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

By Roni Caryn Rabin Middle-aged and older adults who sought hospital or emergency room care because of cannabis use were almost twice as likely to develop dementia over the next five years, compared with similar people in the general population, a large Canadian study reported on Monday. When compared with adults who sought care for other reasons, the risk of developing dementia was still 23 percent higher among users of cannabis, the study also found. The study included the medical records of six million people in Ontario from 2008 to 2021. The authors accounted for health and sociodemographic differences between comparison groups, some of which play a role in cognitive decline. The data do not reveal how much cannabis the subjects had been using, and the study does not prove that regular or heavy cannabis use plays a causal role in dementia. But the finding does raise serious concerns that require further exploration, said Dr. Daniel T. Myran, the first author of the study, which was published in JAMA Neurology. “Figuring out whether or not cannabis use or heavy regular chronic use causes dementia is a challenging and complicated question that you don’t answer in one study,” said Dr. Myran, an assistant professor of family medicine at University of Ottawa. “This contributes to the literature and to a sign, or signal, of concern.” Dr. Myran’s previous research has found that patients with cannabis use disorder died at almost three times the rate of individuals without the disorder over a five-year period. He has also reported that more cases of schizophrenia and psychosis in Canada have been linked to cannabis use disorder since the drug was legalized. © 2025 The New York Times Company

Keyword: Alzheimers; Drug Abuse
Link ID: 29745 - Posted: 04.16.2025

By Azeen Ghorayshi The percentage of American children estimated to have autism spectrum disorder increased in 2022, continuing a long-running trend, according to data released on Tuesday by the Centers for Disease Control and Prevention. Among 8-year-olds, one in 31 were found to have autism in 2022, compared with 1 in 36 in 2020. That rate is nearly five times as high as the figure in 2000, when the agency first began collecting data. The health agency noted that the increase was most likely being driven by better awareness and screening, not necessarily because autism itself was becoming more common. That diverged sharply from the rhetoric of the nation’s health secretary, Robert F. Kennedy Jr., who on Tuesday said, “The autism epidemic is running rampant.” Mr. Kennedy has repeatedly tried to connect rising autism rates with vaccines, despite dozens of studies over decades that failed to establish such a link. The health secretary nonetheless has initiated a federal study that will revisit the possibility and has hired a well-known vaccine skeptic to oversee the effort. Mr. Kennedy recently announced an effort by the Department of Health and Human Services to pinpoint the “origins of the epidemic” by September, an initiative that was greeted with skepticism by many autism experts. “It seems very unlikely that it is an epidemic, in the way that people define epidemics,” said Catherine Lord, a psychologist and autism researcher at the David Geffen School of Medicine at the University of California, Los Angeles. A significant part of the increase instead can be attributed to the expansion of the diagnosis over the years to capture milder cases, Dr. Lord said, as well as decreased stigma and greater awareness of support services. Still, she left open the possibility that other factors are contributing to more children developing autism. “We can account for a lot of the increase but perhaps not all of it,” Dr. Lord said. “But whatever it is, it’s not vaccines,” she added. © 2025 The New York Times Company

Keyword: Autism
Link ID: 29744 - Posted: 04.16.2025

By Carl Zimmer The human brain is so complex that scientific brains have a hard time making sense of it. A piece of neural tissue the size of a grain of sand might be packed with hundreds of thousands of cells linked together by miles of wiring. In 1979, Francis Crick, the Nobel-prize-winning scientist, concluded that the anatomy and activity in just a cubic millimeter of brain matter would forever exceed our understanding. “It is no use asking for the impossible,” Dr. Crick wrote. Forty-six years later, a team of more than 100 scientists has achieved that impossible, by recording the cellular activity and mapping the structure in a cubic millimeter of a mouse’s brain — less than one percent of its full volume. In accomplishing this feat, they amassed 1.6 petabytes of data — the equivalent of 22 years of nonstop high-definition video. “This is a milestone,” said Davi Bock, a neuroscientist at the University of Vermont who was not involved in the study, which was published Wednesday in the journal Nature. Dr. Bock said that the advances that made it possible to chart a cubic millimeter of brain boded well for a new goal: mapping the wiring of the entire brain of a mouse. “It’s totally doable, and I think it’s worth doing,” he said. More than 130 years have passed since the Spanish neuroscientist Santiago Ramón y Cajal first spied individual neurons under a microscope, making out their peculiar branched shapes. Later generations of scientists worked out many of the details of how a neuron sends a spike of voltage down a long arm, called an axon. Each axon makes contact with tiny branches, or dendrites, of neighboring neurons. Some neurons excite their neighbors into firing voltage spikes of their own. Some quiet other neurons. Human thought somehow emerges from this mix of excitation and inhibition. But how that happens has remained a tremendous mystery, largely because scientists have been able to study only a few neurons at a time. In recent decades, technological advances have allowed scientists to start mapping brains in their entirety. In 1986, British researchers published the circuitry of a tiny worm, made up of 302 neurons. In subsequent years, researchers charted bigger brains, such as the 140,000 neurons in the brain of a fly. © 2025 The New York Times Company

Keyword: Brain imaging; Development of the Brain
Link ID: 29743 - Posted: 04.12.2025

By Michael Schulson Two years ago, at a Stop & Shop in Rhode Island, the Danish neuroscientist and physician Henriette Edemann-Callesen visited an aisle stocked with sleep aids containing melatonin. She looked around in amazement. Then she took out her phone and snapped a photo to send to colleagues back home. “It was really pretty astonishing,” she recalled recently. In Denmark, as in many countries, the hormone melatonin is a prescription drug for treating sleep problems, mostly in adults. Doctors are supposed to prescribe it to children only if they have certain developmental disorders that make it difficult to sleep — and only after the family has tried other methods to address the problem. But at the Rhode Island Stop & Shop, melatonin was available over the counter, as a dietary supplement, meaning it receives slightly less regulatory scrutiny, in some respects, than a package of Skittles. Many of the products were marketed for children, in colorful bottles filled with liquid drops and chewable tablets and bright gummies that look and taste like candy. A quiet but profound shift is underway in American parenting, as more and more caregivers turn to pharmacological solutions to help children sleep. What makes that shift unusual is that it’s largely taking place outside the traditional boundaries of health care. Instead, it’s driven by the country’s sprawling dietary supplements industry, which critics have long said has little regulatory oversight — and which may get a boost from Secretary of Health and Human Services Robert F. Kennedy Jr., who is widely seen as an ally to supplement makers. Thirty years ago, few people were giving melatonin to children, outside of a handful of controlled experiments. Even as melatonin supplements grew in popularity among adults in the late 1990s in the United States and Canada, some of those products carried strict warnings not to give them to younger people. But with time, the age floor dropped, and by the mid-2000s, news reports and academic surveys suggest some early adopters were doing just that. (Try it for ages 11-and-up only, one CNN report warned at the time.) By 2013, according to a Wall Street Journal article, a handful of companies were marketing melatonin products specifically for kids.

Keyword: Biological Rhythms; Development of the Brain
Link ID: 29740 - Posted: 04.12.2025

Jon Hamilton Researchers created an assembloid by integrating four organoids that represent the four components of the human sensory pathway, along which pain stimuli signals are conveyed to the brain. Stimulation of the sensory organoid (top) by pain-inducing substances, such as capsaicin, triggers neuronal activity in that organoid which is then transmitted to the adjacent spinal-cord organoid, the thalamic organoid and, finally, to the cortical organoid (bottom) Researchers integrated four organoids that represent the four components of the human sensory pathway, along which pain signals are conveyed to the brain. Stimulation of the sensory organoid (top) by substances, such as capsaicin, triggers neuronal activity that is then transmitted throughout the rest of the organoids. Pasca lab/Stanford Medicine Scientists have re-created a pain pathway in the brain by growing four key clusters of human nerve cells in a dish. This laboratory model could be used to help explain certain pain syndromes, and offer a new way to test potential analgesic drugs, a Stanford team reports in the journal Nature. "It's exciting," says Dr. Stephen Waxman, a professor at Yale School of Medicine who was not involved in the research. © 2025 npr

Keyword: Pain & Touch; Development of the Brain
Link ID: 29739 - Posted: 04.12.2025

By Rodrigo Pérez Ortega It’s clear a child’s early experiences can leave a lasting imprint on how their brain forms and functions. Now, a new study reveals how various environmental factors, including financial struggles and neighborhood safety, affect the quality of the brain’s white matter—the wiring that connects different brain regions—and in turn, a child’s cognitive abilities. The work, published today in the Proceedings of the National Academy of Sciences, also points to social factors that can boost resilience in a young brain. “It’s a really impressive, compelling paper about the long-term consequences of growing up in undersupported environments,” says John Gabrieli, a neuroscientist at the Massachusetts Institute of Technology who was not involved in the study. White matter consists of nerve fibers facilitating communication between brain regions. They are sheathed in an insulating material called myelin that gives white matter its color. Much of the research to date on how the brain supports cognition has focused on gray matter, tissue mostly made of the cell bodies of neurons that process information, which shows up as gray on brain scans. But complex cognitive tasks are “a symphony of a network” formed by multiple brain areas, Gabrieli says. “And the white matter is what mediates that communication.” Previous studies have linked poverty and childhood trauma—among other adverse environments—with a lower quality of white matter in children and lower scores on cognitive tests. However, these studies included a small number or participants and only looked at one or a few environmental variables at a time. For a more complete picture, developmental neuroscientist Sofia Carozza at Brigham and Women’s Hospital and colleagues analyzed data from more than 9000 participants in the Adolescent Brain Cognitive Development (ABCD) Study. Funded by the National Institutes of Health and established in 2015, ABCD is the largest longitudinal study of brain development in a representative group of U.S. children. Surveys of participants and their parents provide data on their home environment, including household income and parents’ level of education. At age 9 or 10, ABCD participants got a form of magnetic resonance imaging that measures the movement of water in the brain. From the strength of this directional signal, researchers can infer how robust and organized the bundles of white matter fibers are, and whether they have signs of deterioration or damage. © 2025 American Association for the Advancement of Science.

Keyword: Development of the Brain; Learning & Memory
Link ID: 29736 - Posted: 04.09.2025

Ian Sample Science editor Researchers who tracked cases of dementia in Welsh adults have uncovered the strongest evidence yet that the shingles vaccination reduces the risk of developing the devastating brain disease. Health records of more than 280,000 older adults revealed that those who received a largely discontinued shingles vaccine called Zostavax were 20% less likely to be diagnosed with dementia over the next seven years than those who went without. Pascal Geldsetzer, at Stanford University, said: “For the first time we are able to say much more confidently that the shingles vaccine causes a reduction in dementia risk. If this truly is a causal effect, we have a finding that’s of tremendous importance.” The researchers took advantage of a vaccination rollout that took place in Wales more than a decade ago. Public health policy dictated that from 1 September 2013, people born on or after 2 September 1933 became eligible for the Zostavax shot, while those who were older missed out. The policy created a natural experiment where the older population was sharply divided into two groups depending on their access to the vaccine. This allowed the researchers to compare dementia rates in older people born weeks apart but on either side of the vaccine eligibility divide. After accounting for the fact that not all those eligible for the vaccine received it, the researchers found vaccination led to a 20% reduction in dementia risk, with the strongest effect in women. Anupam Jena, a professor of healthcare policy at Harvard Medical School, said the implications were profound. © 2025 Guardian News & Media Limited

Keyword: Alzheimers; Neuroimmunology
Link ID: 29732 - Posted: 04.05.2025

Jon Hamilton New tests of blood and spinal fluid could help doctors quickly identify patients who would most benefit from treatment. New tests of blood and spinal fluid could help doctors quickly identify patients who would most benefit from treatment. Andrew Brookes/Getty Images When doctors suspect Alzheimer's, they can order a blood test to learn whether a patient's brain contains the sticky amyloid plaques that are a hallmark of the disease. But the results of that test won't tell the whole story, says Dr. Randall Bateman, a neurology professor at Washington University in St. Louis. "People can have a head full of amyloid, but no dementia or memory loss," Bateman says. So he and a team of scientists have developed a new blood test that can show whether Alzheimer's has actually begun to affect a person's thinking and memory. It joins another new test, this one of spinal fluid, that can predict whether the brain changes associated with Alzheimer's are likely to affect cognitive function. "It's a strong indicator of memory impairment," says Tony Wyss-Coray, a neurology professor at Stanford University. Both tests, described in the journal Nature Medicine, could help doctors identify patients who are likely to benefit from drugs that can clear the brain of amyloid plaques. Both were developed with funding from the National Institutes of Health. © 2025 npr

Keyword: Alzheimers
Link ID: 29725 - Posted: 04.02.2025

By Sergiu P. Pasca The unbearable inaccessibility of the human brain has been a major barrier to understanding both how the human nervous system assembles itself and how psychiatric and neurological disorders emerge. But thanks to new advances, it is becoming possible to access functional aspects of human brain development and function that were previously out of reach. This progress has been driven primarily by advances in stem cell technologies, which make it possible to recapitulate developmental processes outside the human body. The journey began decades ago with the ability to grow stem cells in a dish, followed by the use of developmental signals to guide them into becoming neural cells. The field was truly catalyzed by the discovery of cell reprogramming and the democratization of stem cell technologies it enabled. Starting more than 15 years ago, my team and others began creating neurons from patients—initially rather inefficiently, but then with increasing ease as culture systems became more sophisticated. For example, cortical neurons derived from people with Timothy syndrome—a genetic form of autism and epilepsy caused by a mutation in a calcium channel present in excitable cells—revealed calcium deficits following depolarization. Some of these defects became more apparent when moving beyond traditional 2D preparations, such as when looking at the morphology of human neurons. For more than a decade, we and others have developed methods for growing these cells into more complex 3D structures, known as organoids, that mimic some of the structure and function of regions of the nervous system, offering a new window into human neurobiology and disease. Giving cells this third dimension of freedom unleashes self-organization: Mirroring in-vivo development, organoids generate diverse neural and glial cell types, starting from radial glia to intermediate progenitors, deep and superficial layer neurons and then astrocytes. These organoids can be maintained in vitro for years. Fascinatingly, developmental timing in organoids is largely preserved. For example, neurons maintained in culture for about nine months can transition to a postnatal state simply by surviving long enough in the dish. This observation in organoids offers a fundamental insight into development: Brain cells have an intrinsic, species-specific developmental “timer.” © 2025 Simons Foundation

Keyword: Development of the Brain
Link ID: 29724 - Posted: 04.02.2025

By Christina Caron Health Secretary Robert F. Kennedy Jr. has often criticized prescription stimulants, such as Adderall, that are primarily used to treat attention deficit hyperactivity disorder. “We have damaged this entire generation,” he said last year during a podcast, referring to the number of children taking psychiatric medications. “We have poisoned them.” In February, the “Make America Healthy Again” commission, led by Mr. Kennedy, announced plans to evaluate the “threat” posed by drugs like prescription stimulants. But are they a threat? And if so, to whom? Like many medications, prescription stimulants have potential side effects, and there are people who misuse them. Yet these drugs are also considered some of the most effective and well-researched treatments that psychiatry has to offer, said Dr. Jeffrey H. Newcorn, the director of the Division of A.D.H.D. and Learning Disorders at the Icahn School of Medicine at Mount Sinai in New York. Here are some answers to common questions and concerns about stimulants. What are prescription stimulants? Prescription stimulants are drugs that help change the way the brain works by increasing the communication among neurons. They are divided into two classes: methylphenidates (like Ritalin, Focalin and Concerta) and amphetamines (like Vyvanse and Adderall). © 2025 The New York Times Company

Keyword: ADHD; Drug Abuse
Link ID: 29723 - Posted: 04.02.2025

By RJ Mackenzie New footage documents microglia pruning synapses at high resolution and in real time. The recordings, published in January, add a new twist to a convoluted debate about the range of these cells’ responsibilities. Microglia are the brain’s resident immune cells. For about a decade, some have also credited them with pruning excess synaptic connections during early brain development. But that idea was based on static images showing debris from destroyed synapses within the cells—which left open the possibility that microglia clean up after neurons do the actual pruning. In the January movies, though, a microglia cell expressing a green fluorescent protein clearly reaches out a ghostly green tentacle to a budding presynapse on a neuron and lifts it away, leaving the neighboring blue axon untouched. “Their imaging is superb,” says Amanda Sierra, a researcher at the Achucarro Basque Center for Neuroscience, who was not involved in the work. But “one single video, or even two single videos, however beautiful they are, are not sufficient evidence that this is the major mechanism of synapse elimination,” she says. In the new study, researchers isolated microglia and neurons from mice and grew them in culture with astrocytes, labeling the microglia, synapses and axons with different fluorescent dyes. Their approach ensured that the microglia formed ramified processes—thin, branching extensions that don’t form when they are cultured in isolation, says Ryuta Koyama, director of the Department of Translational Neurobiology at Japan’s National Center of Neurology and Psychiatry, who led the work. “People now know that ramified processes of microglia are really necessary to pick up synapses,” he says. “In normal culture systems, you can’t find ramified processes. They look amoeboid.” © 2025 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 29720 - Posted: 03.27.2025

By Catherine Offord Scientists say they have found a long–sought-after population of stem cells in the retina of human fetuses that could be used to develop therapies for one of the leading causes of blindness. The use of fetal tissue, a source of ethical debate and controversy in some countries, likely wouldn’t be necessary for an eventual therapy: Transplanting similar human cells generated in the lab into the eyes of mice with retinal disease protected the animals’ vision, the team reported this week in Science Translational Medicine. “I see this as potentially a very interesting advancement of this field, where we are really in need of a regenerative treatment for retinal diseases,” says Anders Kvanta, a retinal specialist at the Karolinska Institute who was not involved in the work. He and others note that more evidence is needed to show the therapeutic usefulness of the newly described cells. The retina, a layer of light-sensing tissue at the back of the eye, can degenerate with age or because of an inherited condition such as retinitis pigmentosa, a rare disease that causes gradual breakdown of retinal cells. Hundreds of millions of people worldwide are affected by retinal degeneration, and many suffer vision loss or blindness as a result. Most forms can’t be treated. Scientists have long seen a potential solution in stem cells, which can regenerate and repair injured tissue. Several early-stage clinical trials are already evaluating the safety and efficacy of transplanting stem cells derived from cell lines established from human embryos, for example, or adult human cells that have been reprogrammed to a stem-like state. Other approaches include transplanting so-called retinal progenitor cells (RPCs)—immature cells that give rise to photoreceptors and other sorts of retinal cells—from aborted human fetuses. Some researchers have argued that another type of cell, sometimes referred to as retinal stem cells (RSCs), could also treat retinal degeneration. These cells’ long lifespans and ability to undergo numerous cells divisions could make them better candidates to regenerate damaged tissue than RPCs. RSCs have been found in the eyes of zebrafish and some other vertebrates, but evidence for their existence in mammals has been controversial. Reports announcing their discovery in adult mice in the early 2000s were later discounted.

Keyword: Vision; Stem Cells
Link ID: 29719 - Posted: 03.27.2025

Ari Daniel Tristan Yates has no doubt about her first memory, even if it is a little fuzzy. "I was about three and a half in Callaway Gardens in Georgia," she recalls, "just running around with my twin sister trying to pick up Easter eggs." But she has zero memories before that, which is typical. This amnesia of our babyhood is pretty much the rule. "We have memories from what happened earlier today and memories from what happened earlier last week and even from a few years ago," says Yates, who's a cognitive neuroscientist at Columbia University. "But all of us lack memories from our infancy." Is that because we don't make memories when we're babies, or is there something else responsible? Now, in new research published by Yates and her colleagues in the journal Science, they propose that babies are able to form memories, even if they become inaccessible later in life. These results might reveal something crucial about the earliest moments of our development. "That's the time when we learn who our parents are, that's when we learn language, that's when we learn how to walk," Yates says. "What happens in your brain in the first two years of life is magnificent," says Nick Turk-Browne, a cognitive neuroscientist at Yale University. "That's the period of by far the greatest plasticity across your whole life span. And better understanding how your brain learns and remembers in infancy lays the foundation for everything you know and do for the rest of your life. © 2025 npr

Keyword: Learning & Memory; Development of the Brain
Link ID: 29715 - Posted: 03.22.2025

By Paula Span Joan Presky worries about dementia. Her mother lived with Alzheimer’s disease for 14 years, the last seven in a memory-care residence, and her maternal grandfather developed dementia, too. “I’m 100 percent convinced that this is in my future,” said Ms. Presky, 70, a retired attorney in Thornton, Colo. Last year, she spent almost a full day with a neuropsychologist, undergoing an extensive evaluation. The results indicated that her short-term memory was fine — which she found “shocking and comforting” — and that she tested average or above in every cognitive category but one. She’s not reassured. “I saw what Alzheimer’s was like,” she said of her mother’s long decline. “The memory of what she went through is profound for me.” The prospect of dementia, which encompasses Alzheimer’s disease and a number of other cognitive disorders, so frightens Americans that a recent study projecting steep increases in cases over the next three decades drew enormous public attention. The researchers’ findings, published in January in Nature Medicine, even showed up as a joke on the Weekend Update segment of “Saturday Night Live.” “Dementia is a devastating condition, and it’s very much related to the oldest ages,” said Dr. Josef Coresh, director of the Optimal Aging Institute at NYU Langone Health and the senior author of the study. “The globe is getting older.” Now the findings are being challenged by other dementia researchers who say that while increases are coming, they will be far smaller than Dr. Coresh and his co-authors predicted. © 2025 The New York Times Company

Keyword: Alzheimers
Link ID: 29713 - Posted: 03.22.2025

Nicola Davis Science correspondent Cat owners are being asked share their pet’s quirky traits and even post researchers their fur in an effort to shed light on how cats’ health and behaviour are influenced by their genetics. The scientists behind the project, Darwin’s Cats, are hoping to enrol 100,000 felines, from pedigrees to moggies, with the DNA of 5,000 cats expected to be sequenced in the next year. The team say the goal is to produce the world’s largest feline genetic database. “Unlike most existing databases, which tend to focus on specific breeds or veterinary applications, Darwin’s Cats is building a diverse, large-scale dataset that includes pet cats, strays and mixed breeds from all walks of life,” said Dr Elinor Karlsson, the chief scientist at the US nonprofit organisation Darwin’s Ark, director of the vertebrate genomics group at the Broad Institute of MIT and Harvard and associate professor at the UMass Chan medical school. “It’s important to note, this is an open data project, so we will share the data with other scientists as the dataset grows,” she added. The project follows on the heels of Darwin’s Dogs, a similar endeavour that has shed light on aspects of canine behaviour, disease and the genetic origins of modern breeds. Darwin’s Cats was launched in mid-2024 and already has more than 3,000 cats enrolled, although not all have submitted fur samples. Participants from all parts of the world are asked to complete a number of free surveys about their pet’s physical traits, behaviour, environment, and health. © 2025 Guardian News & Media Limited

Keyword: Genes & Behavior; Development of the Brain
Link ID: 29708 - Posted: 03.19.2025

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 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 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