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

Sydney Lupkin Jerry Abrams, a 64-year-old marketing strategist in Minneapolis, used to run marathons. But two decades of degenerative spine disease have left him unable to run — and he's grieving. For Abrams, losing running felt like "the loss of a loved one – that friend who's been with you every day you needed him. "You know, having that taken away from you because of pain is the hardest thing of all," he says. The constant pain in his lower back makes running impossible. Sometimes, when the pain isn't under control, he can't get out of bed. Abrams has tried taking opioids. They help, but he feels he has to be careful because they're potentially addictive. He's also worried about building up a tolerance to them "I don't ever want to be in a situation where I need surgery and need to recover and opioid medication no longer does what it needs to do," he explains. The Food and Drug Administration approved a new non-opioid drug earlier this year called Journavx. It's a pill for severe acute pain that works by blocking plain signals from where someone hurts. It's offered hope for the 1 in 5 Americans who suffer from chronic pain, but it's also just out of reach. Journavx is the first new kind of painkiller in more than 20 years, and the medical community is cautiously optimistic that Journavx doesn't have the same addictive potential as opioids do. But the new pills are expensive, and not everyone has been able to access them, thanks to a narrowly-focused FDA approval and limited insurance coverage Abrams' doctor wanted him to be able to try Journavx. But the FDA only approved the medication for short-term use for acute pain, which is usually defined as lasting less than three months, such as right after surgery. Because Abrahm's pain is chronic, his insurance wouldn't cover it. A single Journavx pill costs around $15 without insurance, according to Vertex Pharmaceuticals, the drug's manufacturer. © 2025 npr

Keyword: Pain & Touch; Drug Abuse
Link ID: 29849 - Posted: 07.12.2025

Heidi Ledford Telltale features in standard brain images can reveal how quickly a person is ageing, a study of more than 50,000 brain scans has shown1. Pivotal features include the thickness of the cerebral cortex — a region that controls language and thinking — and the volume of grey matter that it contains. These and other characteristics can predict how quickly a person’s ability to think and remember will decline with age, as well as their risk of frailty, disease and death. Although it’s too soon to use the new results in the clinic, the test provides advantages over previously reported ‘clocks’ — typically based on blood tests — that purport to measure the pace of ageing, says Mahdi Moqri, a computational biologist who studies ageing at Harvard Medical School in Boston, Massachusetts. “Imaging offers unique, direct insights into the brain’s structural ageing, providing information that blood-based or molecular biomarkers alone can’t capture,” says Moqri, who was not involved in the study. The results were published today in Nature Aging. Genetics, environment and disease all affect the speed of biological ageing. As a result, chronological age does not always reflect the pace at which time takes its toll on the body. Researchers have been racing to develop measures to fill that gap. Ageing clocks could be used early in life to assess an individual’s risk of age-related illness, when it might still be possible to intervene. They could also aid testing of treatments aimed at slowing ageing, by providing a marker to track the effects of the intervention in real time. © 2025 Springer Nature Limited

Keyword: Development of the Brain; Brain imaging
Link ID: 29848 - Posted: 07.02.2025

By Mohana Ravindranath A new analysis of data gathered from a small Indigenous population in the Bolivian Amazon suggests some of our basic assumptions about the biological process of aging might be wrong. Inflammation is a natural immune response that protects the body from injury or infection. Scientists have long believed that long-term, low-grade inflammation — also known as “inflammaging” — is a universal hallmark of getting older. But this new data raises the question of whether inflammation is directly linked to aging at all, or if it’s linked to a person’s lifestyle or environment instead. The study, which was published today, found that people in two nonindustrialized areas experienced a different kind of inflammation throughout their lives than more urban people — likely tied to infections from bacteria, viruses and parasites rather than the precursors of chronic disease. Their inflammation also didn’t appear to increase with age. Scientists compared inflammation signals in existing data sets from four distinct populations in Italy, Singapore, Bolivia and Malaysia; because they didn’t collect the blood samples directly, they couldn’t make exact apples-to-apples comparisons. But if validated in larger studies, the findings could suggest that diet, lifestyle and environment influence inflammation more than aging itself, said Alan Cohen, an author of the paper and an associate professor of environmental health sciences at Columbia University. “Inflammaging may not be a direct product of aging, but rather a response to industrialized conditions,” he said, adding that this was a warning to experts like him that they might be overestimating its pervasiveness globally. “How we understand inflammation and aging health is based almost entirely on research in high-income countries like the U.S.,” said Thomas McDade, a biological anthropologist at Northwestern University. But a broader look shows that there’s much more global variation in aging than scientists previously thought, he added. © 2025 The New York Times Company

Keyword: Development of the Brain; Neuroimmunology
Link ID: 29847 - Posted: 07.02.2025

By Laura Sanders GLP-1 drugs may possess a new power: Easing migraines. In a small, preliminary study, a GLP-1 drug nearly halved the number of days people spent with a migraine in a given month. The results, presented June 21 at the European Academy of Neurology Congress in Helsinki, Finland, expand the possible benefits of the powerful new class of obesity and diabetes drugs. These pernicious, debilitating headaches are estimated to affect one billion people worldwide. Earlier studies have shown that GLP-1 agonists can reduce the pressure inside the skull, a squeeze that’s been implicated in migraines. Neurologist Simone Braca of the University of Naples Federico II in Italy and his colleagues explored whether liraglutide, an older relative of Ozempic and Wegovy, might help migraine sufferers. Thirty-one adults, 26 of them women, got daily injections of liraglutide for 12 weeks. These adults all had obesity and continued to take their current migraine medicines too. At the start of the experiment, participants had headaches on about 20 days out of a month. After 12 weeks of liraglutide, the average number dropped to about 11 days. “Basically, we observed that patients saw their days with headache halved, which is huge,” Braca says. Participants’ weight stayed about the same during the trial, suggesting that headache reductions weren’t tied to weight loss. If the results hold up in larger studies, they may point to treatments for migraine sufferers who aren’t helped by existing drugs. The results may also lead to a deeper understanding of the role of pressure inside the head in migraines, Braca says. © Society for Science & the Public 2000–2025.

Keyword: Obesity; Pain & Touch
Link ID: 29846 - Posted: 07.02.2025

By Claudia López Lloreda When it comes to cognition and behavior, neurons usually take center stage. They famously drive everything from thoughts to movements by way of synaptic communication, with the help of neuromodulators such as dopamine, norepinephrine and certain immune molecules that regulate neuronal activity and plasticity. But astrocytes play essential roles in these processes behind the scenes, according to four independent studies published in the past two months. Rather than acting solely on neurons, neuromodulators also act on astrocytes to influence neuronal function and behavior—making astrocytes crucial intermediates in activities previously attributed to direct communication between neurons, the studies suggest. For instance, norepinephrine sensitizes astrocytes to neurotransmitters and prompts them to regulate circuit computations, synapse function and various behaviors across diverse animal models, three of the studies—all published last month in Science—show. “Do neurons actually signal through astrocytes in a meaningful way during normal behavior or normal circuit function?” asks Marc Freeman, senior scientist at Oregon Health & Science University and principal investigator on one of the Science studies. These new findings “argue very strongly the answer is yes.” Astrocytes can also detect peripheral inflammation and modify the neurons that drive a stress-induced fear behavior in mice, according to the fourth study, published in April in Nature. Although astrocytes are no longer thought of as simply support cells, they were still “not really considered for having a real plasticity and a real important role,” says Caroline Menard, associate professor of psychiatry and neurosciences at the University of Laval, who was not involved in any of the new studies. Now “there’s more consideration from the field that behavior is not only driven by neurons, but there’s other cell types involved.” © 2025 Simons Foundation

Keyword: Glia; Learning & Memory
Link ID: 29845 - Posted: 07.02.2025

Humberto Basilio Mindia Wichert has taken part in plenty of brain experiments as a cognitive-neuroscience graduate student at the Humboldt University of Berlin, but none was as challenging as one he faced in 2023. Inside a stark white room, he stared at a flickering screen that flashed a different image every 10 seconds. His task was to determine what familiar object appeared in each image. But, at least at first, the images looked like nothing more than a jumble of black and white patches. “I’m very competitive with myself,” says Wichert. “I felt really frustrated.” Cognitive neuroscientist Maxi Becker, now at Duke University in Durham, North Carolina, chose the images in an attempt to spark a fleeting mental phenomenon that people often experience but can’t control or fully explain. Study participants puzzling out what is depicted in the images — known as Mooney images, after a researcher who published a set of them in the 1950s1 — can’t rely on analytical thinking. Instead, the answer must arrive all at once, like a flash of lightning in the dark (take Nature’s Mooney-images quiz below). Becker asked some of the participants to view the images while lying inside a functional magnetic resonance imaging (fMRI) scanner, so she could track tiny shifts in blood flow corresponding to brain activity. She hoped to determine which regions produce ‘aha!’ moments. Over the past two decades, scientists studying such moments of insight — also known as eureka moments — have used the tools of neuroscience to reveal which regions of the brain are active and how they interact when discovery strikes. They’ve refined the puzzles they use to trigger insight and the measurements they take, in an attempt to turn a self-reported, subjective experience into something that can be documented and rigorously studied. This foundational work has led to new questions, including why some people are more insightful than others, what mental states could encourage insight and how insight might boost memory. © 2025 Springer Nature Limited

Keyword: Attention; Learning & Memory
Link ID: 29844 - Posted: 06.28.2025

By Katrina Miller Take a look at this video of a waiting room. Do you see anything strange? Perhaps you saw the rug disappear, or the couch pillows transform, or a few ceiling panels evaporate. Or maybe you didn’t. In fact, dozens of objects change in this video, which won second place in the Best Illusion of the Year Contest in 2021. Voting for the latest version of the contest opened on Monday. Illusions “are the phenomena in which the physical reality is divorced from perception,” said Stephen Macknik, a neuroscientist at SUNY Downstate Health Sciences University in Brooklyn. He runs the contest with his colleague and spouse, Susana Martinez-Conde. By studying the disconnect between perception and reality, scientists can better understand which brain regions and processes help us interpret the world around us. The illusion above highlights change blindness, the brain’s failure to notice shifts in the environment, especially when they occur gradually. To some extent, all sensory experience is illusory, Dr. Martinez-Conde asserts. “We are always constructing a simulation of reality,” she said. “We don’t have direct access to that reality. We live inside the simulation that we create.” She and Dr. Macknik have run the illusion contest since 2005. What began as a public outreach event at an academic conference has since blossomed into an annual competition open to anyone in the world. They initially worried that people would run out of illusions to submit. “But that actually never happened,” Dr. Martinez-Conde said. “What ended up happening instead is that people started developing illusions, actually, with an eye to competing in the contest.” © 2025 The New York Times Company

Keyword: Vision; Attention
Link ID: 29843 - Posted: 06.28.2025

By Gordy Slack, MindSite News Lauren Kennedy West was still a teenager when she began to smell and hear things that weren’t there. Then to see things, too, that were invisible to others. Meanwhile, her moods began to intensify, sometimes turning very, very dark. “It was confusing, disturbing, and depressing,” she recalls. She had periods of elation, too. But when she came down from these, she’d keep descending until she hit emotional bottom. It got so bad that in her early 20s, at college, Kennedy West tried to end her life twice. Finally, when she was 25, she was diagnosed with schizoaffective disorder, a form of schizophrenia with powerful mood swings. The medications she was prescribed eased her worst symptoms, she said, but they also had troubling side effects that ranged from extreme weight gain and “dry mouth” to feeling lethargic and an episodic condition called oculogyric crisis which causes people to continually, involuntarily, gaze upward. Worst of all, she said, was the feeling of being “emotionally blunted.” Learning that she’d likely be taking those medications for the rest of her life was a blow, but the diagnosis gave Kennedy West a meaningful framework for her struggle. To be as stable, happy, and engaged as possible she would have to cultivate acceptance of her condition and the limitations it imposed, she was told. Driven by a hope that others might be spared the disabling confusion and depression she suffered before her diagnosis, Kennedy West and her partner started a YouTube Channel, which they called “Living Well with Mental Illness” (now “Living Well with Schizophrenia“) In frequent posts, Kennedy West recounted her own struggles and triumphs and interviewed experts on mental illness and related subjects. In early 2023, Christopher Palmer was a guest on the channel.

Keyword: Schizophrenia
Link ID: 29842 - Posted: 06.28.2025

By Sydney Wyatt The shape and density of dendritic spines fluctuate in step with the estrous cycle in the hippocampus of living mice, a new study shows. And these structural changes coincide with shifts in the stability of place fields encoded by place cells. “You can literally see these oscillations in hippocampal spines, and they keep time with the endocrine rhythms being produced by the ovaries,” says study investigator Emily Jacobs, associate professor of psychological and brain sciences at the University of California, Santa Barbara. She and her colleagues used calcium imaging and surgically implanted microperiscopes to view the dynamics of the dendritic spines in real time. The findings, published in Neuron in May, replicate and expand upon a series of cross-sectional studies of rat brain tissue in the early 1990s that documented sex hormone receptors in the hippocampus and showed that changes in estradiol levels across the estrous cycle track with differences in dendritic spine density. “The field of neuroendocrinology was really changed in the early ’90s because of this discovery,” Jacobs says. The new work is a “very important advancement,” says John Morrison, professor of neurology at the University of California, Davis, who was not involved in the research. It shows that spines change across the natural cycle of living mice, supporting estradiol’s role in this process, and it links these changes to electrophysiological differences, he says. “The most surprising part of this study is that everything seems to follow each other. Usually biology doesn’t cooperate like this,” Morrison says. Before the early 1990s, estrogens were viewed only as reproductive hormones, and their effects in the brain were thought to be limited to the hypothalamus, says Catherine Woolley, professor of neurobiology at Northwestern University, who worked on the classic rat hippocampus studies when she was a graduate student in the lab of the late Bruce McEwen. For that reason, her rat hippocampus results were initially met with “resistance,” she adds. A leader in the field once told her to “get some better advice” from her adviser “because estrogens are reproductive hormones, and they don’t have effects in the hippocampus,” she recalls. © 2025 Simons Foundation

Keyword: Hormones & Behavior; Learning & Memory
Link ID: 29841 - Posted: 06.28.2025

By Nazeefa Ahmed Humans prefer fruit at its sweetest, whereas many birds happily snack on the sourest of the bunch, from zesty lemons to unripe honey mangoes. Researchers may now know why. A study published today in Science suggests birds have evolved a specialized taste receptor that’s suppressed by high acidity, which effectively dulls the sharp, sour taste of fruits they eat. The finding reveals the evolutionary history of the pucker-inducing diets of many fruit-eating birds around the world—and may also help explain birds’ knack for survival, by broadening their potential food sources. The study is a “robust” addition to our understanding of how birds taste sour foods, which is still a research area in its infancy, says Leanne Grieves, an ornithologist at Cornell University’s Lab of Ornithology. Scientists identified a sour taste receptor in vertebrates—known as OTOP1—only 7 years ago, and few studies focus on why birds eat what they eat, rather than simply what they eat. Grieves, who studies birds’ sense of smell but who was not involved with the current work, adds that the new study “provides a really nice starting point.” To examine how birds approach sour-tasting foods, scientists exposed OTOP1 receptors from mice, domestic pigeons, and canaries to various acidic solutions. The activity of the mouse version of the receptor increased with greater acidity—meaning more acidic foods register to mice, and other mammals like us, as increasingly sour. However, the pigeon and canary versions of OTOP1 became less active in solutions about as acidic as a lemon. As a result, the birds wouldn’t perceive as much of a sour taste, allowing them to take advantage of the fruits mammals can’t stomach. Determining why bird OTOP1 reacted differently was a challenge, according to study author Hao Zhang, an evolutionary biologist at the Chinese Academy of Sciences (CAS). So, the researchers mutated sections of the gene that encodes the OTOP1 receptor, which let them identify four candidate amino acids within the protein that are responsible for sour tolerance. One of them, known as G378, is found almost exclusively in songbirds such as the canary—a species that showed greater sour tolerance than the pigeon, which lacks this variance. “A single amino acid in the bird OTOP1 can increase sour tolerance,” says study author Lei Luo, a biologist at CAS. © 2025 American Association for the Advancement of Science.

Keyword: Chemical Senses (Smell & Taste); Evolution
Link ID: 29840 - Posted: 06.21.2025

James Doubek Researchers have some new evidence about what makes birds make so much noise early in the morning, and it's not for some of the reasons they previously thought. For decades, a dominant theory about why birds sing at dawn — called the "dawn chorus" — has been that they can be heard farther and more clearly at that time. Sound travels faster in humid air and it's more humid early in the morning. It's less windy, too, which is thought to lessen any distortion of their vocalizations. But scientists from the Cornell Lab of Ornithology's K. Lisa Yang Center for Conservation Bioacoustics and Project Dhvani in India combed through audio recordings of birds in the rainforest. They say they didn't find evidence to back up this "acoustic transmission hypothesis." It was among the hypotheses involving environmental factors. Another is that birds spend their time singing at dawn because there's low light and it's a bad time to look for food. "We basically didn't find much support for some of these environmental cues which have been purported in literature as hypotheses" for why birds sing more at dawn, says Vijay Ramesh, a postdoctoral research associate at Cornell and the study's lead author. The study, called "Why is the early bird early? An evaluation of hypotheses for avian dawn-biased vocal activity," was published this month in the peer-reviewed journal Philosophical Transactions of the Royal Society B. The researchers didn't definitively point to one reason for why the dawn chorus is happening, but they found support for ideas that the early morning racket relates to birds marking their territory after being inactive at night, and communicating about finding food. © 2025 npr

Keyword: Animal Communication; Evolution
Link ID: 29839 - Posted: 06.21.2025

By Nala Rogers Coffer illusion What do you see when you stare at this grid of line segments: a series of rectangles, or a series of circles? The way you perceive this optical illusion, known as the Coffer illusion, may tie back to the visual environment that surrounds you, a recent preprint suggests.Anthony Norcia/Smith-Kettlewell Eye Research Institute Himba people from rural Namibia can see right through optical illusions that trick people from the United States and United Kingdom. Even when there’s no “right” or “wrong” way to interpret an image, what Himba people see is often vastly different from what people see in industrialized societies, a new preprint suggests. That could mean people’s vision is fundamentally shaped by the environments they’re raised in—an old but controversial idea that runs counter to the way human perception is often studied. For example, when presented with a grid of line segments that can be seen as either rectangles or circles—an optical illusion known as the Coffer illusion—people from the U.S. and U.K. almost always see rectangles first, and they often struggle to see circles. The researchers suspect this is because they are surrounded by rectangular architecture, an idea known as the carpentered world hypothesis. In contrast, the traditional villages of Himba people are composed of round huts surrounding a circular livestock corral. People from these villages almost always see circles first, and about half don’t see rectangles even when prompted. “I’m surprised that you can’t see the round ones,” says Uapwanawa Muhenije, a Himba woman from a village in northern Namibia, speaking through an interpreter over a Zoom interview. “I wonder how you can’t see them.” Muhenije didn’t participate in the research because her village is less remote than those in the study, and it includes rectangular as well as circular buildings. She sees both shapes in the Coffer illusion easily. Although the study found dramatic differences in how people see four illusions, “the one experiment that’s going to overwhelm people is this Coffer,” says Jules Davidoff, a psychologist at the University of London who was not involved in the study. “There are other striking cultural differences in perception, but the one that they’ve produced here is a real humdinger.” The findings were published as a preprint on the PsyArXiv in February and updated this week. © 2025 American Association for the Advancement of Science.

Keyword: Vision; Development of the Brain
Link ID: 29838 - Posted: 06.21.2025

Katie Kavanagh Scientists have identified a group of neurons that might explain the mechanism behind how stress gives rise to problems with sleep and memory. The study — published last week in The Journal of Neuroscience1 — shows that neurons in a brain area called the hypothalamus mediate the effects of stress on sleep and memory, potentially providing a new target for the treatment of stress-related sleep disorders. Previous work has shown that in the hypothalamus, neurons in a structure called the paraventricular nucleus communicate with other areas important for sleep and memory. The neurons of the paraventricular nucleus release a hormone called corticotropin and have a role in regulating stress. But the neural mechanisms underlying the effect of stress on sleep and memory have remained elusive. For co-author Shinjae Chung, a neuroscientist at the University of Pennsylvania in Philadelphia, the question of exactly how stress affects these processes is personal, because, she says, “I experience a lot of sleep problems when I’m stressed”. She adds that “when I have an exam deadline, I have a tendency to have bad sleep that really affects my score the next day”. To study how neurons in the paraventricular nucleus translate stress into sleep and memory problems, the researchers put laboratory mice through a stressful experience by physically restraining the animals in a plastic tube. The team then tested the creatures’ spatial memory and monitored their brain activity as they slept. © 2025 Springer Nature Limited

Keyword: Sleep; Stress
Link ID: 29837 - Posted: 06.21.2025

Diana Kwon There might be a paradox in the biology of ageing. As humans grow older, their metabolisms tend to slow, they lose muscle mass and they burn many fewer calories. But certain cells in older people appear to do the exact opposite — they consume more energy than when they were young. These potential energy hogs are senescent cells, older cells that have stopped dividing and no longer perform the essential functions that they used to. Because they seem idle, biologists had assumed that zombie-like senescent cells use less energy than their younger, actively replicating counterparts, says Martin Picard, a psychobiologist at Columbia University in New York City. But in 2022, Gabriel Sturm, a former graduate student of Picard’s, painstakingly observed the life course of human skin cells cultured in a dish1 and, in findings that have not yet been published in full, found that cells that had stopped dividing had a metabolic rate about double that of younger cells. For Picard and his colleagues, the energetic mismatch wasn’t a paradox at all: ageing cells accumulate energetically costly forms of damage, such as alterations in DNA, and they initiate pro-inflammatory signalling. How that corresponds with the relatively low energy expenditure for ageing organisms is still unclear, but the researchers hypothesize that this tension might be an important driver of many of the negative effects of growing old, and that the brain might be playing a key part as mediator2. As some cells get older and require more energy, the brain reacts by stripping resources from other biological processes, which ultimately results in outward signs of ageing, such as greying hair or a reduction in muscle mass (see ‘Energy management and ageing’). Picard and his colleagues call this concept the ‘brain–body energy-conservation model’. And although many parts of the hypothesis are still untested, scientists are working to decipher the precise mechanisms that connect the brain to processes associated with ageing, such as senescence, inflammation and the shortening of telomeres — the stretches of repetitive DNA that cap the ends of chromosomes and protect them. © 2025 Springer Nature Limited

Keyword: Obesity; Stress
Link ID: 29836 - Posted: 06.18.2025

By Michael A. Yassa For nearly three decades, Alzheimer’s disease has been framed as a story about amyloid: A toxic protein builds up, forms plaques, kills neurons and slowly robs people of their memories and identity. The simplicity of this “amyloid cascade hypothesis” gave us targets, tools and a sense of purpose. It felt like a clean story. Almost too clean. We spent decades chasing it, developing dozens of animal models and pouring billions into anti-amyloid therapies, most of which failed. The few that made it to market offer only modest benefits, often with serious side effects. Whenever I think about this, I can’t help but picture Will Ferrell’s Buddy the Elf, in the movie “Elf,” confronting the mall Santa: “You sit on a throne of lies.” Not because anyone meant to mislead people (though maybe some did). But because we wanted so badly for the story to be true. So what happened? This should have worked … right? I would argue it was never going to work because we have been thinking about Alzheimer’s the wrong way. For decades, we have treated it as a single disease with a single straight line from amyloid to dementia. But what if that’s not how it works? What if Alzheimer’s only looks like one disease because we keep trying to force it into a single narrative? If that’s the case, then the search for a single cause—and a single cure—was always destined to fail. ”What if Alzheimer’s only looks like one disease because we keep trying to force it into a single narrative? If that’s the case, then the search for a single cause—and a single cure—was always destined to fail. Real progress, I believe, requires two major shifts in how we think. First, we have to let go of our obsession with amyloid. © 2025 Simons Foundation

Keyword: Alzheimers
Link ID: 29835 - Posted: 06.18.2025

By Amber Dance Back in 2008, neurovirologist Renée Douville observed something weird in the brains of people who’d died of the movement disorder ALS: virus proteins. But these people hadn’t caught any known virus. Instead, ancient genes originally from viruses, and still lurking within these patients’ chromosomes, had awakened and started churning out viral proteins. Our genomes are littered with scraps of long-lost viruses, the descendants of viral infections often from millions of years ago. Most of these once-foreign DNA bits are a type called retrotransposons; they make up more than 40 percent of the human genome. Pie chart shows that retrotransposons make up nearly half the human genome. Our genomes are riddled with DNA from ancient viral infections known as jumping genes. The majority of these are retrotransposons, which copy themselves via RNA intermediates; a smaller portion are cut-and-paste DNA transposons. Many retrotransposons seem to be harmless, most of the time. But Douville and others are pursuing the possibility that some reawakened retrotransposons may do serious damage: They can degrade nerve cells and fire up inflammation and may underlie some instances of Alzheimer’s disease and ALS (amyotrophic lateral sclerosis, or Lou Gehrig’s disease). The theory linking retrotransposons to neurodegenerative diseases — conditions in which nerve cells decline or die — is still developing; even its proponents, while optimistic, are cautious. “It’s not yet the consensus view,” says Josh Dubnau, a neurobiologist at the Renaissance School of Medicine at Stony Brook University in New York. And retrotransposons can’t explain all cases of neurodegeneration. Yet evidence is building that they may underlie some cases. Now, after more than a decade of studying this possibility in human brain tissue, fruit flies and mice, researchers are putting their ideas to the ultimate test: clinical trials in people with ALS, Alzheimer’s and related conditions. These trials, which borrow antiretroviral medications from the HIV pharmacopeia, have yielded preliminary but promising results. © 2025 Annual Reviews

Keyword: ALS-Lou Gehrig's Disease ; Alzheimers
Link ID: 29834 - Posted: 06.18.2025