By Siddhant Pusdekar The food we eat, the air we breathe, and our daily activities all shape how our minds work. Yet most brain research focuses on a narrow slice of humanity: people in high-income countries in the Northern Hemisphere. That leaves a vast gap in our understanding of how neural activity varies across cultures, environments, and lifestyles. A team of researchers from Tanzania and India has taken a step toward closing that gap. In a study published this week in eNeuro, they describe a strategy for collecting data from the brains of diverse groups—from hunter-gatherers to urban dwellers—using electroencephalography (EEG). The technology relies on portable headsets, widely used in clinical settings, that record the brain’s electrical activity through electrodes placed on the scalp. The researchers trained trusted community members as “surveyors,” who visited participants where they live and work to gather EEG data and conduct surveys about their lifestyles and experiences. The initial effort, which involved nearly 8000 volunteers across Tanzania and India, shows that this kind of data collection in low- and middle-income countries is feasible and affordable, the researchers say. The work cost them $50 for each person studied, a fraction of equivalent, large-scale studies conducted in research labs. A: I think mental health is one of the defining health issues in India. When we survey 18- to 24-year-olds, 50% tell us that almost every other day of the month they don’t feel like going to work or college. India is a young country and is increasingly relying on its youth to grow its economy. If they can’t function in their daily activities, you can’t expect them to be productive and contribute to the economy.

Keyword: Brain imaging
Link ID: 29869 - Posted: 07.26.2025

By Diana Kwon A new sensor makes it possible for the first time to simultaneously track dopamine and up to two additional molecules in the brains of living animals. The sensor, dubbed HaloDA1.0, uses a novel dopamine-tagging system that emits light at the far-red end of the color spectrum, according to the team behind the work. “There’s a real need to monitor multiple relevant molecules, as they’re doing here,” says Nicolas Tritsch, assistant professor of neuroscience at McGill University, who was not involved in the study. Because dopamine is involved in a range of key brain functions, when studying its effects on a cell it’s important to consider other neuromodulators that are released at the same time, as well as the signaling cascades these molecules may trigger, Tritsch says. Most dopamine-tracking strategies genetically encode a naturally occurring fluorescent protein into dopamine receptors; when dopamine attaches to the modified receptors, the fluorescent protein changes shape and emits light. But naturally occurring fluorescent proteins have a limited color palette, which has made it difficult to develop sensors that can go beyond two-color imaging, says study investigator Yulong Li, professor of life sciences at Peking University. Instead of genetically encoding a fluorescent protein, HaloDA1.0 attaches a synthetic molecule called HaloTag to dopamine receptors. This tag binds tightly to previously developed artificial dyes that change shape and fluoresce in the far-red spectrum when dopamine binds to its receptors. Because the dyes fluoresce at the far end of the red spectrum, it leaves room for other sensors to glow at different wavelengths. © 2025 Simons Foundation

Keyword: Brain imaging
Link ID: 29868 - Posted: 07.26.2025

Maria Godoy Back in the 1800s, obesity was almost nonexistent in the United States. Over the last century, it's become common here and in other industrialized nations, though it remains rare among people who live more traditional lifestyles, such as the Hadza hunter-gatherers of Tanzania. So what's changed? One common explanation is that as societies have developed, they've also become more sedentary, and people have gotten less active. The assumption is that as a result, we burn fewer calories each day, contributing to an energy imbalance that leads to weight gain over time, says Herman Pontzer, a professor of evolutionary biology and global health at Duke University who studies how human metabolism has evolved. Sponsor Message But in a major new study published in the journal PNAS, Pontzer and an international team of collaborators found that's not the case. They compared the daily total calorie burn for people from 34 different countries and cultures around the world. The people involved ran the spectrum from hunter-gatherers and farming populations with low obesity rates, to people in more sedentary jobs in places like Europe and the U.S., where obesity is widespread. "Surprisingly, what we find is that actually, the total calories burned per day is really similar across these populations, even though the lifestyle and the activity levels are really different," says Pontzer. And that finding offers strong evidence that diet — not a lack of physical activity — is the major driver of weight gain and obesity in our modern world. © 2025 npr

Keyword: Obesity
Link ID: 29867 - Posted: 07.26.2025

By Sofia Caetano Avritzer The original paleo diet might have included fewer succulent steaks and more juicy maggots. Neandertals are often depicted at the top of the food chain for their time, consuming as much meat as lions or hyenas. But maggots growing on rotting meat might have been the real signature dish of the Neandertal diet, researchers report July 25 in Science Advances. The idea that Neandertals were extreme carnivores comes partly from the high levels of a specific type of nitrogen called N-15 in their bones. Nitrogen has two stable forms. N-14 is lighter and a lot more common in nature, while N-15 is heavier and much rarer. When an animal eats a plant with both types of nitrogen, it will keep more N-15 than N-14 in its body after digestion. If that animal gets eaten, its predator will have an even higher proportion of N-15. That makes this molecule more prominent in animals that eat a lot of meat, says Melanie Beasley, a biological anthropologist at Purdue University in West Lafayette, Ind. The proportion of N-15 to N-14 found in Neandertal bones is similar to that found in animals like hyenas, which eat almost exclusively meat, Beasley says. But humans can’t consume as much meat as specialized carnivores, says Karen Hardy, a prehistoric archeologist at the University of Glasgow in Scotland. Without a balanced diet, the human body transforms protein into energy instead of using it to develop muscle, hormones and more. This creates toxic waste products that can cause nausea, diarrhea and even death. So, if Neandertals probably couldn’t eat as much meat as lions or hyenas, where does all the N-15 come from? Rotting meat. © Society for Science & the Public 2000–2025.

Keyword: Evolution; Obesity
Link ID: 29866 - Posted: 07.26.2025

By Michael S. Rosenwald Sarah Morlok Cotton, the last surviving member of a set of identical quadruplets who charmed Depression-era America with song-and-dance performances, and then took part in a landmark psychological study after being diagnosed with schizophrenia, died on July 7 in Belleville, Mich. She was 95. Her death, at an adult foster home, was confirmed by her son David Cotton. The Morlok Quads, as they came to be known, were a medical marvel and attracted crowds of people to Edward W. Sparrow Hospital in Lansing, Mich., shortly after they were born there on May 19, 1930. Newspapers held naming contests, and the winning entry suggested names that derived from the first letters of the hospital: Edna, Wilma, Sarah and Helen. The quadruplets’ middle names were simply initials denoting their birth order. (Sarah, the third born, was C.) Donations poured in almost immediately. The city of Lansing provided the family with a rent-free home. The Massachusetts Carriage Company sent a custom-made baby carriage with four seats. Businessmen opened bank accounts for each child. “Lansing’s Morlok quadruplets,” The Associated Press wrote, “are the most famous group of babies on the American continent.” The Morloks charged visitors 25 cents to visit their home and see the babies. Carl Morlok, who ran for constable of Lansing in 1931, used photos of his daughters on his campaign ads with the slogan, “We will appreciate your support.” He won in a landslide. Amid the commotion, Sadie Morlok tried to provide her daughters with a sense of normalcy. “Our mother used to dress us in pretty little identical crocheted sweaters and bonnets in spring and summer, or snow pant outfits in winter,” Mrs. Cotton wrote in her autobiography, “The Morlok Quadruplets: The Alphabet Sisters” (2015). “Then, she would carefully seat two of us facing the other two in the carriage and go for a nice stroll around the block to give us sunshine and a breath.” © 2025 The New York Times Company

Keyword: Schizophrenia; Genes & Behavior
Link ID: 29865 - Posted: 07.26.2025

Katie Kavanagh How does your brain wake up from sleep? A study of more than 1,000 arousals from slumber has revealed precisely how the brain bestirs itself during the transition to alertness1 — a finding that might help to manage sleep inertia, the grogginess that many people feel when hitting the snooze button. Recordings of people as they woke from the dream-laden phase of sleep showed that the first brain regions to rouse are those associated with executive function and decision-making, located at the front of the head. A wave of wakefulness then spreads to the back, ending with an area associated with vision. The findings could change how we think of waking up, says Rachel Rowe, a neuroscientist at the University of Colorado Boulder, who was not involved with the work. The results emphasize that “falling asleep and waking up aren’t simply reverse processes, but really waking up is this ordered wave of activation that moves from the front to the back of the brain”, whereas falling asleep seems to be less linear and more gradual. The study was published today in Current Biology1. The wide-awake brain shows a characteristic pattern of electrical activity, recorded by sensors on the scalp — it looks like a jagged line made up of small, tightly packed peaks and valleys. Although the pattern looks similar during rapid eye movement (REM) sleep, when vivid dreams occur, this stage features a lack of skeletal-muscle movement. The peaks are taller during most stages of non-REM sleep, which ranges from light to very deep slumber. Scientists already knew that the ‘awakened’ signature occurs at different times in different brain regions, but common imaging techniques did not allow these patterns to be explored on a precise timescale. © 2025 Springer Nature Limited

Keyword: Sleep; Attention
Link ID: 29864 - Posted: 07.19.2025

Jon Hamilton After about age 40, our brains begin to lose a step or two. Each year, our reaction time slows by a few thousandths of a second. We're also less able to recall items on a shopping list. Those changes can be signs of a disease, like Alzheimer's. But usually, they're not. "Both of those things, memory and processing speed, change with age in a normal group of people," says Matt Huentelman, a professor at TGen, the Translational Genomics Research Institute, in Phoenix. Huentelman should know. He helps run MindCrowd, a free online cognitive test that has been taken by more than 700,000 adults. About a thousand of those people had test scores indicating that their brain was "exceptional," meaning they performed like a person 30 years younger on tests of memory and processing speed. Genetics played a role, of course. But Huentelman and a team of researchers have been focusing on other differences. A key protein called Reelin may help stave off Alzheimer's disease, according to a growing body of research. A protein called Reelin keeps popping up in brains that resist aging and Alzheimer's "We want to study these exceptional performers because we think they can tell us what the rest of us should be doing," he says. Early results suggest that sleep and maintaining cardiovascular health are a good start. Other measures include avoiding smoking, limiting alcohol and getting plenty of exercise. Huentelman was one of several dozen researchers who met in Miami this summer to discuss healthy brain aging. The event was hosted by the McKnight Brain Research Foundation, which funds studies on age-related cognitive decline and memory loss. To preserve cognitive function in later life, "we're going to have to understand [brain] aging at a mechanistic level," says Alice Luo Clayton, a neuroscientist who is the group's chief executive officer. © 2025 npr

Keyword: Development of the Brain
Link ID: 29863 - Posted: 07.19.2025

By Katarina Zimmer Using a tiny, spherical glass lens sandwiched between two brass plates, the 17th century Dutch microscopist Antonie van Leeuwenhoek was the first to officially describe red blood cells and sperm cells in human tissues, and observe “animalcules” — bacteria and protists — in the water of a lake. Increasingly powerful light microscopes followed, revealing cell organelles like the nucleus and energy-producing mitochondria. But by 1873, scientists realized there was a limit to the level of detail. When light passes through a lens, the light gets spread out through diffraction. This means that two objects can’t be distinguished if they’re less than roughly 250 nanometers (250 billionths of a meter) apart — instead, they’ll appear as a blur. That put the inner workings of cell structures off limits. Electron microscopy, which uses electron beams instead of light, offers higher resolution. But the resulting black-and-white images make it hard tell proteins apart, and the method only works on dead cells. Now, however, optics engineers and physicists have developed sophisticated tricks to overcome the diffraction limit of light microscopes, opening up a new world of detail. These “super-resolution” light microscopy techniques can distinguish objects down to 100 nanometers and sometimes even less than 10 nanometers. Scientists attach tiny, colored fluorescent tags to individual proteins or bits of DNA, often in living cells where they can watch them in action. As a result, they are now filling in key knowledge gaps about how cells work and what goes wrong in neurological diseases and cancers, or during viral infections. “We can really see new biology — things that we were hoping to see but hadn’t seen before,” says molecular cell biologist Lothar Schermelleh, who directs an imaging center at the University of Oxford in the United Kingdom. Here’s some of what scientists are learning in this new age of light microscopy. Overcoming the diffraction limit

Keyword: Brain imaging
Link ID: 29862 - Posted: 07.19.2025

By Tom Zeller Jr. During the week between two experimental infusions at the Danish Headache Center, where I had agreed to be a test subject, I rented a small flat in central Copenhagen, near Assistens Cemetery. This is where many notable Danes have been laid to rest, and I took some time that September to visit the monuments, which were shrouded in manicured stands of mature poplars and willows. The accompanying article is adapted from “The Headache: The Science of a Most Confounding Affliction — and a Search for Relief,” by Tom Zeller Jr. (Mariner Books, 310 pages). Copyright © 2025. Reprinted by permission. The grave of Niels Bohr, one of the 20th century’s leading figures in theoretical physics, is marked by a gray stone pillar with an owl perched on top. Hans Christian Andersen, the author who gave us “The Little Mermaid” and “The Ugly Duckling,” among other treasured stories, resides here too. But it felt most appropriate to my mission that Danish philosopher Søren Kierkegaard, who thought suffering was where life’s meaning is forged, occupied his own leafy corner of the park. In the Kierkegaardian tradition, suffering is redemptive — the feedstock of enlightenment — and rather than wallow in its insults and pains, the sufferer should embrace its power to transform. “Even the heaviest suffering cannot be heavier than a mountain,” he once wrote. “And thus, if the sufferer believes that his suffering is beneficial to him — yes, then he moves mountains. In order to move a mountain, you must get under it.” I was thinking of Kierkegaard when I first presented my arm to Lanfranco Pellesi, then a researcher at the Danish Headache Center, for my initial infusion. Pellesi had an early interest in studying near-death experiences, before turning his attention to pain, and then from pain to headaches. It struck me as such an obvious trajectory — one that followed an almost inevitable path — and I asked him how he made sense of that progression. “I think probably it links to the problem of conscience — where it is, where it’s not.”

Keyword: Pain & Touch
Link ID: 29861 - Posted: 07.19.2025

By Tina Hesman Saey A large-scale study of proteins in blood and cerebrospinal fluid could pave the way for improved blood tests to diagnose multiple brain diseases — and potential early warning signs of disease risk — researchers report July 15 in several papers in Nature Medicine and Nature Aging. Proteins do much of the work to keep cells and bodies working. Trouble with these building blocks can spell disease; protein misfolding, for instance, links many brain diseases. The results, drawn from samples from 18,645 people, reveal biochemical fingerprints of neurodegenerative disorders such as Alzheimer’s, Parkinson’s, frontotemporal dementia and amyotrophic lateral sclerosis, or ALS. These tests could also help identify disease subtypes and track progression before symptoms emerge. Such well-validated and robust results are “more likely to ultimately translate into something that’s medically actionable,” says Andrew Saykin, director of the Indiana Alzheimer’s Disease Research Center in Indianapolis, which contributed samples to the effort. In one key finding, researchers discovered that individuals carrying a form of the APOE gene called APOE4 — the biggest genetic risk factor for developing Alzheimer’s — share a blood signature regardless of diagnosis. That signature appeared not only in people with Alzheimer’s but also in those with other brain diseases or no neurodegeneration at all, neuroscientist Caitlin Finney and colleagues report in Nature Medicine. The APOE4 protein signature involves proteins that respond to infection and inflammation, hinting at how the variant predisposes carriers to brain diseases. It also suggests that the APOE4 protein may be involved in the early stages of multiple diseases. © Society for Science & the Public 2000–2025.

Keyword: Development of the Brain; Alzheimers
Link ID: 29860 - Posted: 07.16.2025

By Celina Zhao You could be 45 on paper but 60 in your kidneys. Turns out, your organs have birthdays of their own — and how well they’re faring may set the pace for your health, researchers report July 9 in Nature Medicine. Using data from nearly 45,000 people, scientists developed a blood-based test to estimate the biological age of 11 organs, providing a measure of how healthy or worn down each organ is. When a person has an organ substantially “older” than their actual age, disease risks tied to that organ surge. Conversely, extremely youthful brains and immune systems are linked to living longer, the results suggest. “The fact that [the researchers] can create an organ age using proteins — and use it to predict diseases that you would expect to be predicted from that organ — is quite amazing,” says Sarah Harris, a molecular biologist at the University of Edinburgh who was not involved in the study. Aging is far from a uniform process; each organ follows its own clock of decline. One way to track this hidden timeline, previously discovered by Stanford neurology researchers Hamilton Oh and Tony Wyss-Coray, is through the thousands of proteins coursing through our blood. Some unmistakably originate in the liver, while others can be traced to the lungs. Analyzing these proteins can reveal clues about how each organ is holding up. In the new study, the team zeroed in on thousands of patients from the UK Biobank, a long-term database tracking the health of individuals ages 40 to 70 for up to 17 years. By assessing proteins in the blood, the team determined the average protein signature for, say, a 40-year-old liver or 70-year-old arteries. © Society for Science & the Public 2000–2025.

Keyword: Development of the Brain
Link ID: 29859 - Posted: 07.16.2025

Sally Adee Keith Krehbiel lived with Parkinson’s disease for nearly 25 years before agreeing to try a brain implant that might alleviate his symptoms. He had long been reluctant to submit to the surgery. “It was a big move,” he says. But by 2020, his symptoms had become so severe that he grudgingly agreed to go ahead. Deep-brain stimulation involves inserting thin wires through two small holes in the skull into a region of the brain associated with movement. The hope is that by delivering electrical pulses to the region, the implant can normalize aberrant brain activity and reduce symptoms. Since the devices were first approved almost three decades ago, some 200,000 people have had them fitted to help calm the tremors and rigidity caused by Parkinson’s disease. But about 40,000 of those who received devices made after 2020 got them with a special feature that has largely not yet been turned on. The devices can read brain waves and then adapt and tailor the rhythm of their output, in much the same way as a pacemaker monitors and corrects the heart’s electrical rhythms, says Helen Bronte-Stewart, a neurologist at Stanford University in California. Bronte-Stewart received approval to start a clinical trial of this new technology, known as adaptive deep-brain stimulation (aDBS), the same week that Krehbiel was preparing for surgery. He recalls the phone call in which she asked him if he wanted to be her first participant: “I said, ‘Boy, do I!’” Five years on, the results of this 68-person trial, called ADAPT-PD, are under review for publication. Although the exact details are still under wraps, they were convincing enough to earn approval for the technology earlier this year from both US and European regulators. © 2025 Springer Nature Limited

Keyword: Parkinsons
Link ID: 29858 - Posted: 07.16.2025

By Celina Ribeiro Some say it was John Sattler’s own fault. The lead-up to the 1970 rugby league grand final had been tense; the team he led, the South Sydney Rabbitohs, had lost the 1969 final. Here was an opportunity for redemption. The Rabbitohs were not about to let glory slip through their fingers again. Soon after the starting whistle, Sattler went in for a tackle. As he untangled – in a move not uncommon in the sport at the time – he gave the Manly Sea Eagles’ John Bucknall a clip on the ear. Seconds later – just three minutes into the game – the towering second rower returned favour with force: Bucknall’s mighty right arm bore down on Sattler, breaking his jaw in three places and tearing his skin; he would later need eight stitches. When his teammate Bob McCarthy turned to check on him, he saw his captain spurting blood, his jaw hanging low. Forty years later Sattler would recall that moment. One thought raged in his shattered head: “I have never felt pain like this in my life.” But he played on. Tackling heaving muscular players as they advanced. Being tackled in turn, around the head, as he pushed forward. All the while he could feel his jaw in pieces. At half-time the Rabbitohs were leading. In the locker room, Sattler warned his teammates, “Don’t play me out of this grand final.” McCarthy told him, “Mate, you’ve got to go off.” He refused. “I’m staying.” Sattler played the whole game. The remaining 77 minutes. At the end, he gave a speech and ran a lap of honour. The Rabbitohs had won. The back page of the next day’s Sunday Mirror screamed “BROKEN JAW HERO”. © 2025 Guardian News & Media Limited

Keyword: Pain & Touch
Link ID: 29857 - Posted: 07.16.2025

By Shaena Montanari Leafcutter ants’ roles can be reprogrammed by manipulating two neuropeptides, according to a new study. These ants are known for their rigorous division of labor in a caste system, with groups performing roles ranging from cutting leaves to nest defense to tending the fungus that is their food source. Despite physical differences among the ants—the heads of the nest defender ants can be five times the size of the fungal carers’ heads, for instance—it’s still possible to “pharmacologically reprogram them to assume some of the roles that typically other castes assume,” indicating behavioral flexibility, says Daniel Kronauer, professor at Rockefeller University, who was not involved in the work. The researchers induced the behavioral changes by first using RNA sequencing to uncover target neuropeptides and then manipulating neuropeptide levels in the ants. The study was published in June in Cell. The work illustrates the close relationship between neuropeptides and behavior, says Shelley Berger, professor of cell and developmental biology at the University of Pennsylvania and principal investigator of the study. Defender ants are “so big and awkward and clumsy,” she says, but after a certain neuropeptide level is lowered, the ant becomes a “nurse tending to the brood.” The study shows the “importance of neuropeptides as these molecular controllers of incredibly complex” behavioral traits, says Zoe Donaldson, professor of behavioral neuroscience at the University of Colorado Boulder, who was not involved in the study. “I think it’s a really elegant demonstration of just how powerful they are.” Almost all species of ants live in colonies, but leafcutter ants (Atta cephalotes) have a particularly intricate labor division, says study investigator Karl Glastad, assistant professor of biology at the University of Rochester. He and Berger previously explored hormonal controls of social behavior in Florida carpenter ants, which have two worker subtypes, but leafcutter ants are a “really elaborated version” of that species, Glastad says. © 2025 Simons Foundation

Keyword: Hormones & Behavior; Evolution
Link ID: 29856 - Posted: 07.16.2025

Smriti Mallapaty A gene variant known to increase the risk of Alzheimer’s disease also makes people vulnerable to a host of other age-related brain disorders, from Parkinson’s disease to motor neuron disease. The gene variant, a version of apolipoprotein E called APOE ε4, produces a distinct set of proteins that contribute to chronic inflammation, finds an analysis1 using the largest proteomics database for neurodegenerative disease. Neurodegenerative diseases affect more than 57 million people worldwide. Researchers know that people who carry the APOE ε4 variant have an increased risk of developing late-onset Alzheimer’s disease, but studies are beginning to implicate this version, or allele, of APOE in other neurodegenerative diseases. Caitlin Finney and Artur Shvetcov, who study neurodegenerative diseases at the Westmead Institute for Medical Research in Sydney, Australia, and their colleagues wanted to better understand how this genetic risk factor contributes to disease. They took advantage of a newly established proteomics database that allowed them to look beyond individual diseases, says Finney. The Global Neurodegeneration Proteomics Consortium (GNPC) data set2 includes samples from more than 18,600 individuals, mainly of European ancestry, including many with Alzheimer’s, Parkinson’s, a form of motor neuron disease called amyotrophic lateral sclerosis (ALS) and types of dementia, as well as individuals without neurological disorders. The consortia collected around 250 million measurements of proteins found in the blood and cerebrospinal fluid, which surrounds the brain and spinal cord, taken at some two dozen clinics across the United States and Europe. “It’s one of the most powerful databases that we have available for proteomics right now,” says Maryam Shoai, a bioinformatician at University College London. Predicting risk © 2025 Springer Nature Limited

Keyword: Alzheimers; Parkinsons
Link ID: 29855 - Posted: 07.16.2025

By Jan Hoffman Jamie Mains showed up for her checkup so high that there was no point in pretending otherwise. At least she wasn’t shooting fentanyl again; medication was suppressing those cravings. Now it was methamphetamine that manacled her, keeping her from eating, sleeping, thinking straight. Still, she could not stop injecting. “Give me something that’s going to help me with this,” she begged her doctor. “There is nothing,” the doctor replied. Overcoming meth addiction has become one of the biggest challenges of the national drug crisis. Fentanyl deaths have been dropping, in part because of medications that can reverse overdoses and curb the urge to use opioids. But no such prescriptions exist for meth, which works differently on the brain. In recent years, meth, a highly addictive stimulant, has been spreading aggressively across the country, rattling communities and increasingly involved in overdoses. Lacking a medical treatment, a growing number of clinics are trying a startlingly different strategy: To induce patients to stop using meth, they pay them. The approach has been around for decades, but most clinics were uneasy about adopting it because of its bluntly transactional nature. Patients typically come in twice a week for a urine drug screen. If they test negative, they are immediately handed a small reward: a modest store voucher, a prize or debit card cash. The longer they abstain from use, the greater the rewards, with a typical cumulative value of nearly $600. The programs, which usually last three to six months, operate on the principle of positive reinforcement, with incentives intended to encourage repetition of desired behavior — somewhat like a parent who permits a child to stay up late as a reward for good grades. Research shows that the approach, known in addiction treatment as “contingency management,” or CM, produces better outcomes for stimulant addiction than counseling or cognitive behavioral therapy. Follow-up studies of patients a year after they successfully completed programs show that about half remained stimulant-free. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29854 - Posted: 07.16.2025

Mariana Lenharo A speedy imaging method can map the nerves running from a mouse’s brain and spinal cord to the rest of its body at micrometre-scale resolution, revealing details such as individual fibres travelling from a key nerve to distant organs1. Previous efforts have mapped the network of connections between nerve cells, known as the connectome, in the mouse brain. But tracing the complex paths of nerves through the rest of the body has been challenging. To do so, the creators of the new map used a custom-built microscope to scan exposed tissue, completing the process in just 40 hours. Nerves look blue in the reconstructed view of a genetically engineered mouse (left) whose neurons produce a fluorescent marker. In a separate animal (right), antibodies detail the sympathetic nerves (purple). Credit: M.-Y. Shi et al./Cell (CC-BY-4.0) The method, described today in Cell, is an important technical achievement, says Ann-Shyn Chiang, a neuroscientist at the National Tsing Hua University in Hsinchu, Taiwan, who was not involved with the research. “This work is a major step forward in expanding connectomics beyond the brain,” he says. To prepare a mouse’s body for the scan, researchers treat it with chemicals that make its tissues transparent by removing fat, calcium and other components that block light. This provides a clear view of the nerves, which have been labelled with fluorescent marker proteins. The see-through body is then placed into a device that combines a slicing tool and a microscope that takes 3D images. A piston gradually pushes the mouse towards the slicing blade, 400 micrometres at a time. After each slice, a microscope images the newly exposed surface of the mouse, capturing details up to 600 micrometres deep — roughly the thickness of six sheets of paper — below the surface. The body then advances for the next cut. The cycle repeats around 200 times without pause, to cover the entire body. The images are then combined. © 2025 Springer Nature Limited

Keyword: Brain imaging; Development of the Brain
Link ID: 29853 - Posted: 07.12.2025

By Claudia López Lloreda Neural progenitor cells exist in the adult human hippocampus all the way into old age, a new transcriptomics study published today in Science suggests. The results strengthen the claim that adults can form new neurons, according to the team behind the work. But not everyone is convinced that the study shows progenitors are prevalent enough in adulthood to really matter. “Look, there might be something,” says Juan Arellano, a research scientist in neuroscience at Yale University who was not involved with the study. But the cells seem to be rare, because the team could not identify them without the help of a machine-learning algorithm, he adds. “Are they really so relevant in the circuit?” Although the researchers did not quantify the number of cells in their study, newborn neurons are highly excitatory and plastic, so they might still contribute functionally even if there are few, says study investigator Ionut Dumitru, research specialist in Jonas Frisén’s lab at the Karolinska Institutet. Proliferating neurons in adults were first documented in a 1998 study that used a synthetic nucleoside to track newly synthesized DNA in newborn cells. Subsequent work involving carbon dating, lineage tracing and tissue-staining techniques bolstered the idea that people can continue to produce new neurons after childhood. But other studies that stained for cellular markers of neurogenesis suggest that few neurons are born in adults, and the rate of neurogenesis declines dramatically during the first few years of life. These results led some researchers in the field to question the extent and role of neurogenesis in the adult brain, says Shawn Sorrells, assistant professor of neuroscience at the University of Pittsburgh, who conducted some of these cellular marker studies but was not involved with the new one. © 2025 Simons Foundation

Keyword: Neurogenesis; Development of the Brain
Link ID: 29852 - Posted: 07.12.2025

By Dan Falk I’ve been fascinated by time for as long as I can remember. In my undergraduate physics classes, time always lurked in the background—it was the “t” that the professors sprinkled into their equations—but it was never quite clear what time actually was. Years later, I wrote a book about time, but even with chapters on Newton and Einstein, and a solid dose of philosophy, something was missing. Nautilus Members enjoy an ad-free experience. Log in or Join now . For starters, we know clocks and watches work, but how do we tell time? If you’re watching network TV and a commercial break begins, you know you have time to use the bathroom or perhaps make a sandwich—in fact, you can probably arrange to be back in front of the TV just as the ads are ending. What makes you so good at judging these intervals of time? I figured that Dean Buonomano, being a neuroscientist, might have some of the answers. Buonomano is known for developing the idea that the key mechanism is not a single clock-like structure in the brain but rather networks of neurons working together, known as “neural dynamics.” But as Buonomano sees it, the brain does much more than keep track of time; in fact, it might be said to create it. It’s thanks to our brains that we feel time’s “flow,” even though nothing in physics points to such a flow out there in the world. Perhaps even more crucially, the brain allows us to engage in “mental time travel”—the ability to recall past events and imagine future happenings. This capability, he argues, was essential in shaping humanity’s path from the African savannah to today’s globe-spanning civilization. © 2025 NautilusNext Inc.,

Keyword: Attention
Link ID: 29851 - Posted: 07.12.2025

By Ellen Barry Few practices in mental health are debated more than the long-term use of antidepressant medications, which are prescribed to roughly one in nine adults in the United States, according to data from the Centers for Disease Control and Prevention. A reassessment began in 2019, when two British researchers published a study that found that 56 percent of patients suffered from withdrawal symptoms when they stopped antidepressant medications and that 46 percent of those described their symptoms as severe. The findings made headlines in Britain and had a powerful ripple effect, forcing changes to psychiatric training and prescribing guidelines. And they fed a growing grass-roots movement calling to rein in the prescription of psychotropic drugs that has, in recent months, gained new influence in the United States with the rise of Robert F. Kennedy Jr. as health secretary. A new study, published on Wednesday in the journal JAMA Psychiatry, makes the case that these warnings were overblown. The authors of the new paper found that a week after quitting antidepressants, patients reported symptoms like dizziness, nausea and vertigo, but that they remained, on average, “below the threshold for clinically significant” withdrawal. Dr. Sameer Jauhar, one of the authors, said the new analysis should reassure both patients and prescribers. “The messaging that came out in 2019 was all antidepressants can cause this and this can happen in this proportion of people, and that just doesn’t survive any scientific scrutiny,” said Dr. Jauhar, a professor of psychiatry at Imperial College London. He criticized the earlier study for including data from online surveys as a quantitative measure, for failing to control for the placebo effect, and for failing to distinguish between various types of antidepressants. These methodologies, he said, led to inflated estimates of withdrawal. © 2025 The New York Times Company

Keyword: Depression
Link ID: 29850 - Posted: 07.12.2025