By Claire L. Evans It was the dead of winter in Boston. The surface of the Charles River was frozen solid. But Zachary Kelso (opens a new tab) braved the biting cold to finally put to rest a mystery that has haunted neuroscience labs for over half a century. To do that, Kelso, a research assistant in the Harvard lab of the neuroscientist Sam Gershman (opens a new tab), needed some worms. Specifically, planarians: arrow-headed flatworms, which are among the simplest creatures to possess a brain and a nervous system with bilateral symmetry like ours. Normally, labs order these widely used model organisms from biological supply companies. But the mail-order worms weren’t up to snuff. So Gershman had dispatched Kelso to the Charles’ icy banks to catch some wild ones. “I thought, ‘I’m going to look crazy because I’m using a hammer to beat through the ice,’” Kelso recalled. “So I wore the more business end of business casual.” In philosophy, “qualia” refers to the subjective qualities of our experience: what it’s like for Alice to see blue or for Bob to feel delighted. Qualia are “the ways things seem to us,” as the late philosopher Daniel Dennett put it. In these essays, our columnists follow their curiosity, and explore important but not necessarily answerable scientific questions. It wouldn’t be the last time Kelso found himself in this situation. The Charles River planarians, it turned out, didn’t cut it either. Neither did the worms he sourced while stream-hopping around Eugene, Oregon, in March 2025. Nor did the ones he fished from Michigan lakes that June — this time in thigh-high waders — while picnicking families gawked from shore. Kelso diligently turned over rocks, angled with bits of meat tied to a string, and even followed maps from a vintage guidebook called The Fresh-Water Triclads of Michigan (opens a new tab). But his adventure was fruitless. Sure, he caught plenty of planarians. But back in Gershman’s lab, none of them would do what they were supposed to do. (C) Simons Foundation

Keyword: Learning & Memory; Evolution
Link ID: 30272 - Posted: 06.06.2026

By Erin Garcia de Jesús Buff-tailed bumblebees can figure out on their own how to use a ball as a ladder to nab sugar from an out-of-reach fake flower, researchers report in the June 4 Science. The insects worked out the trick without specific training for the solution, suggesting a remarkable capacity for solving problems. Bumblebees are brainy, with studies showing they may have emotions and can teach one another to score goals in a six-legged version of soccer. The new finding adds yet another skill to their repertoire. “Spontaneous problem-solving is something that has never been shown in any invertebrate before,” says Olli Loukola, a behavioral ecologist at the University of Oulu in Finland. Vertebrates including chimpanzees and parrots can problem solve on their own, although researchers typically focus on captive animals with plenty of experience working out puzzles. “Our study is the first one where we can be 100 percent sure that these individuals don’t have any prior experience about any problem-solving tasks,” Loukola says. Loukola and colleagues first taught bees two necessary associations: Balls are moveable objects and a blue ring — representing a flower — means food. The team then let the bees loose in plexiglass arenas too small for them to fly to reach a blue ring printed on the ceiling. © Society for Science & the Public 2000–2026.

Keyword: Learning & Memory; Intelligence
Link ID: 30271 - Posted: 06.06.2026

By Natalia Mesa Dopamine neurons register surprise: Their activity surges when an experience exceeds expectations and falls silent with disappointment. These prediction errors help brains and artificial-intelligence systems learn from experience by updating future expectations, according to a long-standing model. But because dopamine neurons receive input from several sources, the exact circuit mechanisms that compute the difference have remained mysterious, says Naoshige Uchida, professor of molecular and cellular biology at Harvard University. It turns out that a circuit of just two types of neurons is central to this computation. Dopamine neurons in the ventral tegmental area calculate the error based on input originating from D1 medium spiny neurons in the striatum, according to unpublished mouse data Uchida and his team presented at this year’s Computational and Systems Neuroscience (COSYNE) annual meeting and reported in a preprint posted on bioRxiv in October 2025. This result suggests that “reward learning doesn’t necessarily involve higher-order computation,” says Kauê Costa, assistant professor of psychology at the University of Alabama at Birmingham, who was not involved in the work. “The canonical view is that these types of computations would involve higher-order areas.” But it also bolsters the reward prediction error model, which has come under scrutiny in recent years, says Nathaniel Daw, professor of computational and theoretical neuroscience at Princeton University, who was not involved in the study. “It’s amazing” how much explanatory power the model has had in predicting neuronal responses, he adds. “It’s been a long road to get here. It’s a really beautiful study.” © 2026 Simons Foundation

Keyword: Learning & Memory; Drug Abuse
Link ID: 30270 - Posted: 06.06.2026

By Elizabeth Preston To our human eyes, a mouse’s furred face doesn’t betray much emotion. But if you watch the body language of a mouse who’s reunited with one of her sisters after five days in a cage alone, you might suspect you know what she’s feeling. The formerly isolated mouse chatters in squeaks too high for a human to hear. She follows her sister, crawling beneath the other mouse’s body as if trying to get a hug. She looks like she’s feeling what you or I feel when meeting a long-lost friend or a family member — maybe with more sniffing. Loneliness isn’t just for humans, and neither are its harms. Over the past decade or so, some researchers have come to believe that an animal’s craving for the company of others isn’t just a preference, but a basic, deeply held need. When we don’t socialize enough, we feel the lack like hunger or thirst, they say. When we’ve had our fill of togetherness, we feel satisfied or quenched. The amount of socializing a creature needs may be particular to that species, and even to that individual. Scientists have found within-species social differences in birds, monkeys, fish and even cockroaches. Among humans, “you can feel lonely at a party, or you can feel fine alone in your office,” says Kay Tye, a neuroscientist at the Salk Institute for Biological Studies in California. Whatever the ideal degree of togetherness, Tye and others think that an animal’s need to balance time alone and time with others represents a kind of homeostasis: an equilibrium that’s critical for survival. Today, they are on a hunt to find where, in the brain, this equilibrium is controlled — and hoping their work will hold dividends for lonely humans.

Keyword: Emotions; Evolution
Link ID: 30269 - Posted: 06.06.2026

Ian Sample Claire was in bad shape. She had been brought to the ward on a stretcher and hoisted on to a bed where she lay curled up in a ball. She was unable to speak, her eyes flat and face expressionless. While she could move her right arm a little, her left arm and both legs were immobile. Life had changed dramatically for Claire, a mother of three in her late 30s, many months earlier, when she collapsed while on a night out with friends. A weakness in an artery at the base of her brain had ruptured, spilling blood around her frontal lobe. She was taken to hospital, where surgeons removed two side plate-sized pieces of bone from her skull to relieve the pressure on her brain. She spent months in intensive care. Can a patient with such profound impairment improve in any meaningful way, especially so long after the event? That was the question for Orlando Swayne, a consultant neurologist and co-lead of the pioneering neurorehabilitation unit at the National hospital for Neurology and Neurosurgery, a Victorian redbrick building in Queen Square, central London. It was a few years before the pandemic when Swayne first met Claire on the ward. She made eye contact but showed no other response. He knew from the referring hospital that she could write single-word answers to queries, but these revealed characteristic signs of the brain damage she had sustained. Before leaving her bedside to tend to other patients, Swayne asked if she had any questions. With a pencil clenched in her right hand, she wrote: “Questions, questions, questions,” and then tailed off into a wiggly line. The pathological repetition comes from a failure in the frontal lobe to keep actions moving along in sequence. “There are some patients who start off, when we first work with them, severely impaired – and I mean very severely impaired,” says Swayne. Claire (not her real name) was one such patient. © 2026 Guardian News & Media Limited

Keyword: Stroke; Brain Injury/Concussion
Link ID: 30268 - Posted: 06.03.2026

Jon Hamilton Scientists who've spent decades learning how the brain works say they're now ready to start fixing it when it breaks. That's the premise of the Brain Health accelerator, a collaborative effort launched by the Allen Institute in Seattle, which has become a major player in brain research. The initiative includes plans to develop new genetic therapies — a term that includes gene editing as well as traditional gene therapy — for diseases including Alzheimer's, Parkinson's, ALS, and Huntington's. "The latest genetic treatments allow scientists to control the activity of particular genes," says Ed Lein, who directs the institute's brain health programs. "That opens up the possibility for very specific precision therapies for brain disorders." The accelerator is an outgrowth of the BRAIN Initiative, an ambitious research program unveiled by President Obama in 2013. The goal of this public-private partnership was to create tools that would allow scientists to see the brain's inner workings, and, eventually, to develop treatments. But the effort has progressed far faster than many scientists expected. "I am shocked at how far we've come in the last 10, 12 years," says John Ngai, a senior investigator at the National Institutes of Health who directs the BRAIN Initiative. "It's just been beyond my wildest imagination — and I've been accused of having a pretty good imagination." © 2026 npr

Keyword: Parkinsons; Alzheimers
Link ID: 30267 - Posted: 06.03.2026

By Hannah Thomasy Prairie voles have a reputation as one of the most social rodents, but when Aubrey Kelly tried to use them to study the neurobiology of group dynamics, she discovered limits to their sociability. “Prairie voles are indeed super social with their pair-bond partner and with their offspring,” says Kelly, associate professor of psychology at Emory University. “But if an adult prairie vole encounters a stranger, they’re going to fight—oftentimes to the death.” She shifted her focus to paternal care in the voles but stayed on the lookout for a truly social rodent that lived in rich, complex communities. As a graduate student, she had studied the neural circuitry that contributes to such societies in zebra finches, and she hoped to make similar inroads in mammalian brains. “I got really into the idea of animal societies and how individuals can just get along in big groups, which is something that we do ourselves,” Kelly says. About four years later, a colleague introduced her to spiny mice. Despite their name, these animals are more closely related to gerbils than to laboratory mice. They live in large, flexible, mixed-sex groups and rarely brawl, the colleague told her. Kelly was intrigued—perhaps these groups were the miniature mammal societies she had been searching for. Her subsequent work has demonstrated that, indeed, these critters not only tolerate groups but actually prefer them: When given a choice between associating with two peers or eight peers, they spend the majority of their time with the larger group. Now Kelly is digging into the neural mechanisms underlying this communal lifestyle. Kelly spoke with The Transmitter about spiny mouse “friendships,” custom CRISPR tools and the neurobiology of coexistence. © 2026 Simons Foundation

Keyword: Aggression; Hormones & Behavior
Link ID: 30266 - Posted: 06.03.2026

By Nora Bradford General anesthesia shuts off conscious awareness, but what do our brains process while we’re under? Individual neurons in a brain region known for its role in memory consolidation can detect unexpected sounds, decode the nuances of language and even predict upcoming word types in a sentence, all while a patient is fully anesthetized, researchers report May 6 in Nature. Scientists have been gathering mounting evidence that even when unconscious, our brains can track certain aspects of speech. “The field was already moving toward a more nuanced picture [of what the unconscious brain can do], but this study pushes the boundary considerably further,” says Athena Akrami, a neuroscientist at University College London who was not involved with the research. To peer into the unconscious brain, neurosurgeon Kalman Katlowitz of Baylor College of Medicine in Houston and colleagues monitored activity in the hippocampi of seven anesthetized patients. The team used a technology developed within the last few years called a Neuropixels probe. These high-density microelectrodes can record the electrical activity of hundreds of individual neurons simultaneously, rather than listening to the collective activity of groups of neurons. The team inserted these probes into patients’ hippocampi, in tissue slated for surgical removal as part of epilepsy treatment. While the patients were under general anesthesia, the researchers played various sounds through headphones. For some patients, this consisted of a series of uniform pure tones interspersed with occasional, unexpected “oddball” tones of a different frequency. For others, the researchers played 10 to 20 minutes of educational videos and storytelling podcasts, like The Moth Radio Hour, to evaluate how the brain processes natural speech. © Society for Science & the Public 2000–2026.

Keyword: Consciousness; Sleep
Link ID: 30265 - Posted: 06.03.2026

By Elizabeth Pennisi Homing pigeons don’t rely on gut instinct to return to the roost. But a nearby organ — the liver — might point the way. White blood cells in the birds’ livers accumulate iron and act as an internal compass when clouds block the sun that normally helps them navigate, researchers report May 28 in Science. While scientists generally agree that some animals use Earth’s magnetic field to guide migrations, they had not pinned down how, and the new work offers a surprising explanation. For decades, researchers have fiercely debated first if and then how birds sense magnetic fields and use them for navigation. One prominent idea involves proteins in their eyes undergoing a reaction in magnetic fields. No one has been able to prove exactly how this so-called “quantum effect” is in play. Other animals that orient using Earth’s magnetism, such as bats and sharks, lack the proteins, so the debate languished unresolved. Ornithologist Martin Wikelski of the Max Planck Institute of Animal Behavior in Radolfzell, Germany, and immunologist Christian Kurts of the University of Bonn in Germany stumbled on another idea more than a decade ago at a conference coffee break. Kurts mentioned how frustrated he was that immune system cells called macrophages in mouse spleens would stick to magnetic columns in instruments used to separate different types of cells, ruining his experiments. The reason the macrophages were sticking, he discovered, was that they accumulated and recycled damaged red blood cells’ iron atoms, which aligned in magnetic fields. © Society for Science & the Public 2000–2026

Keyword: Animal Migration; Neuroimmunology
Link ID: 30264 - Posted: 05.30.2026

By Sara Novak Whether tucked away in a colony of coral, hidden in the darkness of an aquatic cave or floating catatonic just above the ocean floor, fish take opportunities for rest and recovery, just as we do. Like humans, most fish are diurnal, meaning they sleep mostly at night; while they don’t have eyelids, and therefore can’t shut out the darkness, light does disrupt their sleep. And just like us, when they snooze they’re motionless and slow to respond to environmental stimuli. If you deprive them of sleep, they will make up for the loss by sleeping longer the next night. Now, a new study, released this month in Nature Communications, shows just how much fish sleep really does resemble our own. By tracking eye movements of zebrafish, the researchers were able to identify four different substates of sleep, akin to the “stages” of sleep that scientists have described in humans. “There’s complexity to their sleep structure,” said Jennifer Mengbo Li, a co-author of the study and a neuroscientist at the Max Planck Institute for Biological Cybernetics in Germany. Three of the four substates happen at night, lasting a total of 10 hours. The first — and deepest — is characterized by a stone-cold stare. As the waking hours near, a second, lighter substate sets in: The zebrafish’s eyes twitch, sideways in the same direction, before moving slowly back to center. In the third substate, entered as morning approaches, both eyes turn to the same side and stay there. During the fourth and final substate, which takes place in brief bursts during the day, the zebrafish’s eyes move back and forth, as if sweeping the surroundings for potential risks. But the eyes can be deceiving: These five-to-10-minute naps are deep enough that much of the brain activity is suppressed, and the zebrafish are hard to wake up. © 2026 The New York Times Company

Keyword: Sleep; Evolution
Link ID: 30263 - Posted: 05.30.2026

By Claudia López Lloreda Neurons in the visual cortex decode an object’s orientation—horizontal, vertical or anything in between—using information from non-orientation-tuned neurons in the thalamus, according to David Hubel and Torsten Wiesel’s Nobel Prize-winning work in cats in the 1950s and ’60s. In other species, though, the process remained unclear. Thalamic neurons in mice, for example, show orientation selectivity, subsequent studies suggested. New mouse findings—realized by imaging individual synapses on cortical neurons and distinguishing which inputs come from the thalamus versus the neighboring cortex during visual processing—help resolve the discrepancy. Signals coming into the primary visual cortex, or V1, from the thalamus are not orientation tuned, but those from other parts of the cortex are, confirming that orientation tuning occurs in the visual cortex, the new study reveals. This study is the first “to get a map of thalamic receptive field location at the level of seeing almost all the spines that receive thalamic input,” says Jose Manuel Alonso, professor of biological and vision sciences at the State University of New York College of Optometry, who was not involved with the work. “This is unbelievably beautiful.” What’s more, the Hubel and Wiesel model of orientation selectivity “is preserved through evolution,” Alonso adds. “In the mouse, this pathway from the thalamus to the V1 is really organized as the Hubel and Wiesel suggested it should be,” says Anton Arkhipov, investigator at the Allen Institute, who was not involved with the study. © 2026 Simons Foundation

Keyword: Vision; Evolution
Link ID: 30262 - Posted: 05.30.2026

By Bethany Brookshire Once people understood glucagonlike peptide 1 (GLP-1) drugs’ potential for weight loss, the race among pharmaceutical companies was on. Among the current options, Wegovy can help people lose an average of 10 percent of their body weight in a year, while people taking Zepbound have had about a 15 percent loss, on average, in the same period. Soon the most powerful GLP-1 treatment to date could hit the market: retatrutide. Already popular on the online peptide gray market, the new drug, originally developed by Eli Lilly, caused participants in a recent clinical study to lose more than a quarter of their body weight over 80 weeks at the highest dose—results comparable to bariatric surgery. U.S. Food and Drug Administration approval could soon follow. But bodies don’t just drop weight with no potential adverse effects. Weight loss on its own can change muscle, bone and more. As new-generation GLP-1 drugs promote higher rates of loss, clinicians want to ensure that the desire to shed pounds and see improvements such as better cardiovascular health are balanced with the very real risks that may come with the treatment. Fat, Muscle or Bone? People typically lose weight when they eat fewer calories than their body expends. A common way to cut calories is to diet, while bariatric surgery removes or changes part of the gastrointestinal tract to reduce food—and therefore calorie—absorption. GLP-1 is a gut hormone released in response to a meal that helps people feel full. It also increases insulin release and reduces glucose in the blood. Semaglutide (sold as Ozempic and Wegovy by Novo Nordisk) binds to the hormone’s receptor for longer periods of time, making people feel fuller for longer and eat less. Newer versions of GLP-1 drugs, such as tirzepatide (sold as Zepbound and Mounjaro by Eli Lilly) and Novo Nordisk’s upcoming drug CagriSema target more than one type of gut hormone receptor, while retatrutide hits three. © 2026 SCIENTIFIC AMERICAN

Keyword: Obesity
Link ID: 30261 - Posted: 05.30.2026

Andrew Gregory in Chicago Poor sleep may be fuelling the global rise in under-50s being diagnosed with cancer, two large studies suggest. The number of younger people diagnosed with the disease has risen by almost 80% in three decades. Worldwide cases of early-onset cancer increased from 1.82m in 1990 to 3.26m in 2019, while cancer deaths among people in their 40s, 30s or younger rose by 27%. Experts are still trying to understand the reasons behind the increase. However, research presented at the world’s largest cancer conference, the American Society of Clinical Oncology’s annual meeting in Chicago, suggests irregular sleeping patterns in younger people may be a contributing factor. Two studies led by MD Anderson Cancer Center in Houston, Texas, one of the world’s leading cancer research organisations, analysed health data for more than 18 million adults in the US aged between 18 and 50. Researchers found that people with poor sleeping patterns were more likely to develop early-onset bowel, breast, uterine or ovarian cancer. In some cases, under-50s diagnosed with insomnia were three times more likely to develop cancer within five years. “These findings suggest that sleep disruption may represent a clinically relevant, potentially modifiable risk factor in early-onset cancer risk stratification and warrants further investigation,” the researchers said. © 2026 Guardian News & Media Limited

Keyword: Sleep
Link ID: 30260 - Posted: 05.30.2026

R. J. Mackenzie At dawn in late January 1998, two men entered the home of Betty Black in Farmers Branch, a suburb of Dallas, Texas. They killed her in an apparent burglary gone wrong. A few hours later, an eyewitness — Black’s neighbour — described what she had seen to police. She said that two white men with long hair had got out of a car and walked towards Black’s house in the early morning light. The neighbour, Jill Barganier, went to the police station the next day and identified Richard Childs, a white man with long hair, as the car’s driver. Childs would later confess to his involvement and serve 16 years in prison. Over the next week, the police homed in on 28-year-old Charles Don Flores as the second suspect. Flores had been seen with Childs on the morning of the murder, but he was a Latino man with short hair. On 4 February, Barganier was called to the police station. There, in an attempt to jog her memory, an officer used ‘forensic hypnosis’, a discredited practice that has since been discontinued in Texas and many other jurisdictions. During the session, he suggested to Barganier that one of the men might have had “neatly trimmed” hair. She once again described the passenger as a white man with long hair and then helped police to produce a composite sketch that looked nothing like Flores. She studied another photo line-up consisting of Flores and five other Latino men with short hair; she didn’t recognize any of them. More than a year later, however, in March 1999, Barganier’s memory had changed. She testified in court that Flores was in the car, saying that she was “over 100 percent” sure that he was the man she had seen. In the absence of DNA evidence connecting Flores to the crime, this testimony became the cornerstone of the prosecution’s case. A jury convicted Flores of capital murder, and he is currently on death row. © 2026 Springer Nature Limited

Keyword: Attention; Learning & Memory
Link ID: 30259 - Posted: 05.27.2026

By Laura Sanders This is a two-part series on Parkinson’s, detailing the daily struggles with the disease, new treatment programs and how patients’ lives have been impacted by emerging therapies. You can read the first part here. The night before he had brain surgery to treat his Parkinson’s disease symptoms, Robert Goings couldn’t sleep. “He was pacing all night,” says his wife, Diana. That’s because it hurt to stop moving. Normally, Goings’ restless movements, stiffness and muscle cramps were eased by medicine. But doctors wanted his symptoms unmasked for the procedure, which meant he was feeling them full blast. “My legs would cramp up, my arms, you know, everything would cramp up without the medication,” Goings says. The next morning, last November 5, Goings, who at age 68 had been living with increasingly disruptive symptoms for years, slid into an MRI machine at Oregon Health and Science University, or OHSU, in Portland. While Goings was inside the MRI tube, doctors aimed 1,024 ultrasound beams at several spots deep in his brain, burning the problematic tissue there. Afterward, Goings was wheeled to a recovery room. “He held out his hand — dead still,” Diana says. She remembers thinking, “Oh my God, I don’t believe this. It’s gone. Absolutely gone.” In opting for this treatment, called high-intensity focused ultrasound, Goings has joined a small but growing number of people choosing to control their Parkinson’s symptoms with permanent lesions in their brain. Already, an estimated 50 to 60 people have undergone the surgery at OHSU, where the treatment calendar is booked up months in advance. © Society for Science & the Public 2000–2026.

Keyword: Parkinsons
Link ID: 30258 - Posted: 05.27.2026

By Holly Barker Neurons in the locus coeruleus, which provides norepinephrine to the rest of the brain and spinal cord, are more spatially and functionally diverse than previously thought, a new preprint finds. The work reveals how such a small structure located deep in the brainstem can influence a range of functions in multiple brain regions. Locus coeruleus neurons show gene expression variations that track with differences in the cells’ shape and projection targets, the study found. And neurons that occupy opposite ends of the structure respond differently to the rewards mice receive during a learning task, suggesting that the neurons facilitate learning in distinct ways. “This is the bread-and-butter work that the locus coeruleus field needed,” says Nelson Totah, associate professor of neurophysiology and pharmacology at the University of Helsinki, who was not involved in the study. “What they did here was not ask flashy questions [but] answer fundamental questions about this evolutionarily ancient nucleus, so I’m really glad to see this work.” The locus coeruleus—which translates from Latin to “blue spot”—is named for the blue pigmented cells that synthesize norepinephrine. The structure was long thought to consist of homogeneous neurons that secrete norepinephrine in synchrony. But over the past two decades it has become increasingly clear that the region is structurally and functionally heterogeneous: It has two distinct neuronal subtypes that fire asynchronously and drive opposite behaviors in rats, according to papers published in 2018 and 2017, respectively. The new findings suggest that the structure’s neurons are even more diverse and follow a precise organizational pattern: From one end of the region to the other, neurons show a spatial gradient in gene expression differences that map onto variations in the cells’ morphology, electrical activity and target regions, the new study found. © 2026 Simons Foundation

Keyword: Brain imaging; Learning & Memory
Link ID: 30257 - Posted: 05.27.2026

By Ellen Barry Most years, when thousands of psychiatrists gather for the annual meeting of the American Psychiatric Association, they walk past a scattering of protesters. There are Scientologists with megaphones; Falun Gong groups doing their exercises; and, often, former patients, saying they have been harmed by medications or electroconvulsive therapy. This year, though, the profession is facing criticism from the highest levels of the federal government. The American Psychiatric Association gathered just 10 days after Health Secretary Robert F. Kennedy Jr. announced a set of policies to encourage doctors to deprescribe, or assist patients in stopping, the most widely prescribed class of antidepressants. A current of anxiety ran through the meeting, held here this week. Many physicians in the crowd said they worried that Mr. Kennedy’s statements would prompt people to refuse medications, or to quit them and relapse. The plenary session erupted in applause when Dr. Marketa Wills, the organization’s chief executive, declared, “We will never support governmental interference in the practice of medicine.” “We are standing tall for evidence-based care,” she continued. “We are standing tall against stigma, oversimplification, and anything that would move patients further away from the care that they need.” But there were also signs that the field’s leaders are engaging, albeit cautiously, with Mr. Kennedy’s effort to curb overprescribing. Numerous sessions offered training in helping patients taper off medications. In July, the association’s president will take part in a panel convened by the Department of Health and Human Services to develop clinical guidance on tapering antidepressants. In an interview, Dr. Wills said she had been “encouraged” by the invitation to participate in the panel, and she credited the administration with “putting mental health front and center.” © 2026 The New York Times Company

Keyword: Depression
Link ID: 30256 - Posted: 05.27.2026

Simon Spichak Acute stress makes it difficult to link memories of past events with fresh information, a study1 suggests. The results help to explain why people struggle to show insight under pressure. The study, published today in Science Advances, combined brain imaging and psychological testing to show how stress disrupts people’s ability to tap into records of previous experiences and make deductions. The combination of behavioural testing and neural imaging “to actually see what’s going awry is really compelling”, says Brice Kuhl, a neuroscientist at the University of Oregon in Eugene, who was not involved in the study. Only connect The brain connects new and old information to make inferences through a cognitive process called integration. For example, if you have a memory of your friend wearing a bright green jacket, and you see a bright green jacket on a park bench, you might integrate your memory and the visual input to infer that your friend is at the park. This ability can be impaired in individuals with some mental-health conditions, such as anxiety disorders and psychosis. The brain area called the hippocampus is essential for integration. Since it is also particularly vulnerable to stress, Lars Schwabe, a cognitive psychologist at the University of Hamburg in Germany, and his colleagues decided to test how acute stress would affect the brain’s ability to integrate information and make inferences. Memory task On the experiment’s first day, 121 participants were asked to memorize a series of paired images, each containing one image of an animal and one image of either a face or a scene. © 2026 Springer Nature Limited

Keyword: Stress; Learning & Memory
Link ID: 30255 - Posted: 05.23.2026

By Sarah Kliff and Margot Sanger-Katz On a sunny Wednesday morning last month, dozens of preschoolers filed into a Compleat Kidz autism clinic in Concord, N.C. One wore light-up sneakers. Another had a Spider-Man lunchbox. They settled into tiny green cubicles, each accompanied by a staff member, and started their work. A decade ago, this Charlotte suburb had no clinics providing therapy to children with autism. Now it has 12. Inside this one, children buzzed with activity as they worked long sessions with therapists. One 6-year-old girl, exhausted after hours of therapy, fell fast asleep in her therapist’s lap. Soon, a supervisor, Stephen Schroeder, intervened. “How long?” Mr. Schroeder asked Courtney Evans, the therapist. “I set the timer for 7. We’re almost done,” Ms. Evans said. A couple of minutes later, she nudged the child awake. The girl cried. At Compleat Kidz, a fast-growing chain of autism clinics based in North Carolina, the policy is firm: Naps cannot be longer than seven minutes before children are awakened to resume therapy. The company says this is necessary to prevent fraud since clinics can be paid only when children are awake and getting services. But it also allows the clinic to bill insurers or Medicaid for more hours. Across the United States, where treatment for autistic children was once fairly rare, thousands of clinics have sprung up, turning a once obscure therapy into a multibillion-dollar industry. The growth has been fueled by rising autism diagnoses, state insurance mandates and a federal requirement that Medicaid cover the therapy. Private equity investors have rushed into the business, buying up chains and opening new clinics.. © 2026 The New York Times Company

Keyword: Autism
Link ID: 30254 - Posted: 05.23.2026

By Meghan Rosen Neurologist David Standaert can often tell if someone has Parkinson’s disease in a matter of minutes. Maybe their hand trembles and one of their arms doesn’t swing as much as the other when they walk. Maybe their voice sounds softer than usual, and they have a stillness to their body and a masklike look on their face, with little expressivity or blinking. “I always tell patients, ‘It’s not any one thing that tells me you have Parkinson’s. It’s all of these things together,’ ” he says. But Standaert’s is a rare skill. A movement disorder specialist at the University of Alabama at Birmingham, he has been diagnosing people with the disease for decades. He’s one of fewer than 1,000 doctors in the United States trained to spot and treat the sometimes-subtle signs of Parkinson’s. That’s a problem because more than 1 million people in the country have the disease, and the number is climbing as the population ages. “There are nowhere near enough movement disorder specialists to go diagnosing all these people,” Standaert says. A lack of specialists is just one of the problems that plagues Parkinson’s diagnosis, which has proved difficult in part because the disease is so complicated. Over time, and for reasons scientists don’t fully understand, particular nerve cells deep in the brain become damaged and die. For patients, this can manifest as tremors and a constellation of other symptoms that start mild and progressively worsen. Eventually, as muscles stiffen and swallowing becomes difficult, people may become bedridden, in need of round-the-clock care. But Parkinson’s disease varies tremendously, Standaert says. Which symptoms arise, how severe they are and how quickly they progress differ from person to person. “I have seen tens of thousands of patients with Parkinson’s disease, and no two are the same,” he says. © Society for Science & the Public 2000–2026.

Keyword: Parkinsons
Link ID: 30253 - Posted: 05.23.2026