By Gina Kolata Women’s brains are superior to men’s in at least in one respect — they age more slowly. And now, a group of researchers reports that they have found a gene in mice that rejuvenates female brains. Humans have the same gene. The discovery suggests a possible way to help both women and men avoid cognitive declines in advanced age. The study was published Wednesday in the journal Science Advances. The journal also published two other studies on women’s brains, one on the effect of hormone therapy on the brain and another on how age at the onset of menopause shapes the risk of getting Alzheimer’s disease. The evidence that women’s brains age more slowly than men’s seemed compelling. Researchers, looking at the way the brain uses blood sugar, had already found that the brains of aging women are years younger, in metabolic terms, than the brains of aging men. Other scientists, examining markings on DNA, found that female brains are a year or so younger than male brains. And careful cognitive studies of healthy older people found that women had better memories and cognitive function than men of the same age. Dr. Dena Dubal, a professor of neurology at the University of California, San Francisco, set out to understand why. “We really wanted to know what could underlie this female resilience,” Dr. Dubal said. So she and her colleagues focused on the one factor that differentiates females and males: the X chromosome. Females have two X chromosomes; males have one X and one Y chromosome. Early in pregnancy, one of the X chromosomes in females shuts down and its genes go nearly silent. But that silencing changes in aging, Dr. Dubal found. © 2025 The New York Times Company

Keyword: Alzheimers; Sexual Behavior
Link ID: 29704 - Posted: 03.12.2025

By Kelly Servick New York City—A recent meeting here on consciousness started from a relatively uncontroversial premise: A newly fertilized human egg isn’t conscious, and a preschooler is, so consciousness must emerge somewhere in between. But the gathering, sponsored by New York University (NYU), quickly veered into more unsettled territory. At the Infant Consciousness Conference from 28 February to 1 March, researchers explored when and how consciousness might arise, and how to find out. They also considered hints from recent brain imaging studies that the capacity for consciousness could emerge before birth, toward the end of gestation. “Fetal consciousness would have been a less central topic at a meeting like this a few years ago,” says Claudia Passos-Ferreira, a bioethicist at NYU who co-organized the gathering. The conversation has implications for how best to care for premature infants, she says, and intersects with thorny issues such as abortion. “Whatever you claim about this, there are some moral implications.” How to define consciousness is itself the subject of debate. “Each of us might have a slightly different definition,” neuroscientist Lorina Naci of Trinity College Dublin acknowledged at the meeting before describing how she views consciousness—as the capacity to have an experience or a subjective point of view. There’s also vigorous debate about where consciousness arises in the brain and what types of neural activity define it. That makes it hard to agree on specific markers of consciousness in beings—such as babies—that can’t talk about their experience. Further complicating the picture, the nature of consciousness could be different for infants than adults, researchers noted at the meeting. And it may emerge gradually versus all at once, on different timescales for different individuals.

Keyword: Consciousness; Development of the Brain
Link ID: 29703 - Posted: 03.12.2025

By Mark Humphries There are many ways neuroscience could end. Prosaically, society may just lose interest. Of all the ways we can use our finite resources, studying the brain has only recently become one; it may one day return to dust. Other things may take precedence, like feeding the planet or preventing an asteroid strike. Or neuroscience may end as an incidental byproduct, one of the consequences of war or of thoughtlessly disassembling a government or of being sideswiped by a chunk of space rock. We would prefer it to end on our own terms. We would like neuroscience to end when we understand the brain. Which raises the obvious question: Is this possible? For the answer to be yes, three things need to be true: that there is a finite amount of stuff to know, that stuff is physically accessible and that we understand all the stuff we obtain. But each of these we can reasonably doubt. The existence of a finite amount of knowledge is not a given. Some arguments suggest that an infinite amount of knowledge is not only possible but inevitable. Physicist David Deutsch proposes the seemingly innocuous idea that knowledge grows when we find a good explanation for a phenomenon, an explanation whose details are hard to vary without changing its predictions and hence breaking it as an explanation. Bad explanations are those whose details can be varied without consequence. Ancient peoples attributing the changing seasons to the gods is a bad explanation, for those gods and their actions can be endlessly varied without altering the existence of four seasons occurring in strict order. Our attributing the changing seasons to the Earth’s tilt in its orbit of the sun is a good explanation, for if we omit the tilt, we lose the four seasons and the opposite patterns of seasons in the Northern and Southern hemispheres. A good explanation means we have nailed down some property of the universe sufficiently well that something can be built upon it. © 2025 Simons Foundation

Keyword: Consciousness
Link ID: 29702 - Posted: 03.12.2025

By Meghan Rosen and Laura Sanders Millions of Americans take antidepressants to help manage everything from depression and anxiety to post-traumatic stress disorder. Now, the Trump administration has announced that these drugs, which have been in use for decades and gone through rigorous testing, will be subject to new scrutiny. Invoking a burden of chronic disease, including in children, the administration has pledged to, in its words, “assess the prevalence of and threat posed by” certain commonly prescribed medications. In the coming months, its “Make America Healthy Again” commission plans to review a slew of existing medications, including SSRIs, or selective serotonin reuptake inhibitors. More than 10 percent of U.S. adults took antidepressants over the previous 30 days, data from 2015 to 2018 show. And SSRIs are among the most widely prescribed of those drugs. U.S. Health and Human Services Secretary Robert F. Kennedy Jr. has long questioned the safety of antidepressants and other psychiatric medicines, making misleading and unsubstantiated claims about the drugs. For instance, as recently as his January confirmation hearings, he likened taking SSRIs to having a heroin addiction. He also has suggested — without evidence — that SSRIs play a role in school shootings. With the executive order and statements like these, “it’s implied there is something nefarious or harmful” about antidepressants and related medications, says Lisa Fortuna, chair of the American Psychiatric Association’s Council on Children, Adolescents and Their Families. “People may think that they’re dangerous drugs.” © Society for Science & the Public 2000–2025

Keyword: Depression; Sexual Behavior
Link ID: 29701 - Posted: 03.12.2025

By Angie Voyles Askham Synaptic plasticity in the hippocampus involves both strengthening relevant connections and weakening irrelevant ones. That sapping of synaptic links, called long-term depression (LTD), can occur through two distinct routes: the activity of either NMDA receptors or metabotropic glutamate receptors (mGluRs). The mGluR-dependent form of LTD, required for immediate translation of mRNAs at the synapse, appears to go awry in fragile X syndrome, a genetic condition that stems from loss of the protein FMRP and is characterized by intellectual disability and often autism. Possibly as a result, mice that model fragile X exhibit altered protein synthesis regulation in the hippocampus, an increase in dendritic spines and overactive neurons. Treatments for fragile X that focus on dialing down the mGluR pathway and tamping down protein synthesis at the synapse have shown success in quelling those traits in mice, but they have repeatedly failed in human clinical trials. But the alternative pathway—via the NMDA receptor—may provide better results, according to a new study. Signaling through the NMDA receptor subunit GluN2B can also decrease spine density and alleviate fragile-X-linked traits in mice, the work shows. “You don’t have to modulate the protein synthesis directly,” says Lynn Raymond, professor of psychiatry and chair in neuroscience at the University of British Columbia, who was not involved in the work. Instead, activation of part of the GluN2B subunit can indirectly shift the balance of mRNAs that are translated at the synapse. “It’s just another piece of the puzzle, but I think it’s a very important piece,” she says. Whether this insight will advance fragile X treatments remains to be seen, says Wayne Sossin, professor of neurology and neurosurgery at Montreal Neurological Institute-Hospital, who was not involved in the study. Multiple groups have cured fragile-X-like traits in mice by altering what happens at the synapse, he says. “Altering translation in a number of ways seems to change the balance that is off when you lose FMRP. And it’s not really clear how specific that is for FMRP.” © 2025 Simons Foundation

Keyword: Development of the Brain; Learning & Memory
Link ID: 29700 - Posted: 03.12.2025

By Pam Belluck Postpartum depression affects about one in every seven women who give birth, but little is known about what happens in the brains of pregnant women who experience it. A new study begins to shed some light. Researchers scanned the brains of dozens of women in the weeks before and after childbirth and found that two brain areas involved in the processing and control of emotions increased in size in women who developed symptoms of postpartum depression. The results, published Wednesday in the journal Science Advances, constitute some of the first evidence that postpartum depression is associated with changes in the brain during pregnancy. Researchers found that women with symptoms of depression in the first month after giving birth also had increases in the volume of their amygdala, a brain area that plays a key role in emotional processing. Women who rated their childbirth experience as difficult or stressful — a perception that is often associated with postpartum depression — also showed increases in the volume of the hippocampus, a brain area that helps regulate emotions. “This is really the first step in trying to understand how does the brain change in people who have a normal course of pregnancy and then those who experience perinatal depression, and what can we do about it,” said Dr. Sheila Shanmugan, an assistant professor of psychiatry, obstetrics-gynecology and radiology at the University of Pennsylvania who was not involved in the study. “The big takeaways are about how there are these really profound brain changes during pregnancy and how now we’re seeing it in depression circuitry specifically,” she said. The study was conducted in Madrid by a team that has led efforts to document the effects of pregnancy on the brain. It is part of a growing body of research that has found that certain brain networks, especially those involved in social and emotional processing, shrink during pregnancy, possibly undergoing a fine-tuning process in preparation for parenting. Such changes correspond with surges in pregnancy hormones, especially estrogen, and some last at least two years after childbirth, researchers have found. © 2025 The New York Times Company

Keyword: Hormones & Behavior; Depression
Link ID: 29699 - Posted: 03.08.2025

By Katherine Bourzac Women tend to live longer than men and are often more resilient to cognitive decline as they age. Now researchers might have uncovered a source for this resilience: the second X chromosome in female cells that was previously considered ‘silent’. In work published today in the journal Science Advances1, a team reports that, at least in female mice, ageing activates expression of genes on what is usually the ‘silent’, or inactivated, X chromosome in cells in the hippocampus, a brain region crucial to learning and memory. And when the researchers gave mature mice of both sexes a type of gene therapy to boost expression of one of those genes, it improved their cognition, as measured by how well they explored a maze. Assuming these results can be confirmed in humans, the team suggests it could mean that women’s brains are being protected by their second X chromosome as they age — and that the finding could translate into future therapies boosting cognition for everyone. “The X chromosome is powerful,” says Rachel Buckley, a neurologist who studies sex differences in Alzheimer’s disease at Massachusetts General Hospital in Charlestown, and who was not involved in the research. This kind of work, she says, is helping researchers to understand “where female resilience lies and how to harness it”. (This article uses ‘women’ and ‘female’ to describe people with two X chromosomes and no Y chromosome, reflecting the language of the study. Nature recognizes that not all people who identify as women have this chromosomal make-up.) Double dose Female cells typically have two X chromosomes, one from each parent; male cells usually have one X and one Y. Early in development, one of the two X chromosomes in female cells is inactivated — coated in various proteins and RNA molecules that prevent its genes from being expressed. Which one is ‘silenced’ — meaning which parent it comes from — is random, and the tissues in the body are a mosaic of both types. © 2025 Springer Nature Limited

Keyword: Sexual Behavior; Stress
Link ID: 29698 - Posted: 03.08.2025

Andrew Gregory Health editor Doctors in London have successfully restored a sense of smell and taste in patients who lost it due to long Covid with pioneering surgery that expands their nasal airways to kickstart their recovery. Most patients diagnosed with Covid-19 recover fully. But the infectious disease can lead to serious long-term effects. About six in every 100 people who get Covid develop long Covid, with millions of people affected globally, according to the World Health Organization. Losing a sense of smell and taste are among more than 200 different symptoms reported by people with long Covid. Now surgeons at University College London Hospitals NHS Foundation Trust (UCLH) have cured a dozen patients, each of whom had suffered a profound loss of smell after a Covid infection. All had experienced the problem for more than two years and other treatments, such as smell training and corticosteroids, had failed. In a study aiming to find new ways to resolve the issue, surgeons tried a technique called functional septorhinoplasty (fSRP), which is typically used to correct any deviation of the nasal septum, increasing the size of nasal passageways. This boosts airflow into the olfactory region, at the roof of the nasal cavity, which controls smell. Doctors said the surgery enabled an increased amount of odorants – chemical compounds that have a smell – to reach the roof of the nose, where sense of smell is located. They believe that increasing the delivery of odorants to this area “kickstarts” smell recovery in patients who have lost their sense of smell to long Covid. © 2025 Guardian News & Media Limited

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29697 - Posted: 03.08.2025

By Felicity Nelson A region in the brainstem, called the median raphe nucleus, contains neurons that control perseverance and exploration.Credit: K H Fung/Science Photo Library Whether mice persist with a task, explore new options or give up comes down to the activity of three types of neuron in the brain. In experiments, researchers at University College London (UCL) were able to control the three behaviours by switching the neurons on and off in a part of the animals’ brainstem called the median raphe nucleus. The findings are reported in Nature today1. “It’s quite remarkable that manipulation of specific neural subtypes in the median raphe nucleus mediates certain strategic behaviours,” says neuroscientist Roger Marek at the Queensland Brain Institute in Brisbane, Australia, who was not involved in the work. Whether these behaviours are controlled in the same way in humans needs to be confirmed, but if they are, this could be relevant to certain neuropsychiatric conditions that are associated with imbalances in the three behavioural strategies, says Sonja Hofer, a co-author of the paper and a systems neuroscientist at UCL. For instance, an overly high drive to persist with familiar actions and repetitive behaviours can be observed in people with obsessive–compulsive disorder and autism, she says. Conversely, pathological disengagement and lack of motivation are symptoms of major depressive disorder, and an excessive drive to explore and inability to persevere with a task is seen in attention deficit hyperactivity disorder. “It could be that changes in the firing rate of specific median raphe cell types could contribute to certain aspects of these conditions,” says Hofer. © 2025 Springer Nature Limited

Keyword: Attention
Link ID: 29696 - Posted: 03.08.2025

Nicola Davis Science correspondent Which songs birds sing can – as with human music – be influenced by age, social interactions and migration, researchers have found. Not all birds learn songs, but among those that do, individuals, neighbourhoods and populations can produce different collections of tunes, akin to different music albums. Now researchers have found that changes in the makeup of a group of birds can influence factors including which songs they learn, how similar those songs are to each other and how quickly songs are replaced. Dr Nilo Merino Recalde, the first author of the study, from the University of Oxford, said: “This is very interesting, I think, partly because it shows that there are all these kind of common elements at play when it comes to shaping learned traits, [similar to] what happens with human languages and human music.” But he said the parallels had their limits. “The function and the role of human music and language is very, very different to the function of birdsong,” he said. “Birdsong is used to repel rivals, to protect territories, to entice mates, this kind of thing. And that also shapes songs.” Writing in the journal Current Biology, Recalde and colleagues describe how they used physical tracking as well as artificial intelligence to match recorded songs to individual male great tits living in Wytham Woods in Oxford. In total, the study encompassed 20,000 hours of sound recordings and more than 100,000 songs, captured over three years. The researchers used their AI models to analyse the repertoires of individual birds, those within neighbourhoods and across the entire population to explore how similar the various songs were. As a result, the team were able to unpick how population turnover, immigration and age structure influenced the songs. © 2025 Guardian News & Media Limited

Keyword: Animal Communication; Language
Link ID: 29695 - Posted: 03.08.2025

By Tim Vernimmen On a rainy day in July 2024, Tim Bliss and Terje Lømo are in the best of moods, chuckling and joking over brunch, occasionally pounding the table to make a point. They’re at Lømo’s house near Oslo, Norway, where they’ve met to write about the late neuroscientist Per Andersen, in whose lab they conducted groundbreaking experiments more than 50 years ago. The duo only ever wrote one research paper together, in 1973, but that work is now considered a turning point in the study of learning and memory. Published in the Journal of Physiology, it was the first demonstration that when a neuron — a cell that receives and sends signals throughout the nervous system — signals to another neuron frequently enough, the second neuron will later respond more strongly to new signals, not for just seconds or minutes, but for hours. It would take decades to fully understand the implications of their research, but Bliss and Lømo had discovered something momentous: a phenomenon called long-term potentiation, or LTP, which researchers now know is fundamental to the brain’s ability to learn and remember. Today, scientists agree that LTP plays a major role in the strengthening of neuronal connections, or synapses, that allow the brain to adjust in response to experience. And growing evidence suggests that LTP may also be crucially involved in a variety of problems, including memory deficits and pain disorders. Bliss and Lømo never wrote another research article together. In fact, they would soon stop working on LTP — Bliss for about a decade, Lømo for the rest of his life. Although the researchers knew they had discovered something important, at first the paper “didn’t make a big splash,” Bliss says. By the early 1970s, neuroscientist Eric Kandel had demonstrated that some simple forms of learning can be explained by chemical changes in synapses — at least in a species of sea slug. But scientists didn’t yet know if such findings applied to mammals, or if they could explain more complex and enduring types of learning, such as the formation of memories that may last for years.

Keyword: Learning & Memory
Link ID: 29694 - Posted: 03.05.2025

By Sydney Wyatt Numerous actions by the Trump administration over the past month have caused confusion and fear throughout the U.S. scientific community. In response, a group called Stand Up for Science, which says it opposes attacks on science and on efforts to improve diversity, equity and inclusion (DEI) in research, has planned rallies on 7 March in Washington, D.C., and across the United States. “The biggest thing for us is that science is for everyone, in that it benefits every person,” says rally co-organizer Colette Delawalla, a graduate student in clinical psychology at Emory University. “It doesn’t matter who you voted for. It doesn’t even matter if you voted or not.” The event is reminiscent of the 2017 March for Science, which drew more than 1 million attendees in 600 cites around the world to show support for scientific research and protest proposed budget cuts to the U.S. National Institutes of Health and other federal agencies during Donald Trump’s first term as president. Scientists were divided in their views about that march, with some criticizing it for a lack of concrete goals and others saying it engaged more people with science and policy than ever before. This year is no different. Some scientists say protests do little to change minds, whereas others say it can raise awareness. The effectiveness of a protest depends on several factors, including the clarity of its goals, the scope of the target audience, the tactics used and whether the movement continues after the initial event, says Susan Olzak, professor emerita of sociology at Stanford University. “Temporary, fleeting protests are not likely to have much of an effect on anything, but if you have a sustained campaign, then you’re more likely to have some kind of impact, even if it’s just on public opinion,” Olzak says. © 2025 Simons Foundation

Keyword: Miscellaneous
Link ID: 29693 - Posted: 03.05.2025

By Jyoti Madhusoodanan In June 2021, 63-year-old Lisa Daurio was making the two-hour drive from her hometown of Pueblo, Colorado, to a doctor’s appointment in Denver when she settled on a life-changing decision: She would tell her doctor she was ready to stop taking her weekly injections to treat her multiple sclerosis. Daurio was not cured, but her condition had remained stable for more than a decade. As she got older, her doctor had periodically asked if she wanted to consider halting her medication. It’s an unusual question in modern medicine: Clinicians don’t typically ask people with arthritis, high cholesterol, diabetes, or other chronic conditions whether they’d like to stop taking their medication as they get older. But MS is an unusual disease, the result of immune cells attacking a person’s brain, optic nerves and spinal cord. The subsequent nerve injuries trigger burning pain, numbness, loss of balance, and a range of other symptoms. These hallmark immune assaults and symptoms flare up sporadically in younger adults and, for some people, seem to quiet down as they age into their 50s and beyond. Still, Daurio’s decision to stop wasn’t straightforward. Her MS symptoms began when she was in her late 30s, with a sense of overwhelming fatigue, a numbness in her legs, and a “feeling of fire ants” that ran “from the back of my neck around the front of my face,” she said. She was diagnosed with MS in 2003, when her entire left side went numb, and she thought she was having a stroke. The weekly injections had kept all of those symptoms at bay for more than a decade. When her doctor broached the idea of stopping them, Daurio’s reaction was “it’s working, let’s not mess with what’s not broken,” she said. Staying on her medication wasn’t always easy. For about 10 years, every dose made her feel like she had the flu. After each shot, she spent two days on Tylenol and a steroid named prednisone to cope with the side effects. But Daurio stuck with the regimen because the injection seemed to help; she had not had a single relapse since 2009, and periodic MRI scans showed no new signs of immune attacks on her brain.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 29692 - Posted: 03.05.2025

By Jennifer Couzin-Frankel Sign up for a clinical trial of a psychedelic drug and you’re agreeing to a potentially bizarre experience. “All of a sudden, your dead grandma or Satan is in front of you,” says psychiatrist Charles Raison of the University of Wisconsin–Madison. Some think this consciousness-altering “trip” underlies the potential benefits of drugs such as psilocybin and LSD, which are under study to treat depression, trauma, chronic pain, and more. But the trip can also be a roadblock to assessing the drugs’ effects, making it near-impossible to conceal who is getting an active substance and who’s been assigned to placebo—a trial strategy called blinding that aims to keep participants’ expectations from skewing their response to a drug. This “functional unblinding” is not unique to psychedelics, but it’s especially pronounced in this drug class. The U.S. Food and Drug Administration (FDA) has expressed concern about the issue in psychedelic trials. And it was among the critiques FDA advisers leveled at Lykos Therapeutics, whose application for MDMA to treat post-traumatic stress disorder (PTSD) FDA rejected last summer. Now, scientists and companies are experimenting with trial designs meant to shield participants from recognizing what they’re getting, or to separate expectations from the drug’s impact on health. These include incorporating a range of doses; giving the drug, with permission, to people who are asleep; and misleading participants about how a trial is set up. Companies running large-scale psychedelic trials mostly view unblinding as inevitable. Participants “are going to feel” the drug, “that’s just how it is,” says Rob Barrow, CEO of MindMed, which has late-stage trials underway to test LSD’s ability to ease anxiety. But he believes there are ways to parse a drug’s efficacy even if people know they’re getting it. In one recent trial, MindMed recruited 198 people with anxiety, giving some a placebo and the others LSD at one of four doses. Virtually all who received active drug correctly guessed that they’d gotten it. But those on the two higher doses saw clinically meaningful reduced anxiety, whereas those on the lower doses didn’t. That split means the benefit “has to be due to something other than thinking you’re getting drug,” Barrow says. MindMed is using a lower, nontherapeutic dose as well as a higher dose in an ongoing phase 3 trial, and hopes to report results next year.

Keyword: Depression; Drug Abuse
Link ID: 29691 - Posted: 03.05.2025

Five years ago Italian researchers published a study on the eruption of Mount Vesuvius in A.D. 79. that detailed how one victim of the blast, a male presumed to be in his mid 20s, had been found nearby in the seaside settlement of Herculaneum. He was lying facedown and buried by ash on a wooden bed in the College of the Augustales, a public building dedicated to the worship of Emperor Augustus. Some scholars believe that the man was the center’s caretaker and was asleep at the time of the disaster. In 2018, one researcher discovered black, glossy shards embedded inside the caretaker’s skull. The paper, published in 2020, speculated that the heat of the explosion was so immense that it had fused the victim’s brain tissue into glass. Vesuvius Erupted, but When Exactly? March 2, 2025 Forensic analysis of the obsidian-like chips revealed proteins common in brain tissue and fatty acids found in human hair, while a chunk of charred wood unearthed near the skeleton indicated a thermal reading as high as 968 degrees Fahrenheit, roughly the dome temperature of a wood-fired Neapolitan pizza oven. It was the only known instance of soft tissue — much less any organic material — being naturally preserved as glass. On Thursday, a paper published in Nature verified that the fragments are indeed glassified brain. Using techniques such as electron microscopy, energy dispersive X-ray spectroscopy and differential scanning calorimetry, scientists examined the physical properties of samples taken from the glassy fragments and demonstrated how they were formed and preserved. “The unique finding implies unique processes,” said Guido Giordano, a volcanologist at the Roma Tre University and lead author of the new study. Foremost among those processes is vitrification, by which material is burned at a high heat until it liquefies. To harden into glass, the substance requires rapid cooling, solidifying at a temperature higher than its surroundings. This makes organic glass formation challenging, Dr. Giordano said, as vitrification entails very specific temperature conditions and the liquid form must cool fast enough to avoid being crystallized as it congeals. © 2025 The New York Times Company

Keyword: Brain imaging
Link ID: 29690 - Posted: 03.05.2025

By Holly Barker Hunched over a microscope more than a century ago, Santiago Ramón y Cajal discovered that distinct types of neurons favor different brain regions. Looking at tissue from a pigeon’s cerebellum, he drew Purkinje cells, their dendrites outspread and twisted like a ravaged oak. And drawing from another sample—the first cortical layer of a newborn rabbit’s brain—he traced the tentacled nerve cells that would later bear his name. But the brain’s cellular organization is even more ordered than Ramón y Cajal could have imagined, a new study suggests. Different functional networks—measured using functional MRI—involve distinct blends of cell types, identified from their transcriptional profiles. And a machine-learning tool trained on cell distributions in postmortem tissue can identify functional networks based on these cellular “fingerprints,” the researchers found. The findings could address the gulf between neuroimaging and cell-based research, says the study’s principal investigator, Avram Holmes, associate professor of psychiatry at Rutgers University. “In-vivo imaging studies are almost never linked back to the underlying biological cascades that give rise to the phenotypes,” he says. But the new approach “lets you jump between fields of study—that was very difficult to do in the past.” Using bulk gene-expression data from postmortem human brain tissue—obtained from the Allen Human Brain Atlas—Holmes and his colleagues classified 24 different types of cells. They then mapped the cells’ spatial distribution to two features of large-scale brain organization derived from a popular fMRI atlas: networks, and those networks’ position in the cortical gradient, which is based on location, style of information processing and connectivity pattern. Unimodal sensorimotor networks—those that perceive stimuli and act on them—anchor one end of the gradient, and the other end is occupied by transmodal systems, such as the default mode network, that integrate multiple information streams across the cortex. The remaining networks are parked between these two extremes. © 2025 Simons Foundation

Keyword: Brain imaging
Link ID: 29689 - Posted: 03.01.2025

By Heidi Ledford A slimy barrier lining the brain’s blood vessels could hold the key to shielding the organ from the harmful effects of ageing, according to a study in mice. The study showed that this oozy barrier deteriorates with time, potentially allowing harmful molecules into brain tissue and sparking inflammatory responses. Gene therapy to restore the barrier reduced inflammation in the brain and improved learning and memory in aged mice. The work was published today in Nature1. The finding shines a spotlight on a cast of poorly understood molecules called mucins that coat the interior of blood vessels throughout the body and give mucus its slippery texture, says Carolyn Bertozzi, a Nobel-prizewinning chemist at Stanford University in California and a lead author of the study. “Mucins play a lot of interesting roles in the body,” she says. “But until recently, we didn’t have the tools to study them. They were invisible.” Snotty barrier Mucins are large proteins decorated with carbohydrates that form linkages with one another, creating a water-laden, gel-like substance. They are crucial constituents of the blood–brain barrier, a system that restricts the movement of some molecules from the blood into the brain. Researchers have long sought ways to sneak medicines past this barrier to treat diseases of the brain. Previous work also showed that the integrity of the barrier erodes with age2, suggesting that it could be an important target for therapies to combat diseases associated with ageing, such as Alzheimer’s disease. But scientists knew little about the contribution of mucins to these changes, until Sophia Shi, a graduate student at Stanford, decided to focus on a mucin-rich layer called the glycocalyx, which lines blood vessels. Shi and her colleagues looked at what happens to the glycocalyx in the brain as mice age. “The mucins on the young blood vessels were thick and juicy and plump,” says Bertozzi. “In the old mice, they were thin and lame and patchy.” © 2025 Springer Nature Limited

Keyword: Brain Injury/Concussion; Brain imaging
Link ID: 29688 - Posted: 03.01.2025

By Lola Butcher Last September, Eliezer Masliah, a prominent Alzheimer’s disease researcher, stepped away from his influential position at the National Institutes of Health after the organization, where he oversaw a $2.6 billion budget for neuroscience research, found falsified or fabricated images in his scientific articles. That same month, the Securities and Exchange Commission announced neuroscientist Lindsay Burns, her boss, and their company would pay more than $40 million to settle charges they had made misleading statements about research results from their clinical trial of a possible treatment for Alzheimer’s disease. Also in September: A $30 million clinical trial to study a stroke treatment developed by Berislav Zlokovic, a well-known Alzheimer’s expert, and his colleagues was canceled amid an investigation into whether he had manipulated images and data in research publications. Shortly thereafter, Zlokovic, director of the Zilkha Neurogenetic Institute at the University of Southern California medical school, was placed on indefinite administrative leave. Is there a pattern here? And, if there is, can neurology patients trust treatments that are based on published scientific research? That is what Charles Piller, an investigative reporter for Science magazine, examines in “Doctored: Fraud, Arrogance, and Tragedy in the Quest to Cure Alzheimer’s,” and his analysis is not comforting. As for the first question — is there a pattern? — Piller’s relentless reporting reveals that dozens of neuroscientists, including some of the most prominent in the world, appear to be responsible for inaccurate images in their published research. Those problematic images have prompted many of their articles to be retracted, corrected, or flagged as being “of concern” by the journals in which they were published.

Keyword: Alzheimers
Link ID: 29687 - Posted: 03.01.2025

By Donna L. Maney It’s springtime in your backyard. You watch a pair of little brown songbirds flit about, their white throats flashing in the sun. One of the birds has striking black and white stripes on its crown and occasionally belts out its song, “Old Sam Peabody, Peabody, Peabody.” Its partner is more drab, with tan and gray stripes on its head and brown streaks through its white throat. Knowing the conventional wisdom about songbirds—that the males are flashy show-offs and the females more camouflaged and quiet—you decide to name the singer with bright plumage Romeo and the subtler one Juliet. But later that day you notice Juliet teed up on the fence, belting out a song. Juliet’s song is even louder and showier than Romeo’s. You wonder, Do female birds sing? Then you see Romeo bringing a twig to the pair’s nest, hidden under a shrub. Your field guide says that in this species the female builds the nest by herself. What is going on? Turns out, when you named Romeo and Juliet, you made the same mistake 19th-century artist and naturalist John Audubon did when, in his watercolor of this species, he labeled the bright member of the pair “male” and the drab one “female.” Romeo might look male, even to a bird expert such as Audubon, but will build a nest and lay eggs in it. Juliet, who might look female, has testes and will defend the pair’s territory by singing both alone and alongside Romeo, who also sings. Juliet and Romeo are White-throated Sparrows (Zonotrichia albicollis). At first glance, members of this species of songbird might look rather ordinary. For example, like many other songbirds, one member of each breeding pair of these sparrows has more striking plumage—that is, its appearance is what we would traditionally consider malelike for songbirds. The other bird in the pair is more femalelike, with drabber plumage. © 2024 SCIENTIFIC AMERICAN

Keyword: Sexual Behavior; Evolution
Link ID: 29686 - Posted: 02.26.2025

By Ingrid Wickelgren After shuffling the cards in a standard 52-card deck, Alex Mullen, a three-time world memory champion, can memorize their order in under 20 seconds. As he flips though the cards, he takes a mental walk through a house. At each point in his journey — the mailbox, front door, staircase and so on — he attaches a card. To recall the cards, he relives the trip. This technique, called “method of loci” or “memory palace,” is effective because it mirrors the way the brain naturally constructs narrative memories: Mullen’s memory for the card order is built on the scaffold of a familiar journey. We all do something similar every day, as we use familiar sequences of events, such as the repeated steps that unfold during a meal at a restaurant or a trip through the airport, as a home for specific details — an exceptional appetizer or an object flagged at security. The general narrative makes the noteworthy features easier to recall later. “You are taking these details and connecting them to this prior knowledge,” said Christopher Baldassano (opens a new tab), a cognitive neuroscientist at Columbia University. “We think this is how you create your autobiographical memories.” Psychologists empirically introduced (opens a new tab) this theory some 50 years ago, but proof of such scaffolds in the brain was missing. Then, in 2018, Baldassano found it: neural fingerprints of narrative experience, derived from brain scans, that replay sequentially during standard life events. He believes that the brain builds a rich library of scripts for expected scenarios — restaurant or airport, business deal or marriage proposal — over a person’s lifetime. These standardized scripts, and departures from them, influence how and how well we remember specific instances of these event types, his lab has found. And recently, in a paper published in Current Biology in fall 2024, they showed that individuals can select a dominant script (opens a new tab) for a complex, real-world event — for example, while watching a marriage proposal in a restaurant, we might opt, subconsciously, for either a proposal or a restaurant script — which determines what details we remember. © 2025 Simons Foundation

Keyword: Learning & Memory; Attention
Link ID: 29685 - Posted: 02.26.2025