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

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

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

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

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

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

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

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

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

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

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

Keyword: Alzheimers
Link ID: 29767 - Posted: 04.30.2025

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

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

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

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

By Elise Cutts Food poisoning isn’t an experience you’re likely to forget — and now, scientists know why. A study published April 2 in Nature has unraveled neural circuitry in mice that makes food poisoning so memorable. “We’ve all experienced food poisoning at some point … And not only is it terrible in the moment, but it leads us to not eat those foods again,” says Christopher Zimmerman of Princeton University. Luckily, developing a distaste for foul food doesn’t take much practice — one ill-fated encounter with an undercooked enchilada or contaminated hamburger is enough, even if it takes hours or days for symptoms to set in. The same is true for other animals, making food poisoning one of the best ways to study how our brains connect events separated in time, says neuroscientist Richard Palmiter of the University of Washington in Seattle. Mice usually need an immediate reward or punishment to learn something, Palmiter says; even just a minute’s delay between cause (say, pulling a lever) and effect (getting a treat) is enough to prevent mice from learning. Not so for food poisoning. Despite substantial delays, their brains have no trouble associating an unfamiliar food in the past with tummy torment in the present. Researchers knew that a brain region called the amygdala represents flavors and decides whether or not they’re gross. Palmiter’s group had also shown that the gut tells the brain it’s feeling icky by activating specific “alarm” neurons, called CGRP neurons. “They respond to everything that’s bad,” Palmiter says. © Society for Science & the Public 2000–2025.

Keyword: Learning & Memory; Emotions
Link ID: 29756 - Posted: 04.23.2025

William Wright & Takaki Komiyama Every day, people are constantly learning and forming new memories. When you pick up a new hobby, try a recipe a friend recommended or read the latest world news, your brain stores many of these memories for years or decades. But how does your brain achieve this incredible feat? In our newly published research in the journal Science, we have identified some of the “rules” the brain uses to learn. Learning in the brain The human brain is made up of billions of nerve cells. These neurons conduct electrical pulses that carry information, much like how computers use binary code to carry data. These electrical pulses are communicated with other neurons through connections between them called synapses. Individual neurons have branching extensions known as dendrites that can receive thousands of electrical inputs from other cells. Dendrites transmit these inputs to the main body of the neuron, where it then integrates all these signals to generate its own electrical pulses. It is the collective activity of these electrical pulses across specific groups of neurons that form the representations of different information and experiences within the brain. For decades, neuroscientists have thought that the brain learns by changing how neurons are connected to one another. As new information and experiences alter how neurons communicate with each other and change their collective activity patterns, some synaptic connections are made stronger while others are made weaker. This process of synaptic plasticity is what produces representations of new information and experiences within your brain. In order for your brain to produce the correct representations during learning, however, the right synaptic connections must undergo the right changes at the right time. The “rules” that your brain uses to select which synapses to change during learning – what neuroscientists call the credit assignment problem – have remained largely unclear. © 2010–2025, The Conversation US, Inc.

Keyword: Learning & Memory
Link ID: 29754 - Posted: 04.23.2025

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

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

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 Gayoung Lee edited by Allison Parshall Crows sometimes have a bad rap: they’re said to be loud and disruptive, and myths surrounding the birds tend to link them to death or misfortune. But crows deserve more love and charity, says Andreas Nieder, a neurophysiologist at the University of Tübingen in Germany. They not only can be incredibly cute, cuddly and social but also are extremely smart—especially when it comes to geometry, as Nieder has found. In a paper published on Friday in Science Advances, Nieder and his colleagues report that crows display an impressive aptitude at distinguishing shapes by using geometric irregularities as a cognitive cue. These crows could even discern quite subtle differences. For the experiment, the crows perched in front of a digital screen that, almost like a video game, displayed progressively more complex combinations of shapes. First, the crows were taught to peck at a certain shape for a reward. Then they were presented with that same shape among five others—for example, one star shape placed among five moon shapes—and were rewarded if they correctly picked the "outlier." “Initially [the outlier] was very obvious,” Nieder says. But once the crows appeared to have familiarized themselves with how the “game” worked, Nieder and his team introduced more similar quadrilateral shapes to see if the crows would still be able to identify outliers. “And they could tell us, for instance, if they saw a figure that was just not a square, slightly skewed, among all the other squares,” Nieder says. “They really could do this spontaneously [and] discriminate the outlier shapes based on the geometric differences without us needing them to train them additionally.” Even when the researchers stopped rewarding them with treats, the crows continued to peck the outliers. © 2024 SCIENTIFIC AMERICAN,

Keyword: Evolution; Intelligence
Link ID: 29741 - 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 Yasemin Saplakoglu Humans tend to put our own intelligence on a pedestal. Our brains can do math, employ logic, explore abstractions and think critically. But we can’t claim a monopoly on thought. Among a variety of nonhuman species known to display intelligent behavior, birds have been shown time and again to have advanced cognitive abilities. Ravens plan (opens a new tab) for the future, crows count and use tools (opens a new tab), cockatoos open and pillage (opens a new tab) booby-trapped garbage cans, and chickadees keep track (opens a new tab) of tens of thousands of seeds cached across a landscape. Notably, birds achieve such feats with brains that look completely different from ours: They’re smaller and lack the highly organized structures that scientists associate with mammalian intelligence. “A bird with a 10-gram brain is doing pretty much the same as a chimp with a 400-gram brain,” said Onur Güntürkün (opens a new tab), who studies brain structures at Ruhr University Bochum in Germany. “How is it possible?” Researchers have long debated about the relationship between avian and mammalian intelligences. One possibility is that intelligence in vertebrates — animals with backbones, including mammals and birds — evolved once. In that case, both groups would have inherited the complex neural pathways that support cognition from a common ancestor: a lizardlike creature that lived 320 million years ago, when Earth’s continents were squished into one landmass. The other possibility is that the kinds of neural circuits that support vertebrate intelligence evolved independently in birds and mammals. It’s hard to track down which path evolution took, given that any trace of the ancient ancestor’s actual brain vanished in a geological blink. So biologists have taken other approaches — such as comparing brain structures in adult and developing animals today — to piece together how this kind of neurobiological complexity might have emerged. © 2025 Simons Foundation

Keyword: Intelligence; Evolution
Link ID: 29738 - Posted: 04.09.2025

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