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

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