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

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

By Marta Hill Every year, black-capped chickadees perform an impressive game of hide-and-seek. These highly visual birds cache tens of thousands of surplus food morsels and then recover them during leaner times. Place cells in the hippocampus may help the birds keep track of their hidden bounty, according to a study published 11 June in Nature. The cells activate not only when a bird visits a food stash but also when it looks at the stash from far away, the study shows. “What is really profound about the work is it’s trying to unpack how it is that we’re able to combine visual information, which is based on where we currently are in the world, with our understanding of the space around us and how we can navigate it,” says Nick Turk-Browne, professor of psychology and director of the Wu Tsai Institute at Yale University, who was not involved in the study. With each gaze shift, the hippocampus first predicts what the bird is about to see and then reacts to what it actually sees, the study shows. “It really fits beautifully into this picture of this dual role for the system in representing actual and representing possible,” says Loren Frank, professor of physiology and psychiatry at the University of California, San Francisco, who was not involved in the work. The findings help explain how the various functions of the hippocampus—navigation, perception, learning and memory—work together, Turk-Browne adds. “If we can have a smart, abstract representation of place that doesn’t depend on actually physically being there, then you can imagine how this can be used to construct memories.” © 2025 Simons Foundation

Keyword: Learning & Memory
Link ID: 29827 - Posted: 06.14.2025

By Ellen Barry Thirty-six hours after dropping his date off at her apartment, Bradley Goldman was on a video call with his dating coach, breaking down the events of the evening. Listen to this article with reporter commentary For one thing, he told the coach, he had chosen the wrong venue for someone on the autism spectrum — a bar of the Sunset Strip hipster variety, so loud and overstimulating that he could almost feel himself beginning to dissociate. Mr. Goldman, a tall, rangy 42-year-old who works as an office manager, hadn’t decided in advance of the date whether to mention that he had been diagnosed with autism, or that he was working with a coach. So he deflected, and they found themselves, briefly, in a conversational blind alley. “I struggle with how to disclose,” he said. “Do I say I am ‘neuro-spicy’? Or ‘neurodiverse’? Or do I disclose at all?” His coach, Disa Jean-Pierre, was sympathetic. “You could just wait for it to come up naturally after a few dates,” she suggested. Mr. Goldman thought this over. “I’m still figuring this out,” he said. Nevertheless, it was a solidly enjoyable date, something he credited to the coaching he had received from a team of psychologists at the Semel Institute for Neuroscience and Human Behavior at the University of California, Los Angeles. He had avoided “info dumping” or making too many Jeffrey Dahmer jokes, and he had carefully observed his date’s body language to detect whether she was signaling openness to a good night kiss. (She was.) “She was like, ‘I really want you to let me know you got home,’” he said. “So, that © 2025 The New York Times Company

Keyword: Autism
Link ID: 29826 - Posted: 06.14.2025

By Calli McMurray The hunt for a soulmate can be hard work—particularly for naive neurons. During development, the cells’ axons snake through burgeoning brain areas in search of the perfect dendrite to form a synapse with. Cell surface proteins serve as molecular identification tags to help axons distinguish “Mr. Wrong” dendrite from “Mr. Right,” according to the chemoaffinity hypothesis. But there are too many cells and too few cell surface proteins for this to be the only strategy, says Claude Desplan, professor of biology and neural science at New York University. “There is no way you can find your partner in a big mess of many different thousands of types of neurons. So you do need to reduce the issue.” In this brain region, 50 types of olfactory receptor neurons link up with 50 types of neurons that project to a sensory integration hub called the mushroom body; each synapse type bunches together inside the lobe to form its own distinct glomerulus. The axons of olfactory receptor neurons do not search the entire structure for their postsynaptic partner. Instead, the projection neurons inside the lobe send their dendrites to meet axons traveling along the surface. Once the two join up, they descend to their proper place in the lobe, imaging experiments show. “Axons don’t need to delve deep. They only need to survey the surface in order to find their target,” says the study’s principal investigator, Liqun Luo, professor of biology at Stanford University. To make matters even simpler, the axons stick to a narrow, genetically determined trajectory, Luo says. Cortical regions may achieve a similar simplification through columns and layers: Axons travel to a certain brain region and then plunge to a particular depth, Luo suggests. Genetically altering these trajectories precludes the olfactory receptor neurons from finding their proper mate, additional experiments show. Dendrites from the postsynaptic cell still wait for their partner at the surface, but “they will be sitting there waiting forever,” Luo says. Some cells “are still sticking their dendrites out” in adulthood, and in at least one case the team observed, a cell eventually matched with another partner. © 2025 Simons Foundation

Keyword: Development of the Brain
Link ID: 29823 - Posted: 06.07.2025

Jon Hamilton Get cut off in rush-hour traffic and you may feel angry for the whole trip, or even snap at a noisy child in the back seat. Get an unexpected smile from that same kid and you may feel like rush hour — and even those other drivers — aren't so bad. "The thing about emotion is it generalizes. It puts the brain into a broader state," says Dr. Karl Deisseroth, a psychiatrist and professor at Stanford University. Deisseroth and a team of researchers have come up with an explanation for how that happens. The process involves a signal that, after a positive or negative experience, lingers in the brain, the team reports in the journal Science. Experiences themselves act a bit like piano notes in the brain. Some are staccato, producing only a brief burst of activity that may result in a reflexive response, like honking at another driver, or smiling back at a child. But more profound experiences can be more like a musical note that is held with the sustain pedal and still audible when the next note is played, or the one after that. "You just need it to be sustained long enough to merge with and interact with other notes," Deisseroth says. "And from our perspective, this is exactly what emotion needs." If the team is right, it could help explain the emotional differences seen in some neuropsychiatric conditions. People on the autism spectrum, for example, often have trouble recognizing emotions in others, and regulating their own emotions. Schizophrenia can cause mood swings and reduced emotional expression. © 2025 npr

Keyword: Emotions; Autism
Link ID: 29819 - Posted: 06.04.2025

By Lina Zeldovich When Catherine Lord was a psychology student a half century ago, she took part in a pioneering effort to move kids with autism from psychiatric institutions into the community. Lord was inspired by positive changes in the kids and devoted her life to developing therapies for people with autism and understanding the biology of the condition. Today, Lord is a professor of psychiatry at the University of California, Los Angeles, and renowned worldwide for developing tools to diagnose autism, which have become clinical standards, and for her efforts to improve the lives of people with autism and their families. Along with her research, Lord maintains a clinical practice where she works with people with autism, from toddlers to adults. So I couldn’t think of a better scientist to address the views of autism espoused by Robert F. Kennedy, Jr. Since being appointed as the United States Secretary of Health and Human Services, Kennedy has continued to spread misinformation about the condition, a pattern that began two decades ago when he claimed childhood vaccines cause autism, a charge long ago proven to be false. Earlier this year, Kennedy announced the National Institutes of Health would launch a new study to investigate the causes of autism. To conduct its study, he said, the NIH would gather medical records of Americans with autism from federal and commercial databases. In conversation, Lord spoke with authority and concern as she pointed out the mendacity and danger of Kennedy’s comments, and clarified the state of autism research and science. He has made a variety of statements about autism that suggests he doesn’t really know what he’s talking about. © 2025 NautilusNext Inc.,

Keyword: Autism
Link ID: 29818 - Posted: 06.04.2025

By Laura Dattaro One of Clay Holroyd’s mostly highly cited papers is a null result. In 2005, he tested a theory he had proposed about a brain response to unexpected rewards and disappointments, but the findings—now cited more than 600 times—didn’t match his expectations, he says. In the years since, other researchers have run similar tests, many of which contradicted Holroyd’s results. But in 2021, EEGManyLabs announced that it would redo Holroyd’s original experiment across 13 labs. In their replication effort, the researchers increased the sample size from 17 to 370 people. The results—the first from EEGManyLabs—published in January in Cortex, failed to replicate the null result, effectively confirming Holroyd’s theory. “Fundamentally, I thought that maybe it was a power issue,” says Holroyd, a cognitive neuroscientist at Ghent University. “Now this replication paper quite nicely showed that it was a power issue.” The two-decade tale demonstrates why pursuing null findings and replications—the focus of this newsletter—is so important. Holroyd’s 2002 theory proposed that previously observed changes in dopamine associated with unexpectedly positive or negative results cause neural responses that can be measured with EEG. The more surprising a result, he posited, the larger the response. To test the idea, Holroyd and his colleagues used a gambling-like task in which they told participants the odds of correctly identifying which of four choices would lead to a 10-cent reward. In reality, the reward was random. When participants received no reward, their neural reaction to the negative result was equally strong regardless of which odds they had been given, contradicting the theory. © 2025 Simons Foundation

Keyword: Attention; Learning & Memory
Link ID: 29814 - Posted: 05.31.2025

Jon Hamilton Joe Walsh, 79, is waiting to inhale. He's perched on a tan recliner at the Center for Alzheimer Research and Treatment at Brigham and Women's Hospital in Boston. His wife, Karen Walsh, hovers over him, ready to depress the plunger on a nasal spray applicator. "One, two, three," a nurse counts. The plunger plunges, Walsh sniffs, and it's done. The nasal spray contains an experimental monoclonal antibody meant to reduce the Alzheimer's-related inflammation in Walsh's brain. He is the first person living with Alzheimer's to get the treatment, which is also being tested in people with diseases including multiple sclerosis, ALS and COVID-19. Sponsor Message Health A man genetically destined to develop Alzheimer's isn't showing any symptoms And the drug appears to be reducing the inflammation in Walsh's brain, researchers report in the journal Clinical Nuclear Medicine. "I think this is something special," says Dr. Howard Weiner, a neurologist at Mass General Brigham who helped develop the nasal spray, along with its maker, Tiziana Life Sciences. Whether a decrease in inflammation will bring improvements in Walsh's thinking and memory, however, remains unclear. The experimental treatment is part of a larger effort to find new ways to interrupt the cascade of events in the brain that lead to Alzheimer's dementia. Two drugs now on the market clear the brain of sticky amyloid plaques, clumps of toxic protein that accumulate between neurons. Other experimental drugs have targeted the tau tangles, a different protein that builds up inside nerve cells. © 2025 npr

Keyword: Alzheimers
Link ID: 29813 - Posted: 05.31.2025

By Sydney Wyatt Donald Hebb famously proposed in 1949 that when neurons fire together, the synaptic connections between them strengthen, forming the basis for long-term memories. That theory—which held up in experiments in rat hippocampal slice cultures—has shaped how researchers understand synaptic plasticity ever since. But a new computational modeling study adds to mounting evidence that Hebbian plasticity does not always explain how changing neuronal connections enable learning. Rather, behavioral timescale synaptic plasticity (BTSP), which can strengthen synapses even when neurons fire out of sync, better captures the changes seen in CA1 hippocampal cells as mice learn to navigate a new environment, the study suggests. Hebbian spike-timing-dependent plasticity occurs when a neuron fires just ahead of one it synapses onto, leading to a stronger connection between the two cells. BTSP, on the other hand, relies on a complex spike, or a burst of action potentials, in the postsynaptic cell, which triggers a calcium signal that travels across the dendritic arbor. The signal strengthens synaptic connections with the presynaptic cell that were active within seconds of that spike, causing larger changes in synaptic strength. BTSP helps hippocampal cells establish their place fields, the positions at which they fire, previous work suggests. But it was unclear whether it also contributes to learning, says Mark Sheffield, associate professor of neurobiology at the University of Chicago, who led the new study. The new findings suggest that it does—challenging how researchers traditionally think about plasticity mechanisms in the hippocampus, says Jason Shepherd, associate professor of neurobiology at the University of Utah, who was not involved in the research. “The classic rules of plasticity that we have been sort of thinking about for decades may not be actually how the brain works, and that’s a big deal.” © 2025 Simons Foundation

Keyword: Learning & Memory
Link ID: 29810 - Posted: 05.28.2025

Jon Hamilton A new blood test that detects a hallmark of Alzheimer's is poised to change the way doctors diagnose and treat the disease. The test, the first of its kind to be cleared by the Food and Drug Administration, is for people 55 and older who already have memory problems or other signs and symptoms of Alzheimer's. The results show whether the brain of a person with cognitive symptoms also has amyloid plaques, clumps of toxic proteins that build up in the spaces between brain cells. The presence of plaques in a person with cognitive symptoms usually confirms an Alzheimer's diagnosis. "I think the blood test is going to really revolutionize the way people with Alzheimer's are cared for and diagnosed," says Dr. Howard Fillit, chief science officer at the Alzheimer's Drug Discovery Foundation. "Primary care physicians will now have access to something that can give them a quicker read" on whether a patient has Alzheimer's, says Maria Carrillo, chief science officer of the Alzheimer's Association. One benefit of a readily-available blood test will be more accurate diagnoses, Fillit says, noting that currently, primary care doctors correctly diagnose patients only about 60% of the time. "Specialty neurologists get it right like seventy, eighty percent of the time," He says. "With the blood test, we can get it up to over 90%." A PET scan is the gold standard for detecting the amyloid plaques associated with Alzheimer's. But the technology is costly, and unavailable in many communities. © 2025 npr

Keyword: Alzheimers
Link ID: 29799 - Posted: 05.24.2025

Gemma Conroy Researchers have identified a genetic dial in the human brain that, when inserted in mice, boosts their brain size by about 6.5%.Credit: Sergey Bezgodov/Shutterstock Taking a snippet of genetic code that is unique to humans and inserting it into mice helps the animals to grow bigger brains than usual, according to a report out in Nature today1. The slice of code — a stretch of DNA that acts like a dial to turn up the expression of certain genes — expanded the outer layer of the mouse brain by increasing the production of cells that become neurons. The finding could partially explain how humans evolved such large brains compared with their primate relatives. This study goes deeper than previous work that attempted to unpick the genetic mechanisms behind human brain development, says Katherine Pollard, a bioinformatics researcher at the Gladstone Institute of Data Science and Biotechnology in San Francisco, California. “The story is much more complete and convincing,” she says. How the human brain grew to be so big and complex remains a mystery, says Gabriel Santpere Baró, a neuroscientist who studies genomics at the Hospital del Mar Medical Research Institute in Barcelona, Spain. “We still do not have a definitive answer to how the human brain has tripled in size since our split from chimpanzees” during evolution, he says. Previous studies2,3 have hinted that human accelerated regions (HARs) — short snippets of the genome that are conserved across mammals, but which underwent rapid change in humans after they evolutionarily diverged from chimpanzees — could be key contributors to brain development and size. But the exact mechanisms that underlie the brain-building effects of HARs are yet to be uncovered, says study co-author Debra Silver, a developmental neurobiologist at Duke University in Durham, North Carolina. © 2025 Springer Nature Limited

Keyword: Development of the Brain; Evolution
Link ID: 29791 - Posted: 05.17.2025

By Ajdina Halilovic When Todd Sacktor (opens a new tab) was about to turn 3, his 4-year-old sister died of leukemia. “An empty bedroom next to mine. A swing set with two seats instead of one,” he said, recalling the lingering traces of her presence in the house. “There was this missing person — never spoken of — for which I had only one memory.” That memory, faint but enduring, was set in the downstairs den of their home. A young Sacktor asked his sister to read him a book, and she brushed him off: “Go ask your mother.” Sacktor glumly trudged up the stairs to the kitchen. It’s remarkable that, more than 60 years later, Sacktor remembers this fleeting childhood moment at all. The astonishing nature of memory is that every recollection is a physical trace, imprinted into brain tissue by the molecular machinery of neurons. How the essence of a lived moment is encoded and later retrieved remains one of the central unanswered questions in neuroscience. Sacktor became a neuroscientist in pursuit of an answer. At the State University of New York Downstate in Brooklyn, he studies the molecules involved in maintaining the neuronal connections underlying memory. The question that has always held his attention was first articulated in 1984 (opens a new tab) by the famed biologist Francis Crick: How can memories persist for years, even decades, when the body’s molecules degrade and are replaced in a matter of days, weeks or, at most, months? In 2024, working alongside a team that included his longtime collaborator André Fenton (opens a new tab), a neuroscientist at New York University, Sacktor offered a potential explanation in a paper published in Science Advances. The researchers discovered that a persistent bond between two proteins (opens a new tab) is associated with the strengthening of synapses, which are the connections between neurons. Synaptic strengthening is thought to be fundamental to memory formation. As these proteins degrade, new ones take their place in a connected molecular swap that maintains the bond’s integrity and, therefore, the memory. © 2025 Simons Foundation

Keyword: Learning & Memory
Link ID: 29784 - Posted: 05.11.2025

By Calli McMurray At least six new brain donors who can do a functional MRI scan—that’s what it will take to complete the most comprehensive human brain atlas yet, project investigators say. The Human and Mammalian Brain Atlas (HMBA) aims to capture information about the identity and location of cells across the entire brain and tie it, for the first time, to the functional organization of the cortex. The atlas, one of several projects in the BRAIN Initiative Cell Atlas Network funded by the U.S. National Institutes of Health, stands to be “a quantum jump in the quality of the data and the resolution that we can analyze it,” says David Van Essen, professor of neuroscience at Washington University in St. Louis and an HMBA investigator. The first atlas, published by the Allen Institute in 2011, contains gene expression information across the brain projected onto an MRI reference space. “By today’s standards, that’s really low-resolution information,” but it’s still “used like crazy,” says Ed Lein, co-creator of the first atlas and one of the lead investigators of the HMBA project at the Allen Institute for Brain Science. Subsequent iterations mapped more of the human brain’s cellular and molecular landscape and at higher resolution. A “first draft” cell atlas, Lein says, published in a trove of papers in 2023, employed single-cell sequencing techniques to catalog thousands of cell types in the human brain. But as “exceptional” as these resources are, their utility is limited by a lack of functional information about the brain regions, says Avram Holmes, associate professor of psychiatry at Rutgers University, who is not involved with the project. © 2025 Simons Foundation

Keyword: Development of the Brain; Brain imaging
Link ID: 29782 - Posted: 05.11.2025

By Giorgia Guglielmi Newly formed memories change over the course of a night’s sleep, a new study in rats suggests. The results reveal that memory processing and consolidation is more complex and prolonged than previously understood, says study investigator Jozsef Csicsvari, professor of systems neuroscience at the Institute of Science and Technology Austria. Sleep has long been known to help consolidate memories, though most studies have tracked only a few hours of this process. The new work monitored memory-related brain activity patterns across almost an entire day—representing a significant step forward, says Lisa Genzel, associate professor of neuroscience at Radboud University, who wasn’t involved in the research. That’s “a heroic effort,” she says. Csicsvari and his team implanted wireless electrodes into the hippocampus of three rats and recorded neuronal activity as the animals learned to navigate a maze in search of hidden pieces of food, rested or slept for 16 to 20 hours after, and then revisited the same food locations the following day. The neurons that fired during learning became active again throughout the rest period, especially during sleep, the team found. This reactivation is a key part of memory consolidation, and it doesn’t just happen immediately after learning; instead, it continues for hours, the study shows. And while the animals slept, their brain activity patterns gradually shifted to resemble the post-sleep recall patterns—a change known as “representational drift” that likely helps the brain weave new information into what it already knows, Csicsvari says. Some neuron groups may be more involved than others in updating memories, the work showed. Some cell types remained stable, whereas others changed their activity. For example, hippocampal neurons called CA1 pyramidal cells showed distinct firing patterns during memory reactivation. And interneurons, too, appeared to play a supporting role, mirroring the changes in pyramidal cells. The team published their findings in Neuron in March. © 2025 Simons Foundation

Keyword: Sleep; Learning & Memory
Link ID: 29777 - Posted: 05.07.2025

By Laura Dattaro In 2012, neuroscientists Sebastian Seung and J. Anthony Movshon squared off at a Columbia University event over the usefulness of connectomes—maps of every connection between every cell in the brain of a living organism. Such a map, Seung argued, could crack open the brain’s computations and provide insight into processes such as sensory perception and memory. But Movshon, professor of neural science and psychology at New York University, countered that the relationship between structure and function was not so straightforward—that even if you knew how all of a brain’s neurons connect to one another, you still wouldn’t understand how the organ turns electrical signals into cognition and behavior. The debate in the field continues, even though Seung and his colleagues in the FlyWire Consortium completed the first connectome of a female Drosophila melanogaster in 2023, and even though a slew of new computational models built from that and other connectomes hint that structure does, in fact, reveal something about function. “This is just the beginning, and that’s what’s exciting,” says Seung, professor of neuroscience at the Princeton Neuroscience Institute. “These papers are kicking off a beginning to an entirely new field, which is connectome-based brain simulation.” A simulated fruit fly optic lobe, detailed in a September 2024 Nature paper, for example, accurately predicts which neurons in living fruit flies respond to different visual stimuli. “All the work that’s been done in the past year or two feels like the beginning of something new,” says John Tuthill, associate professor of neuroscience at the University of Washington. Tuthill was not involved in the optic lobe study but used a similar approach to identify a circuit that seems to control walking in flies. Most published models so far have made predictions about simple functions that were already understood from recordings of neural activity, Tuthill adds. But “you can see how this will build up to something that is eventually very insightful.” © 2025 Simons Foundation

Keyword: Brain imaging; Development of the Brain
Link ID: 29769 - Posted: 05.03.2025

Andrew Gregory Health editor Scientists have used living human brain tissue to mimic the early stages of Alzheimer’s disease, the most common form of dementia, in a breakthrough that will accelerate the hunt for a cure. In a world first, a British team successfully exposed healthy brain tissue from living NHS patients to a toxic form of a protein linked to Alzheimer’s – taken from patients who died from the disease – to show how it damages connections between brain cells in real time. The groundbreaking move offered a rare and powerful opportunity to see dementia developing in human brain cells. Experts said the new way of studying the disease could make it easier to test new drugs and boost the chances of finding ones that work. Dementia presents a big threat to health and social care systems across the world. The number of people affected is forecast to triple to nearly 153 million by 2050, which underlines why finding new ways to study the disease and speed up the search for treatments is a health priority. In the study, scientists and neurosurgeons in Edinburgh teamed up to show for the first time how a toxic form of a protein linked to Alzheimer’s, amyloid beta, can stick to and destroy vital connections between brain cells. Tiny fragments of healthy brain tissue were collected from cancer patients while they were undergoing routine surgery to remove tumours at the Royal Infirmary of Edinburgh. Scientists dressed in scrubs were stationed in operating theatres alongside surgical teams, ready to receive the healthy brain tissue, which would otherwise have been discarded. Once the pieces of brain were retrieved, scientists put them in glass bottles filled with oxygenated artificial spinal fluid before jumping into taxis to transport the samples to their lab a few minutes away. © 2025 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29767 - Posted: 04.30.2025

By Lydia Denworth The rattling or whistling noises of regular snorers are famously hard on those who share their beds. Middle-aged men and people who are overweight come frequently to mind as perpetrators because they are the most common sufferers of sleep apnea, often caused by a temporarily collapsing airway that makes the person snore heavily. But recent studies in children and pregnant women have revealed that even mild snoring can negatively affect health, behavior and quality of life. “We know that disordered breathing and disturbed sleep can have myriad physiological effects,” says Susan Redline, a pulmonologist and epidemiologist at Brigham and Women’s Hospital in Boston. “More people have sleep-disordered breathing than have overt apneas. We shouldn’t forget about them.” Almost everyone snores occasionally. Allergies and respiratory infections can trigger it. When the upper airway at the back of the throat narrows, it causes the tissues there to vibrate, creating the familiar rumble. Physicians worry if people habitually snore three or more nights a week, especially if they have other red flags such as unexplained high blood pressure. The category of sleep-disordered breathing includes apnea’s total pause in breathing, shallow breaths called hypopnea, snoring without apneas, and a subtler problem called flow limitation in which the shape of the airway is narrowed but the sleeper makes no noise. The standard measure of severity is the apnea-hypopnea index (AHI), which counts pauses in breathing per hour and associated drops in oxygen levels. The normal level in adults is fewer than five pauses; more than 30 is severe. In children, 10 pauses could be considered moderately severe. © 2025 SCIENTIFIC AMERICAN,

Keyword: Sleep; Development of the Brain
Link ID: 29764 - Posted: 04.30.2025