By Yasemin Saplakoglu When an optometrist shines a bright light into your eyes, a vast, branching tree sprouts in your field of vision. This is the shadow of blood vessels. Though we normally can’t perceive them, these vessels always occlude a portion of what we see, and for an important reason. They power the retina, a thin layer of nerve tissue in the back of the eye that communicates light signals to the brain. The retina is one of the body’s most energetically expensive tissues. Built from complex networks of sometimes more than 100 different types of neurons, retinal tissue consumes two to three times more energy than the same mass of typical brain tissue. That’s why most vertebrate retinas, including our own, are furrowed with dense, branching networks of blood vessels: to deliver oxygen and other ingredients for producing energy. But there’s a significant exception to this rule. Birds have retinas that mostly lack blood vessels. This may seem especially strange given birds’ exceptional vision. The bird retina is “one of the most metabolically active tissues in the animal kingdom, yet it worked with no apparent blood perfusion,” said Christian Damsgaard (opens a new tab), an evolutionary physiologist at Aarhus University. “It was a complete paradox.” For centuries this has puzzled scientists, who figured that the bird retina must obtain oxygen through a unique, undiscovered process. Damsgaard is the lead author of a study, published in the journal Nature (opens a new tab) in January 2026, that showed for the first time that bird retinas don’t have some unusual adaptation for acquiring oxygen — they survive without it entirely. Instead, to bring energy to the tissue, they use a process called anaerobic glycolysis that is significantly less efficient than oxygen-powered metabolism but gets the job done. © 2026.Simons Foundation

Keyword: Vision; Evolution
Link ID: 30247 - Posted: 05.16.2026

By Richard Stone The wind picks up dust from the unpaved road one afternoon in December as Jack van Honk turns into a ramshackle neighborhood in Lambert’s Bay, on the west coast of South Africa. A stocky woman in a red patterned sundress steps out of a small home painted palest sea green, her ochre-dirt yard crowded with potted plants, many medicinal. She smiles broadly, deep wrinkles creasing a face that is cherubic and yet careworn beyond her 47 years. “Doctor! I missed you,” she beams, her husky voice barely more than a hoarse whisper. Maria carries a rare genetic mutation that is almost unknown outside of southern Africa. Its effects have been to calcify a part of the brain called the basolateral amygdala, and to thicken and scar the vocal cords. A friend of Maria with the same condition lives several hours inland, and sometimes they meet when van Honk brings them to Cape Town for brain scans and other tests. “It helps to know I’m not alone,” Maria says. By every measure of daily life — holding down a job, keeping a household running, raising two teenage sons — Maria is competent and engaged. “You talk to her, and you don’t see anything wrong,” says van Honk, a social neuroscientist at the University of Cape Town. She and others he knows with her condition, Urbach-Wiethe disease, “are kind, sweet people by nature.” In an interview in her kitchen, Maria struggles to recollect even a fleeting moment of unhappiness — before mentioning that she kicked out her partner some years ago because of his drinking. Photograph of a woman in a red dress standing in her yard. Maria lives with a rare genetic disorder that damages part of the amygdala — a brain region increasingly linked not just to fear, but to how humans weigh the needs of others.

Keyword: Emotions
Link ID: 30246 - Posted: 05.16.2026

By Pam Belluck Time was running out for Amanda Sifford, she and her doctors could tell. A.L.S., the paralyzing neurological disorder, was stealing her ability to breathe. On a breathing test, her lung function was only at 48 percent of capacity, a sharp drop from 86 percent five months earlier. “I couldn’t take 10 steps and be able to breathe,” she said. “I could no longer step up on a curb.” Ms. Sifford, 58, a school psychologist in Cape Coral, Fla., has lost 14 family members, including her father and grandfather, to a rare genetic form of A.L.S., also known as amyotrophic lateral sclerosis or Lou Gehrig’s disease. Her symptoms had been developing gradually, but her breathing suddenly nose-dived. “It was very scary,” said Dr. Nathan Carberry, one of her neurologists at the University of Miami Health System. “I worried that we were looking at months of life left.” “Was I thinking about dying?” said Ms. Sifford, pausing to collect herself. “I had my affairs in order.” It was May 2023, and the Food and Drug Administration had just approved the first therapy for a genetic form of A.L.S., even though clinical trial results had not yet proven the drug would be effective. The drug, tofersen, made by Biogen and marketed as Qalsody, targets the form of A.L.S. that Ms. Sifford inherited, so Dr. Carberry and Dr. Michael Benatar, the executive director of University of Miami A.L.S. Center, scrambled to establish a clinic to administer it. She began receiving tofersen monthly, through infusions into her spinal canal. © 2026 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 30245 - Posted: 05.16.2026

By Jennie Erin Smith About 20 years ago, neuropathologists began to report an inconvenient finding in the autopsied brains of people with dementia: Most have evidence of more than one disease. Studies since have shown the brains of up to half of people diagnosed with Alzheimer’s disease also have a key feature of Parkinson’s disease—deposits of the protein alpha synuclein. At the same time, up to half of Parkinson’s patients who develop dementia have elevated levels of beta amyloid and tau proteins, hallmarks of Alzheimer’s. Researchers studying neurodegenerative diseases are catching on to the importance of this phenomenon, often called copathology. It complicates current disease classifications, which are tightly linked to their signature proteins. But it also offers clues as to why some dementia patients show faster cognitive decline, and some people on antiamyloid drugs for Alzheimer’s seem to fare worse than others. Copathology “helps explain why symptoms don’t match biomarkers, why trajectories vary so much, and why treatment results are not necessarily what we expect them to be,” neuropathologist Lea Grinberg of the Mayo Clinic told researchers at the Alzheimer’s and Parkinson’s Diseases Conference (AD/PD) in March. Why the diseases overlap so often remains a mystery, but it’s not a coincidence. “It seems that they stimulate each other,” Grinberg says. Tests now being developed to pick up multiple biomarkers should give a clearer picture of these mixed pathologies in living patients. And an upcoming clinical trial will be the first to take aim at a common dementia copathology, testing the amyloid-clearing Alzheimer’s drug donanemab in people who have both amyloid in their brains and dementia with Lewy bodies—abnormal clumps of alpha synuclein. © 2026 American Association for the Advancement of Science.

Keyword: Alzheimers
Link ID: 30244 - Posted: 05.16.2026

By Christina Caron Dr. Kyle Staller is a gastroenterologist, so it may be surprising that many of his patients come to him complaining not only about stomach trouble but about their brains, too. Irritable bowel syndrome and other digestive dysfunction can be accompanied by a mental haze. People experiencing constipation and bloating, for example, may describe “a sense of heaviness or being weighed down both physically and mentally,” said Dr. Staller, who works at Massachusetts General Hospital in Boston. “So many of my patients talk about problems like fatigue, brain fog and feeling sluggish,” he added. Scientists are making progress in understanding how the pathway between the brain and the digestive system influences our overall health. They call it the gut-brain axis, and it has been shown to play a big role in immune system support, anxiety, depression, metabolism and disease prevention. It can also affect mental clarity. We asked scientists and clinicians what to know about the gut and brain fog. How does the gut-brain axis work? There are thousands of fibers running from the brain to the abdomen that are known as the vagus nerve. It is a primary conduit of the gut-brain axis. And as the main nerve of the parasympathetic nervous system, it helps the body rest, digest and deter inflammation. Signals also travel back and forth between the gut and brain via stress hormones and immune cells. Crucially, gut bacteria produce chemical messengers (called neurotransmitters) like serotonin, dopamine and GABA that affect the nervous system. When they enter the bloodstream or stimulate the vagus nerve, they can help improve mood, drive motivation, and calm the nervous system. © 2026 The New York Times Company

Keyword: Attention
Link ID: 30243 - Posted: 05.16.2026

By Hannah Thomasy For nearly a decade, Vincent Bombail has been tickling rats. It’s been a standard technique used in the study of animal happiness. But not all rats particularly enjoy the experience, data show. Female rats prefer gentler, more playful tickling than males, Bombail and his colleagues report April 15 in Biology Letters. The findings suggest that the same physical experience evokes a different emotional response in different individuals, potentially influencing the results of studies on animal happiness. “This research helps us understand these animals as playful but also rich and complex and having opinions,” says Daniel Weary, an animal welfare scientist at the University of British Columbia who was not involved in the study. “Understanding the affective lives of animals is actually one of the coolest and most difficult questions there is in science,” he says. As early as the 1930s, researchers deliberately exposed rats to standardized negative experiences to study the physical effects of stress. Figuring out how to study positive experiences took longer. It wasn’t until the 1990s that researchers developed the standard tickling protocol, where a researcher flips a rat over, pins it on its back and tickles its belly. The protocol is intended to mimic the rough-and-tumble play of young male rats. © Society for Science & the Public 2000–2026.

Keyword: Emotions; Evolution
Link ID: 30242 - Posted: 05.16.2026

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