencephalography readings, spikes were once dismissed by clinicians as benign. But they’re increasingly recognized as far from it. In 2023, a team led by neurologist Jonathan Kleen of UC San Francisco (UCSF) reported that people with temporal lobe epilepsy could not remember or repeat back a word spoken to them during a spike: They went blank. “Imagine this happening when you’re in class, or giving a presentation,” Kleen says. One 2025 study went so far as to conclude that spikes occurring during sleep are the major culprit in long-term memory issues among people with temporal lobe epilepsy. Implantable brain stimulation devices used to suppress seizures can detect spikes and react to them, but they can’t predict them. And this type of treatment, known as closed-loop responsive neurostimulation, can take years to calm epileptic activity. Some antiseizure drugs can also reduce spikes, but treating them “is not as easy as it sounds,” says epileptologist Dániel Fabó of the University of Szeged, who was not involved in the study. Antiepilepsy drugs are tested for their effect on seizures, not spikes, he notes, and using too much of them can affect cognitive function.

Keyword: Epilepsy; Brain imaging
Link ID: 30227 - Posted: 05.02.2026

By Kristen French What is a cat, and how do we know when we’ve encountered one? This question may be harder to answer than it seems. Neuroscientists Lisa Feldman Barrett and Earl Miller say people typically think about categories such as cat and apple backward—bottom-up instead of top-down. In reality, you don’t hear a meow, and see whiskers and paws and then conclude, “Cat!” Before any of this happens, your brain has sent signals about a “cat hypothesis”—and a plan for how to respond to a cat—to your body, based on past experience, Barrett and Miller say. This cat hypothesis, in turn, actively orchestrates what signals your body processes and how. In other words, the brain constructs classifications on the fly, and we’re not even conscious this is happening until after the fact. Barrett, a renowned Harvard neuroscientist and psychologist who has written for Nautilus and is best known for her theory of constructed emotion, teamed up with Miller to review “converging” evidence from a wide range of disciplines: neuroanatomy, electrophysiology, brain imaging, and cognitive science. The pair published their results recently in Nature Reviews: Neuroscience. Their new theory of categories has a lot in common with Barrett’s theory of how emotions work. She argues that emotions aren’t hardwired universal reactions, but are instead predictions constructed rapidly and in the moment from internal bodily sensations, past experiences, and cultural context. While her work on emotions has been highly influential, it remains an active subject of debate in the field of psychology. I spoke with Barrett and Miller about what they call “folk psychology,” and how their theory of categorization relates to so-called beginner’s mind, human bias, and objectivity and mental illness. We also talked about Nobel Laureate Daniel Kahneman’s modes of thinking fast and slow. © Copyright 2026

Keyword: Attention; Emotions
Link ID: 30226 - Posted: 05.02.2026

By Rachel E. Gross The first question Sophie Davies had was: Will it affect my memory? In the three weeks since giving birth, Ms. Davies had been in a downward spiral. She checked herself into the mother-and-baby unit of her hospital in East Anglia, England, where doctors ratcheted up the dose of Prozac she took to manage her obsessive-compulsive disorder. But every morning she woke up in tears, and every time she looked at her baby boy, she felt hollow with guilt. “I’m never going to be able to be a mom,” she recalled thinking, “or if I am, I’m not going to be able to be a good one.” A month in, a hospital worker suggested she try a headset that used an electric current to treat depression. The word “electric” gave Ms. Davies, then 34, pause. It sounded like electroconvulsive therapy, or ECT, the scary-sounding treatment that triggers seizures and can result in memory loss. This therapy was different. Transcranial direct-current stimulation, or tDCS, uses a weak electric current to shock the brain and does not produce seizures. “This is as far from ECT as a jet engine is from my bicycle,” Dr. Mark George, of the Medical University of South Carolina, where he is a leading expert in neuromodulation, a term that encompasses all therapies that use electricity to modify brain function. Ms. Davies did an internet search and confirmed that the side effects of tDCS — ringing in the ears, headaches and mild burns or irritation where the electrode pads touched the forehead — were generally transient and didn’t include amnesia. She decided to give it a try. In England, the brain stimulation device has been approved for treating depression since 2019. It can be prescribed by a doctor or purchased over the counter, where it sells for around $530. © 2026 The New York Times Company

Keyword: Depression; Brain imaging
Link ID: 30225 - Posted: 04.29.2026

Chris Simms Olfactory receptors in the mouse nose have been mapped out in unprecedented detail — overturning researchers’ understanding of how noses build a sense of smell. The research, published today in Cell1, shows how around 1,100 olfactory receptors expressed on sensory neurons are organized in tightly regulated spatial locations in the epithelial tissue that lines the nasal cavity. A second study2 provides a complementary atlas of olfactory receptor expression in the olfactory epithelium and their neural connections to the olfactory bulb in the brain. “For 30 years, we’ve taught students that the mouse olfactory epithelium is divided into a handful of broad zones, within which receptor choice is essentially random,” says Johan Lundström, a psychologist and experimental neuroscientist at the Karolinska Institute in Stockholm. In the study, researchers examined about five million neurons from hundreds of individual mice. They first used single-cell sequencing to identify which smell receptors were expressed by neurons in the nose, and then used spatial transcriptomics to map out where key genes were being expressed. This allowed them to pinpoint where the receptors are and show that they are always arranged in horizontal stripes running from the top of the nose to the bottom. “Each receptor adopts a particular position in the nose. Since there are a thousand positions in the nose, each receptor is expressed basically in a stripe that overlaps with other receptor stripes, in a thousand overlapping stripes,” says study co-author Sandeep Robert Datta, a neurobiologist at Harvard Medical School in Boston, Massachusetts. Datta and his colleagues propose that this spatial mapping is organized during development and is controlled by sets of genes. The authors found that a molecule called retinoic acid had a key role in this process. They discovered a gradient in the amount of retinoic acid present at different points in the nose. By tweaking how much this molecule was expressed, they showed that it helps to control gene activity, guiding each neuron to express the correct type of smell receptor for its location. © 2026 Springer Nature Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 30224 - Posted: 04.29.2026

By Siddhant Pusdekar Transcriptional changes are essential for converting new experiences into memories but may not be required to make memories last, a new study suggests. The findings, published in eNeuro in March, conflict with a model proposing that positive feedback loops of transcription can help maintain long-term memories, says study investigator Irina Calin-Jageman, professor of biological sciences at Dominican University. But they open up a set of hypotheses about how transcription maintains long-term memories and indicate that the handful of genes whose regulation persists for up to two weeks could be “really key,” she adds. The results, obtained in the sea slug Aplysia californica, are “one small step on our way to understanding this very important question of: What is the role of transcription in forming long-term memories?” says Wayne Sossin, distinguished James McGill professor of neurology and neurosurgery at McGill University, who is listed as a reviewer for the paper. Disproving models doesn’t “get the attention it deserves, I think, from the scientific community,” he says, but science is built on overturning theory. Irina Calin-Jageman and her colleagues focused on the transcriptional traces of a partially faded memory in the sea slug. When the animal feels threatened, it retracts a breathing apparatus on its back called a siphon. After traumatic experiences—such as induced shocks—the slug retracts its siphon for longer than usual, previous work showed. Also, sensory neurons in the pleural ganglia change their gene expression patterns and remain more excitable for up to 24 hours, and synaptic changes can last for several days to weeks, depending on the training. © 2026 Simons Foundation

Keyword: Learning & Memory
Link ID: 30223 - Posted: 04.29.2026

By Emma Yasinski “Relapse is a part of recovery”: That’s a common refrain among professionals who treat substance use disorders. Many people who have completed treatment programs return to substance use and reenter treatment multiple times, after days, weeks or even years of sobriety. Marina Wolf, a behavioral neuroscientist at the Oregon Health & Science University, studies how cells in the brain respond to drug exposure in ways that can lead people to develop powerful cravings even months after they stop using drugs such as cocaine, opioids or alcohol. Specifically, she has focused on an aspect of this problem called cue-induced craving, in which people’s brains come to associate a cue — such as seeing a certain location where they previously used drugs — with the desire to use that drug. These learned associations, as she described in the 2025 Annual Review of Pharmacology and Toxicology, are caused by structural changes to the brain — neuroplasticity — as a result of drug use, including the strengthening of connections, called synapses, between specific nerve cells. These changes don’t disappear as soon as a person, or animal, stops using a drug. Cravings, in fact, can strengthen after abstinence, leaving a person vulnerable to resume using. How did you become interested in neuroplasticity and addiction? I never had any formal training in synaptic plasticity or addiction. As a graduate student and then a postdoctoral fellow, I worked on how neurons are regulated by the neurotransmitter dopamine, but we studied dopamine’s role in antipsychotic drug effects, not addiction. But when I was setting up my own lab in the early 1990s, I had a friend from graduate school who was involved in groundbreaking studies to work out synaptic plasticity mechanisms in the brain’s hippocampus, a region of the brain responsible for encoding memories. This was fascinating work that helped demonstrate a critical role for a neurotransmitter called glutamate in synaptic plasticity, so I followed it closely. © 2026 Annual Reviews

Keyword: Drug Abuse
Link ID: 30222 - Posted: 04.29.2026