By Yasemin Saplakoglu Imagine you’re on a first date, sipping a martini at a bar. You eat an olive and patiently listen to your date tell you about his job at a bank. Your brain is processing this scene, in part, by breaking it down into concepts. Bar. Date. Martini. Olive. Bank. Deep in your brain, neurons known as concept cells are firing. You might have concept cells that fire for martinis but not for olives. Or ones that fire for bars — perhaps even that specific bar, if you’ve been there before. The idea of a “bank” also has its own set of concept cells, maybe millions of them. And there, in that dimly lit bar, you’re starting to form concept cells for your date, whether you like him or not. Those cells will fire when something reminds you of him. Concept neurons fire for their concept no matter how it is presented: in real life or a photo, in text or speech, on television or in a podcast. “It’s more abstract, really different from what you’re seeing,” said Elizabeth Buffalo (opens a new tab), a neuroscientist at the University of Washington. For decades, neuroscientists mocked the idea that the brain could have such intense selectivity, down to the level of an individual neuron: How could there be one or more neurons for each of the seemingly countless concepts we engage with over a lifetime? “It’s inefficient. It’s not economic,” people broadly agreed, according to the neurobiologist Florian Mormann (opens a new tab) at the University of Bonn. But when researchers identified concept cells in the early 2000s, the laughter started to fade. Over the past 20 years, they have established that concept cells not only exist but are critical to the way the brain abstracts and stores information. New studies, including one recently published in Nature Communications, have suggested that they may be central to how we form and retrieve memory. © 2025 Simons Foundation

Keyword: Learning & Memory; Attention
Link ID: 29639 - Posted: 01.22.2025

By Holly Barker Previously unrecognized genetic changes on the X chromosome of autistic people could explain the higher prevalence of the condition among men and boys than among women and girls, according to two new studies. About 60 variants are more common in people with autism than in those without the condition, an analysis of roughly 15,000 X chromosomes revealed. Several of the variants are in Xp22.11, a region of the X chromosome linked to autism in boys and men. In the second study, the team pinpointed 27 autism-linked variants in DDX53, one of the genes in the vulnerable region that had not been tied to the condition in past research. Those findings could help explain why autism is diagnosed three to four times more often in boys than girls, according to the study investigators, led by Stephen Scherer, chief of research at SickKids Research Institute. Although that disparity is likely influenced by social factors—male-only studies could lead to autism being less recognizable in women and girls, and girls may be conditioned to mask their autism traits—there is also a clear biological component. The X chromosome plays an outsized role in brain development, and many genes on the chromosome are strongly linked to autism, previous studies have found. Still, the sex chromosomes have been mostly ignored in genetic searches of autism variants, says Aaron Besterman, associate clinical professor of psychiatry at the University of California, San Diego, who was not involved in the work. “It’s been a dirty little secret that for a long time the X chromosome has not been well interrogated from a genetics perspective,” he says. Sex chromosomes are often sidelined because of difficulties interpreting data, given that men possess half the number of X-linked genes as women. What’s more, random inactivation of X chromosomes makes it hard to tell how a single variant is expressed in female tissues. And the existence of pseudoautosomal regions—stretches of DNA that behave like regular chromosomes and escape inactivation—complicates matters further. © 2025 Simons Foundation

Keyword: Autism; Sexual Behavior
Link ID: 29638 - Posted: 01.22.2025

Rachael Elward Lauren Ford Severance, which imagines a world where a person’s work and personal lives are surgically separated, will soon return to Apple TV+ for a second season. While the concept of this gripping piece of science fiction is far-fetched, it touches on some interesting neuroscience. Can a person’s mind really be surgically split in two? Remarkably, “split-brain” patients have existed since the 1940s. To control epilepsy symptoms, these patients underwent a surgery to separate the left and right hemispheres. Similar surgeries still happen today. Later research on this type of surgery showed that the separated hemispheres of split-brain patients could process information independently. This raises the uncomfortable possibility that the procedure creates two separate minds living in one brain. In season one of Severance, Helly R (Britt Lower) experienced a conflict between her “innie” (the side of her mind that remembered her work life) and her “outie” (the side outside of work). Similarly, there is evidence of a conflict between the two hemispheres of real split-brain patients. When speaking with split-brain patients, you are usually communicating with the left hemisphere of the brain, which controls speech. However, some patients can communicate from their right hemisphere by writing, for example, or arranging Scrabble letters. A young patient was asked what job he would like in the future. His left hemisphere chose an office job making technical drawings. His right hemisphere, however, arranged letters to spell “automobile racer”. Split brain patients have also reported “alien hand syndrome”, where one of their hands is perceived to be moving of its own volition. These observations suggest that two separate conscious “people” may coexist in one brain and may have conflicting goals. In Severance, however, both the innie and the outie have access to speech. This is one indicator that the fictional “severance procedure” must involve a more complex separation of the brain’s networks. © 2010–2025, The Conversation US, Inc.

Keyword: Learning & Memory; Consciousness
Link ID: 29635 - Posted: 01.18.2025

By Phie Jacobs For more than 30 years, scientists have known the genetic culprit behind Huntington disease, a devastating neurodegenerative disorder that causes cells deep in the brain to sicken and die. But they couldn’t account for why people who inherit the faulty gene variant take so long to develop symptoms, or why disease progression varies so widely from person to person. A study published today in Cell helps explain: In the brain cells that die off in Huntington, a repetitive stretch of a gene’s DNA gets longer and longer over a person’s life, and this accelerating expansion turns deadly to the cell—and ultimately to the person. The findings represent “a really remarkable insight,” says Leslie Thompson, a neuroscientist at the University of California, Irvine who wasn’t involved in the new research. “This study and some others are changing the way that we’re thinking about the disease.” People who develop Huntington inherit a flawed version of the HTT gene, which produces a protein called huntingtin. This gene contains an unusual stretch of DNA, where a sequence of three of its nucleotide bases—cytosine, adenine, and guanine, or CAG in genetic parlance—are repeated multiple times in a row. And although most people inherit versions of HTT with about 15 to 30 consecutive CAG repeats and never develop Huntington, those with 40 or more in the gene almost always have symptoms later in life, including psychological and cognitive problems and uncontrolled, jerking movements known as chorea. The genetic stutter produces an abnormally large, unstable version of the huntingtin protein, which forms clumps inside brain cells. The condition usually leads to early death, often from issues related to difficulty swallowing, injuries from falls, or suicide. The longer a person’s stretch of repeats, the earlier the disorder rears its head. Scientists originally thought the number of CAG repeats only increased as the HTT gene was passed down through generations; a child of a parent with Huntington might themselves develop the condition at an earlier age. But it turns out the length of this genetic “stutter” can change over a person’s life in at least some of their cells. A 2003 study analyzed brain samples donated by people who had died of Huntington and found shockingly large CAG expansions in a part of the brain known as the striatum.

Keyword: Huntingtons; Genes & Behavior
Link ID: 29634 - Posted: 01.18.2025

By Anna Victoria Molofsky Twenty years ago, a remarkable discovery upended our understanding of the range of elements that can shape neuronal function: A team in Europe demonstrated that enzymatic digestion of the extracellular matrix (ECM)—a latticework of proteins that surrounds all brain cells—could restore plasticity to the visual cortex even after the region’s “critical period” had ended. Other studies followed, showing that ECM digestion could also alter learning in the hippocampus and other brain circuits. These observations established that proteins outside neurons can control synaptic plasticity. We now know that up to 20 percent of the brain is extracellular space, filled with hundreds of ECM proteins—a “matrisome” that plays multiple roles, including modulating synaptic function and myelin formation. ECM genes in the human brain are different than those in other species, suggesting that the proteins they encode could be part of what makes our brains unique and keeps them healthy. In a large population study, posted as a preprint on bioRxiv last year, that examined blood protein biomarkers of organ aging, for example, the presence of ECM proteins was most highly correlated with a youthful brain. Matrisome proteins are also dysregulated in astrocytes from people at high risk for Alzheimer’s disease, another study showed. Despite the influence of these proteins and the ongoing work of a few dedicated researchers, however, the ECM field has not caught on. I would challenge a room full of neuroscientists to name one protein in the extracellular matrix. To this day, the only ECM components most neuroscientists have heard of are “perineuronal nets”—structures that play an important role in stabilizing synapses but make up just a tiny fraction of the matrisome. A respectable scientific journal, covering its own paper that identified a critical impact of ECM, called it “brain goop.” © 2025 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 29633 - Posted: 01.18.2025

By Meghan Rosen Baby Boomers may drive a bigger-than-expected boom in dementia cases. By 2060, 1 million U.S. adults per year will develop dementia, scientists predict January 13 in Nature Medicine. Dementia is a broad term encompassing many symptoms, including memory, reasoning and language difficulties that interfere with people’s daily lives. Researchers estimate that it currently affects more than 6 million people in the United States. “This is a huge problem,” says Josef Coresh, an epidemiologist at New York University’s Grossman School of Medicine. A rise in the projected number of dementia cases is not surprising, given the aging U.S. population ­­— but the extent of the rise stands out, he says. His team predicts that 42 percent of people in the United States who are over 55 years old will develop dementia sometime during their lifetime. That’s about double the percentage estimated by previous researchers. Coresh’s new estimate is based on a study population that’s larger — more than 15,000 people — and more diverse than earlier work. His team followed participants for years, in some cases decades, using several methods to identify dementia cases. They pored over hospital and death records, evaluated participants in person and screened them by phone. For the last decade, the researchers have been calling participants twice a year, Coresh says. That gave the team a window into people’s lives, revealing dementia cases that might otherwise have gone unreported. Though the team focused on dementia in people over age 55, risk doesn’t typically start ticking up for decades. And some populations were at greater risk than others, including women, Black people and those with a particular gene variant linked to Alzheimer’s disease. © Society for Science & the Public 2000–2025.

Keyword: Alzheimers
Link ID: 29627 - Posted: 01.15.2025

By Roni Caryn Rabin Water fluoridation is widely seen as one of the great public health achievements of the 20th century, credited with substantially reducing tooth decay. But there has been growing controversy among scientists about whether fluoride may be linked to lower I.Q. scores in children. A comprehensive federal analysis of scores of previous studies, published this week in JAMA Pediatrics, has added to those concerns. It found a significant inverse relationship between exposure levels and cognitive function in children. Higher fluoride exposures were linked to lower I.Q. scores, concluded researchers working for the National Institute of Environmental Health Sciences. None of the studies included in the analysis were conducted in the United States, where recommended fluoridation levels in drinking water are very low. At those amounts, evidence was too limited to draw definitive conclusions. Observational studies cannot prove a cause-and-effect relationship. Yet in countries with much higher levels of fluoridation, the analysis also found evidence of what scientists call a dose-response relationship, with I.Q. scores falling in lock step with increasing fluoride exposure. Children are exposed to fluoride through many sources other than drinking water: toothpaste, dental treatments and some mouthwashes, as well as black tea, coffee and certain foods, such as shrimp and raisins. Some drugs and industrial emissions also contain fluoride. For every one part per million increase in fluoride in urinary samples, which reflect total exposures from water and other sources, I.Q. points in children decreased by 1.63, the analysis found. “There is concern that pregnant women and children are getting fluoride from many sources,” said Kyla Taylor, an epidemiologist at the institute and the report’s lead author, “and that their total fluoride exposure is too high and may affect fetal, infant and child neurodevelopment.” © 2025 The New York Times Company

Keyword: Intelligence; Development of the Brain
Link ID: 29625 - Posted: 01.11.2025

By Laura Sanders Recovery from PTSD comes with key changes in the brain’s memory system, a new study finds. These differences were found in the brains of 19 people who developed post-traumatic stress disorder after the 2015 terrorist attacks in Paris — and then recovered over the following years. The results, published January 8 in Science Advances, point to the complexity of PTSD, but also to ways that brains can reshape themselves as they recover. With memory tasks and brain scans, the study provides a cohesive look at the recovering brain, says cognitive neuroscientist Vishnu Murty of the University of Oregon in Eugene. “It’s pulled together a lot of pieces that were floating around in the field.” On the night of November 13, 2015, terrorists attacked a crowded stadium, a theater and restaurants in Paris. In the years after, PTSD researchers were able to study some of the people who endured that trauma. Just over half the 100 people who volunteered for the study had PTSD initially. Of those, 34 still had the disorder two to three years later; 19 had recovered by two to three years. People who developed PTSD showed differences in how their brains handled intrusive memories, laboratory-based tests of memory revealed. Participants learned pairs of random words and pictures — a box of tissues with the word “work,” for example. PTSD involves pairs of associated stimuli too, though in much more complicated ways. A certain smell or sound, for instance, can be linked with the memory of trauma. © Society for Science & the Public 2000–2025.

Keyword: Learning & Memory; Stress
Link ID: 29622 - Posted: 01.11.2025

By Angie Voyles Askham Old age is the best predictor of Alzheimer’s disease, Parkinson’s disease and many other neurodegenerative conditions. And yet, as deeply studied as those conditions are, the process of healthy brain aging is not well understood. Without that knowledge, “how can we possibly fix something that goes wrong because of it?” asks Courtney Glavis-Bloom, senior staff scientist at the Salk Institute for Biological Sciences. “We don’t have the basics. It’s like running before we walk.” That said, mounting evidence suggests that aging takes a particular toll on non-neuronal and white-matter cells in mice. For example, white-matter cells display more differentially expressed genes in aged mice than in younger ones, according to a 2023 single-cell analysis of the frontal cortex and striatum. And glia present in white matter show accelerated aging when compared with cells in the cortex across 15 different brain regions, another 2023 mouse study revealed. “Different brain regions show totally different trajectories regarding aging,” says Andreas Keller, head of the Department of Clinical Bioinformatics at the Helmholtz Institute for Pharmaceutical Research Saarland, who worked on the latter study. Some of the cell types with the most extensive aging-related changes in gene expression occur in a small region of the hypothalamus, according to a new single-cell mouse atlas, the largest and broadest to date. Rare neuronal and non-neuronal cell populations within this “hot spot” are particularly vulnerable to the aging process, says Hongkui Zeng, executive vice president and director of the Allen Institute for Brain Science, who led the work. “This demonstrates the power of using the cell-type-specific approach that will identify highly susceptible, rare populations of interest in the brain,” she says. © 2025 Simons Foundation

Keyword: Alzheimers
Link ID: 29620 - Posted: 01.08.2025

Kat Lay Global health correspondent Pills that prevent Alzheimer’s disease or blunt its effects are on the horizon, as the fight against dementia enters a “new era”, experts have said. Scientific advances were on the cusp of producing medicines that could be used even in the most remote and under-resourced parts of the world, thereby “democratising” care, said Jeff Cummings, professor of brain science and health at the University of Nevada. An estimated 50 million people live with dementia globally, more than two-thirds of them in low- and middle-income countries. In 2024, the first drugs that can change the course of Alzheimer’s disease entered the market. Eisai and Biogen’s lecanemab and Eli Lilly’s donanemab were approved by medicine watchdogs in many western countries, including the UK and US. “I’m just so excited about this,” said Cummings. “We are truly in a new era. We have opened the door to understanding and manipulating the biology of Alzheimer’s disease for the benefit of our patients.” Cummings conceded that high prices, complicated administration techniques and requirements for advanced technology to monitor patients meant that those newly approved drugs were “not going to be made widely available in the world”. Neither is yet available on the NHS in the UK because of the high cost – about £20,000 to £25,000 a year for each patient. They require additional tests and scans that would probably double that figure. But Cummings said they offered evidence of how to target dementia and “this learning is going to open the door to new therapies of many types, and those drugs can be exported around the world”. There are currently 127 drugs in trials for Alzheimer’s disease. © 2025 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29619 - Posted: 01.08.2025

By Joshua Cohen For decades, scientists have been trying to develop therapeutics for people living with Alzheimer’s disease, a progressive neurodegenerative disease that is characterized by cognitive decline. Given the global rise in cases, the stakes are high. A study published in The Lancet Public Health reports that the number of adults living with dementia worldwide is expected to nearly triple, to 153 million in 2050. Alzheimer’s disease is a dominant form of dementia, representing 60 to 70 percent of cases. Recent approvals by the Food and Drug Administration have focused on medications that shrink the sticky brain deposits of a protein called amyloid beta. The errant growth of this protein is responsible for triggering an increase in tangled threads of another protein called tau and the development of Alzheimer’s disease — at least according to the dominant amyloid cascade hypothesis, which was first proposed in 1991. Over the past few years, however, data and drugs associated with the hypothesis have been mired in various controversies relating to data integrity, regulatory approval, and drug safety. Nevertheless, the hypothesis still dominates research and drug development. According to Science, in fiscal year 2021 to 2022, the National Institutes of Health spent some $1.6 billion on projects that mention amyloids, about 50 percent of the agency’s overall Alzheimer’s funding. And a close look at the data for recently approved drugs suggests the hypothesis is not wrong, so much as incomplete. A few years ago, Matthew Schrag, a neurologist at Vanderbilt University, discovered possible image tampering in papers that supported the hypothesis, including in an influential 2006 Nature study that was eventually retracted. At roughly the same time, the FDA had been greenlighting medications that target amyloid beta.

Keyword: Alzheimers
Link ID: 29618 - Posted: 01.08.2025

By McKenzie Prillaman A peek into living tissue from human hippocampi, a brain region crucial for memory and learning, revealed relatively few cell-to-cell connections for the vast number of nerve cells. But signals sent via those sparse connections proved extremely reliable and precise, researchers report December 11 in Cell. One seahorse-shaped hippocampus sits deep within each hemisphere of the mammalian brain. In each hippocampus’s CA3 area, humans have about 1.7 million nerve cells called pyramidal cells. This subregion is thought to be the most internally connected part of the brain in mammals. But much information about nerve cells in this structure has come from studies in mice, which have only 110,000 pyramidal cells in each CA3 subregion. Previously discovered differences between mouse and human hippocampi hinted that animals with more nerve cells may have fewer connections — or synapses — between them, says cellular neuroscientist Peter Jonas of the Institute of Science and Technology Austria in Klosterneuburg. To see if this held true, he and his colleagues examined tissue taken with consent from eight patients who underwent brain surgery to treat epilepsy. Recording electrical activity from human pyramidal cells in the CA3 area suggested that about 10 synapses existed for every 800 cell pairs tested. In mice, that concentration roughly tripled. Despite the relatively scant nerve cell connections in humans, those cells showed steady and robust activity when sending signals to one another — unlike mouse pyramidal cells. © Society for Science & the Public 2000–2025

Keyword: Learning & Memory
Link ID: 29616 - Posted: 01.08.2025

By Traci Watson New clues have emerged in the mystery of how the brain avoids ‘catastrophic forgetting’ — the distortion and overwriting of previously established memories when new ones are created. A research team has found that, at least in mice, the brain processes new and old memories in separate phases of sleep, which might prevent mixing between the two. Assuming that the finding is confirmed in other animals, “I put all my money that this segregation will also occur in humans”, says György Buzsáki, a systems neuroscientist at New York University in New York City. That’s because memory is an evolutionarily ancient system, says Buzsáki, who was not part of the research team but once supervised the work of some of its members. The work was published on Wednesday in Nature1. Scientists have long known that, during sleep, the brain ‘replays’ recent experiences: the same neurons involved in an experience fire in the same order. This mechanism helps to solidify the experience as a memory and prepare it for long-term storage. To study brain function during sleep, the research team exploited a quirk of mice: their eyes are partially open during some stages of slumber. The team monitored one eye in each mouse as it slept. During a deep phase of sleep, the researchers observed the pupils shrink and then return to their original, larger size repeatedly, with each cycle lasting roughly one minute. Neuron recordings showed that most of the brain’s replay of experiences took place when the animals’ pupils were small. That led the scientists to wonder whether pupil size and memory processing are linked. To find out, they enlisted a technique called optogenetics, which uses light to either trigger or suppress the electrical activity of genetically engineered neurons in the brain. First, they trained engineered mice to find a sweet treat hidden on a platform. Immediately after these lessons, as the mice slept, the authors used optogenetics to reduce bursts of neuronal firing that have been linked to replay. They did so during both the small-pupil and large-pupil stages of sleep. © 2025 Springer Nature Limited

Keyword: Learning & Memory; Sleep
Link ID: 29615 - Posted: 01.04.2025

By Sarah DeWeerdt A few months ago, Sergiu Paşca, professor of psychiatry and behavioral sciences at Stanford University, shared his lab’s new work at the Gordon Research Conference on Thalamocortical Interactions. His talk concerned assembloids, lab-grown combinations of spherical organoids that mimic different parts of the nervous system. Paşca showed a video depicting waves of calcium signals traveling along a line of organoids modeling sensory neurons; the dorsal root ganglia of the spinal cord; a subcortical structure called the thalamus; and, finally, the cerebral cortex. In the audience, Audrey Brumback, assistant professor of neurology and pediatrics at the University of Texas at Austin, felt something move through her own subcortical structures as she watched the video: a visceral feeling of awe. “I just thought, ‘Holy crap, this is amazing,’” she recalls. “‘The future is now.’” The work, described in a preprint posted on bioRxiv in March, is part of a series of recent studies from Paşca’s lab that highlight the potential of assembloids to help researchers understand brain development at the circuit level, and how these circuits go awry in autism and other neurodevelopmental conditions. Autism, after all, involves differences in how various parts of the brain connect with each other, Brumback points out. “So to be able to model that in vitro is exactly what we need to be doing to be able to understand these network dysfunction disorders,” she says. For example, a lack of synchrony between the cortex and the thalamus is known to be associated with autism and schizophrenia, whereas too much synchrony between the two regions is implicated in absence seizures in epilepsy. Using a two-part assembloid representing this pair of brain structures, Paşca and his team probed the roots of these alterations in a study published 16 October in Neuron. © 2024 Simons Foundation

Keyword: Development of the Brain
Link ID: 29610 - Posted: 12.28.2024

By Emily Baumgaertner When President-elect Donald J. Trump mused in a recent television interview about whether vaccines cause autism — a theory that has been discredited by dozens of scientific studies — autism researchers across the country collectively sighed in frustration. But during the interview, on NBC’s “Meet The Press,” Mr. Trump made one passing comment with which they could agree: “I mean, something is going on,” he said, referring to skyrocketing rates of autism. “I think somebody has to find out.” What is going on? Autism diagnoses are undeniably on the rise in the United States — about 1 in 36 children have one, according to data the Centers for Disease Control and Prevention collected from 11 states, compared with 1 in 150 children in 2000 — and researchers have not yet arrived at a clear explanation. They attribute most of the surge to increased awareness of the disorder and changes in how it is classified by medical professionals. But scientists say there are other factors, genetic and environmental, that could be playing a role too. Autism spectrum disorder, as it is officially called, is inherently wide-ranging, marked by a blend of social and communication issues, repetitive behaviors and thinking patterns that vary in severity. A mildly autistic child could simply struggle with social cues, while a child with a severe case could be nonverbal. There is no blood test or brain scan to determine who has autism, just a clinician’s observations. Because there is no singular cause of autism, scientists say there is therefore no singular driver behind the rise in cases. But at the heart of the question is an important distinction: Are more people exhibiting the traits of autism, or are more people with such traits now being identified? It seems to be both, but researchers really aren’t sure of the math. More than 100 genes have been associated with autism, but the disorder appears to result from a complex combination of genetic susceptibilities and environmental triggers. The C.D.C. has a large-scale study on the risk factors that can contribute to autism, and researchers have examined dozens of potential triggers, including pollution, exposure to toxic chemicals and viral infections during pregnancy. © 2024 The New York Times Company

Keyword: Autism
Link ID: 29609 - Posted: 12.28.2024

By Miryam Naddaf Researchers have identified 13 proteins in the blood that predict how quickly or slowly a person’s brain ages compared with the rest of their body. Their study1, published in Nature Aging on 9 December, used a machine-learning model to estimate ‘brain ages’ from scans of more than 10,000 people. The authors then analysed thousands of scans alongside blood samples and found eight proteins that were associated with fast brain ageing, and five linked to slower brain ageing. “Previous studies mainly focused on the association between the proteins and the chronological age, that means the real age of the individual,” says study co-author Wei-Shi Liu, a neurologist at Fudan University in Shanghai, China. However, studying biomarkers linked to a person’s brain age could help scientists to identify molecules to target in future treatments for age-related brain diseases. “These proteins are all promising therapeutic targets for brain disorders, but it may take a long time to validate them,” says Liu. Using machine learning to analyse brain-imaging data from 10,949 people, Liu and his colleagues created a model to calculate a person’s brain age, on the basis of features such as the brain’s volume, surface area and distribution of white matter. They wanted to identify proteins that are associated with a large brain age gap — the difference between brain age and chronological age. To do this, the researchers analysed levels of 2,922 proteins in blood samples from 4,696 people, more than half of whom were female, and compared them with the same people’s brain ages derived from the scans. They identified 13 proteins that seemed to be connected with large brain age gaps, some of which are known to be involved in movement, cognition and mental health.

Keyword: Development of the Brain
Link ID: 29597 - Posted: 12.11.2024

By Grace Huckins Genes on the X and Y chromosomes—and especially those on the Y—appear to be associated with autism likelihood, according to a study focused on people who have missing or extra sex chromosomes. The findings add to the ongoing debate about whether autism’s sex bias reflects a male vulnerability, a female protective effect or other factors. “The Y chromosome is often left out of genetic discovery studies. We really have not interrogated it in [autism] studies very much,” says Matthew Oetjens, assistant professor of human genetics at Geisinger Medical Center’s Autism and Developmental Medicine Institute, who led the new work. There is a clear sex difference in autism prevalence: Men are about four times as likely as women to have a diagnosis. But uncovering the reasons for that discrepancy has proved challenging and contentious. Multiple biological factors may play a role, in addition to social factors—such as the difficult-to-measure gulfs between how boys and girls are taught to behave. Add on the possibility of diagnostic bias and the question starts to look less like a scientific problem and more like a politically toxic Gordian knot. But there are some threads that researchers can pull to disentangle these effects, as the new study illustrates. People with sex chromosome aneuploidies—or unusual combinations of sex chromosomes, such as XXY in those with Klinefelter syndrome or a single X in Turner syndrome—provide a unique opportunity to examine how adding or taking away chromosomes can affect biology and behavior. Previous studies noted high rates of autism in people with sex chromosome aneuploidies, but those analyses were subject to ascertainment bias; perhaps those people found out about their aneuploidies only after seeking support for their neurodevelopmental conditions. © 2024 Simons Foundation

Keyword: Autism; Sexual Behavior
Link ID: 29596 - Posted: 12.11.2024

By Steven Strogatz Death might seem like a pure loss, the disappearance of what makes a living thing distinct from everything else on our planet. But zoom in closer, to the cellular level, and it takes on a different, more nuanced meaning. There is a challenge in simply defining what makes an individual cell alive or dead. Scientists today are working to understand the various ways and reasons that cells disappear, and what these processes mean to biological systems. In this episode, cellular biologist Shai Shaham talks to Steven Strogatz about the different forms of cell death, their roles in evolution and disease, and why the right kinds and patterns of cell death are essential to our development and well-being. STEVE STROGATZ: In the second that it took you to hit play on this episode, a million cells in your body died. Some were programmed to expire in natural, regulated processes, such as apoptosis. Some terminated their own lives after infection, to stop viral invaders from spreading. Others suffered physical damage and went through necrosis, their membranes splitting open and their contents spilling out. We know there are nearly a dozen different ways for our cells to kick the bucket. And learning how to control these processes can make all the difference in the world to a sick patient. In this episode, we ask cellular biologist Shai Shaham (opens a new tab), how can the death of a cell help other cells around it? And how do these insights help us understand life itself? Shai is a professor at The Rockefeller University (opens a new tab), where he studies programmed cell death during animal development and the complex role that glial cells play in the nervous system. There was an example near and dear to my heart, since we work on C. elegans, which is a nematode worm. And there was a recent description of a nematode that was extracted from permafrost in Siberia where it froze about 40,000 years ago and was revived back in the lab. And so you ask yourself, was that whole organism alive or dead for 40,000 years? © 2024 Simons Foundation

Keyword: Apoptosis; Development of the Brain
Link ID: 29591 - Posted: 12.07.2024

Aswathy Ammothumkandy, Charles Liu, Michael A. Bonaguidi Your brain can still make new neurons when you’re an adult. But how does the rare birth of these new neurons contribute to cognitive function? Neurons are the cells that govern brain function, and you are born with most of the neurons you will ever have during your lifetime. While the brain undergoes most of its development during early life, specific regions of the brain continue to generate new neurons throughout adulthood, although at a much lower rate. Whether this process of neurogenesis actually happens in adults and what function it serves in the brain is still a subject of debate among scientists. Past research has shown that people with epilepsy or Alzheimer’s disease and other dementias develop fewer neurons as adults than people without these conditions. However, whether the absence of new neurons contributes to the cognitive challenges patients with these neurological disorders face is unknown. We are part of a team of stem cell researchers, neuroscientists, neurologists, neurosurgeons and neuropsychologists. Our newly published research reveals that the new neurons that form in adults’ brains are linked to how you learn from listening to other people. Researchers know that new neurons contribute to memory and learning in mice. But in humans, the technical challenges of identifying and analyzing new neurons in adult brains, combined with their rarity, had led scientists to doubt their significance to brain function. To uncover the relationship between neurogenesis in adults and cognitive function, we studied patients with drug-resistant epilepsy. These patients underwent cognitive assessments prior to and donated brain tissue during surgical procedures to treat their seizures. To see whether how many new neurons a patient had was associated with specific cognitive functions, we looked under the microscope for markers of neurogenesis. © 2010–2024, The Conversation US, Inc.

Keyword: Neurogenesis; Learning & Memory
Link ID: 29590 - Posted: 12.07.2024

Amy Fleming Nine years ago, Nikki Schultek, an active and healthy woman in her early 30s, experienced a sudden cascade of debilitating and agonising symptoms – including cognitive and breathing problems and heart arrhythmia – and was investigated for multiple sclerosis. But three brain scans and numerous X-rays later, there was still no diagnosis or treatment plan. “It was like living in a nightmare, imagining not watching my children – three and five years old – grow up,” says Schultek. Now, speaking on a video call from North Carolina, she is as bright as a button and shows no signs of degenerative brain disease. It turned out she had multiple chronic infections, including Borrelia burgdorferi bacteria, which causes Lyme disease and which had stealthily reached her brain. Antibiotics restored her health, but B burgdorferi is hard to eradicate once in the brain. She may need maintenance treatment to keep the disease at bay. Schultek is not the only person whose neurological disorder turned out to be caused by microbes in the brain. A recent paper she jointly lead-authored, published in Alzheimer’s and Dementia, compiled a long list of case reports where infectious disease was discovered to be the primary cause of dementia, meaning that, in many cases, the dementia was reversible. A few of the patients died, but most survived and saw significant improvements in cognitive function, including a man in his 70s who had been diagnosed with Alzheimer’s disease after his swift cognitive decline saw him unable to drive or, eventually, leave the house alone. A sample of his cerebrospinal fluid was taken and revealed a fungal infection caused by Cryptococcus neoformans. Within two years of taking antifungal medication, he was driving again and back at work as a gardener. Richard Lathe, a professor of infectious medicine at the University of Edinburgh and another lead author of the paper, says these patients “were by accident found to be suffering from various fungal, bacterial or viral infections, and when they treated the patient with antifungals, antivirals or antibiotics, the dementia went away”. He, among others, has been investigating the possibility that, like the gut, the brain hosts a community of microbes – an area of largely scientifically uncharted waters, but with huge life-saving potential. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Obesity
Link ID: 29587 - Posted: 12.04.2024