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

By Natalia Mesa In 1967, Howard Fields was drafted into the U.S. military and stationed at the Walter Reed Army Institute of Research in Silver Spring, Maryland. It was the height of the Vietnam War, and Fields, who had recently graduated from Stanford University with an M.D. and Ph.D., was assigned to treat wounded soldiers. Among his patients was a man with median nerve causalgia, a painful condition caused by nerve damage following physical trauma. Treatment options for pain were limited at the time, and Fields decided to try what he later recalled as “this strange therapy” that electrically stimulated the peripheral nerve. “The results were dramatic,” Fields wrote in an autobiographical narrative. “Immediate, complete relief lasting for several hours.” His experience with the Vietnam War would guide his career in research. “He saw a lot of trauma,” says Jennifer Mitchell, professor of neurology at the University of California, San Francisco (UCSF), who was a graduate student in Fields’ lab. “I think he was compelled to help people that were suffering.” Fields died of complications from prostate cancer on 1 May 2026, at the age of 86. He spent his career mapping the pain-modulating circuits in the central nervous system, and his lab was the first to demonstrate the efficacy of opioids for neuropathic pain and topical lidocaine for postherpetic neuralgia. Later, he pivoted to studying addiction and mapped out the mechanisms by which opioids co-opt reward circuitry. His work around the physiology and anatomy of pain circuits made Fields “a giant in the field,” says Mary Heinricher, professor of neurological surgery and biomedical engineering at Oregon Health & Science University, who did a postdoctoral fellowship with Fields. In fact, Heinricher adds, “It wasn’t really a field of research before his generation.” © 2026 Simons Foundation

Keyword: Pain & Touch
Link ID: 30252 - Posted: 05.23.2026

Diana Kwon It is a dogma in neuroscience that certain brain cells respond in the same way to the same thing. Specific neurons always fire, for example, when we see particular shapes and colours; other neurons activate to swing an arm or wiggle a nose. The brain needs this stability, the theory goes, to respond to the outside world in a consistent way. So, when neuroscientist Laura Driscoll began her doctoral research at Harvard University in Cambridge, Massachusetts in 2012, her first task was to establish this baseline by tracking the activity of individual mouse neurons over time. To Driscoll’s surprise, the baseline kept moving. Over the course of several days, many of the cells’ responses had shifted noticeably. Neurons that had fired when a mouse was in a specific location on day one were barely responding in the same spot after a few weeks. “It absolutely defied all of our expectations,” recalls Driscoll, who is now at the Allen Institute in Seattle, Washington. “This was so surprising that my whole project changed.” In 2017, she and her colleagues reported findings from that project that flew in the face of neuroscience dogma. Over a single day, neurons in the parietal cortex, a hub for processing sensory information, fired predictably in response to specific things, such as the position of the mouse in a virtual maze. But over the course of a few weeks, even though the task of navigating the maze remained the same, these activity patterns underwent major reorganization1. Some of the neurons stopped firing in response to stimuli that had previously activated them; others did the reverse. In groups of cells, however, patterns of neuronal activity remained more consistent over time. The results suggested that individual neurons might not have fixed roles, and that the response of single cells might be less important than the activity of whole populations. © 2026 Springer Nature Limited

Keyword: Learning & Memory; Brain imaging
Link ID: 30251 - Posted: 05.20.2026

By Marta Zaraska 05.19.2026 On a blazing hot day in South Africa, female southern pied babblers can’t think straight. The medium-sized black-and-white birds are trying to get at tasty mealworms behind a see-through barrier. On cooler days, the birds can quickly figure out that all they have to do is go around the small wall of plastic. But when the mercury goes up, the birds just keep stubbornly pecking at the barrier. That experiment is part of a growing body of research showing that animals get their minds muddled during heat waves. When it’s hot outside, birds struggle to learn, dogs bite more often, goat-like chamois pick fights. This is bad news not just for those who get on Fido’s toasted nerves. If the animals can’t stay alert enough to find food or avoid predators, their chances of survival go downhill, says Amanda Ridley, a behavioral ecologist at the University of Western Australia who coauthored the pied babbler study. With climate change making heat waves more common, such cognitive impairments across the animal kingdom could ripple through entire ecosystems, putting already fragile species at greater risk. If pollinators forget which flowers to visit, crops and wild plants may fail. If birds can’t find food as easily, their young may not survive. And on a warming planet, a sharp mind is particularly vital. “A changing climate means that your ability to behaviorally adapt is even more important,” Ridley says.

Keyword: Intelligence; Learning & Memory
Link ID: 30250 - Posted: 05.20.2026

Xiaoying You Chinese companies are racing to develop and deploy artificial-intelligence powered brain–computer interfaces (BCIs) that can help people to move, speak and control devices. BCIs, which link a person’s brain to an external device or a computer using sensors placed around or inside the head, have been used in people who are paralysed and those with neurodegenerative diseases over the past decade. In the past few years, companies, mostly in China and the United States, have added large language models to their brain devices. This enables scientists to decode brain activity more accurately than can be achieved using conventional signal-processing and data-analysing technologies, says Li Haifeng, a neuro-computing scientist at Harbin Institute of Technology in China. In China, trials in small numbers of people are underway and some AI-powered brain devices will soon be sold to the public. First trials in people NeuroXess in Shanghai is one company in China that has run small clinical trials, including on their AI-powered brain implant can assist people with paralysis. The implant is placed in a shallow recess in the skull, and its sensors are fitted on the brain’s outer layer, called the cerebral cortex. The system is then connected by wire to a data transmitter that doubles as a battery, which is embedded in the recipient’s chest. In a trial in October, a 28-year-old man with a spinal cord injury who was fitted with the brain implant was able to control appliances by moving a computer cursor with his thoughts to turn them on and off using an app. © 2026 Springer Nature Limited

Keyword: Robotics; Brain imaging
Link ID: 30249 - Posted: 05.20.2026

By Nicole Rust Anthropic’s artificial intelligence (AI), Claude, like other large language models (LLMs), appears to express emotions ranging from joy to despair when interacting with human users. In a report the company shared in April, researchers examined the model’s inner workings to understand why these emotional expressions happen and what they reflect about how Claude works. They concluded that these emotional displays are nontrivial, reflecting more than simple repetitions of patterns in Claude’s training data (the common pairing of the phrases “rainy day” and “feeling sad,” for example). At the same time, they found no evidence that Claude has genuine feelings like our own. Instead, Claude’s emotion equivalents contribute to its ability to adaptively solve complex problems. Like human emotions, this adaptivity comes at a cost, sometimes leading Claude to make irrational decisions. We should not conflate Claude’s emotions with our own, but studying emotion equivalents in Claude and other AIs can help lay the foundation for understanding the mysterious, multifaceted functions that emotions serve in humans. To understand Anthropic’s claims about Claude, we first need to grapple with its definition of “emotion.” For many, the term implies an inner experience—feelings such as happiness, fear or despair. But that is not the only way to define it. Consider “memory.” Like emotion, memory can refer to an inner experience: When we remember, we experience something. Yet when we talk about the memory of our laptop—having it retrieve an image, for example—we do not think of it as having an inner experience. In this second sense, memory is defined functionally; it is simply the capacity to store information for later recall and use. © 2026 Simons Foundation

Keyword: Emotions
Link ID: 30248 - Posted: 05.20.2026

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