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 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

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 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

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

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 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 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

By Sara Talpos It’s been more than 30 years since the award-winning film “Rain Man,” starring Dustin Hoffman and Tom Cruise, put a spotlight on autism — or, more specifically, on a specific type of autism characterized by social awkwardness and isolation and typically affecting males. Yet as far back as the 1980s, at least one prominent autism researcher wondered whether autism’s male skew might simply reflect the fact that autistic females were, for some reason, going undiagnosed. Over the past decade, spurred by the personal testimonies of late-diagnosed women, autism researchers have increasingly examined this question. As it turns out, many autistic women and girls are driven by a powerful desire to avoid social rejection, so powerful, in fact, that they may adopt two broad strategies — camouflaging and masking — to hide their condition in an attempt to better fit in with neurotypical peers and family members. Such behavior is “at odds with the traditional picture of autism,” writes Gina Rippon, an emeritus professor of cognitive neuroimaging at Aston University in Birmingham, England, in her new book “Off the Spectrum: Why the Science of Autism Has Failed Women and Girls.” And while the ability to blend in might seem like a positive, it can ultimately take a heavy toll. Rippon points, for example, to surveys showing that by age 25, about 20 percent of autistic women have been hospitalized for a psychiatric condition, more than twice the rate of autistic men. In the U.S., the rate of autism has been increasing since at least 2000, and many autism researchers, including Rippon, believe more inclusive diagnostic criteria, coupled with increased awareness, have contributed to the rise. Last week, however, Health and Human Services Secretary Robert F. Kennedy Jr. dismissed this idea and insisted that the condition is caused by environmental factors. The National Institutes of Health has begun work on a research initiative that aims to look into this further.

Keyword: Autism; Sexual Behavior
Link ID: 29758 - Posted: 04.26.2025

Smriti Mallapaty Two hotly anticipated clinical trials using stem cells to treat people with Parkinson’s disease have published encouraging results. The early-stage trials demonstrate that injecting stem-cell-derived neurons into the brain is safe1,2. They also show hints of benefit: the transplanted cells can replace the dopamine-producing cells that die off in people with the disease, and survive long enough to produce the crucial hormone. Some participants experienced visible reductions in tremors. The studies, published by two groups in Nature today, are “a big leap in the field”, says Malin Parmar, a stem-cell biologist at Lund University, Sweden. “These cell products are safe and show signs of cell survival.” Japan’s big bet on stem-cell therapies might soon pay off with breakthrough therapies The trials were mainly designed to test safety and were small, involving 19 individuals in total, which is not enough to indicate whether the intervention is effective, says Parmar. “Some people got slightly better and others didn’t get worse,” says Jeanne Loring, a stem-cell researcher at Scripps Research in La Jolla, California. This could be due to the relatively small number of cells transplanted in these first early-stage trials. Parkinson’s is a progressive neurological condition driven by the loss of dopamine-producing neurons, which causes tremors, stiffness and slowness in movement. There is currently no cure for the condition, which is projected to affect 25 million people globally by 2050. Cell therapies are designed to replace damaged neurons, but previous trials using fetal tissue transplants have had mixed results. The latest findings are the first among a handful of global trials testing more-advanced cell therapies. © 2025 Springer Nature Limited

Keyword: Parkinsons; Stem Cells
Link ID: 29751 - Posted: 04.19.2025