By Bob Holmes Like many of the researchers who study how people find their way from place to place, David Uttal is a poor navigator. “When I was 13 years old, I got lost on a Boy Scout hike, and I was lost for two and a half days,” recalls the Northwestern University cognitive scientist. And he’s still bad at finding his way around. The world is full of people like Uttal — and their opposites, the folks who always seem to know exactly where they are and how to get where they want to go. Scientists sometimes measure navigational ability by asking someone to point toward an out-of-sight location — or, more challenging, to imagine they are someplace else and point in the direction of a third location — and it’s immediately obvious that some people are better at it than others. “People are never perfect, but they can be as accurate as single-digit degrees off, which is incredibly accurate,” says Nora Newcombe, a cognitive psychologist at Temple University who coauthored a look at how navigational ability develops in the 2022 Annual Review of Developmental Psychology. But others, when asked to indicate the target’s direction, seem to point at random. “They have literally no idea where it is.” While it’s easy to show that people differ in navigational ability, it has proved much harder for scientists to explain why. There’s new excitement brewing in the navigation research world, though. By leveraging technologies such as virtual reality and GPS tracking, scientists have been able to watch hundreds, sometimes even millions, of people trying to find their way through complex spaces, and to measure how well they do. Though there’s still much to learn, the research suggests that to some extent, navigation skills are shaped by upbringing. Nurturing navigation skills

Keyword: Learning & Memory
Link ID: 29255 - Posted: 04.13.2024

By Joanne Silberner In March, the sons of Gabriel García Márquez, the Nobel Prize-winning Colombian writer, published a posthumous novel against the specific wishes their father expressed before he died in 2014 at the age of 87. García Márquez had struggled through several versions of the book as dementia set in, and, perhaps stung by uncharacteristic negative reviews from his previous novel, didn’t want the new one published. “Until August,” the story of a woman who travels to her mother’s grave once a year and takes a new lover on each visit, got mixed reviews. Some were outright harsh. In The New York Times, Michael Greenberg wrote “It would be hard to imagine a more unsatisfying goodbye.” García Márquez’s decline, he continued, “seems to have been steep enough to prevent him from holding together the kind of imagined world that the writing of fiction demands.” Wendy Mitchell, who was an administrator with England’s National Health Service until her diagnosis of early-onset Alzheimer’s disease in 2014, recalled the moment she learned of the publication plans last year. “I type every day for fear of dementia snatching away that creative skill, which I see as my escape from dementia,” she wrote last October in The Guardian. “Maybe Márquez thought the same?” The novel’s publication raises some vital questions about living with an aging and perhaps ailing brain. What do mild cognitive impairment and dementia do to our creativity? How do these conditions affect our ability to use words, formulate sentences, and craft stories? Neuroscientists have been exploring these questions for several decades. First, a few definitions. People with mild cognitive impairment have lost more of their cognitive functioning than others their age, and often struggle to remember things. But they’re capable of managing daily activities like dressing, eating, bathing, and finding their way around. In dementia, cognitive difficulties have increased enough to interfere with daily life, and personality changes are more likely.

Keyword: Alzheimers
Link ID: 29254 - Posted: 04.13.2024

By Nicole Rust We readily (and reasonably) accept that the causes of memory dysfunction, including Alzheimer’s disease, reside in the brain. The same is true for many problems with seeing, hearing and motor control. We acknowledge that understanding how the brain supports these functions is important for developing treatments for their corresponding dysfunctions, including blindness, deafness and Parkinson’s disease. Applying the analogous assertion to mood—that understanding how the brain supports mood is crucial for developing more effective treatments for mood disorders, such as depression—is more controversial. For brain researchers unfamiliar with the controversy, it can be befuddling. You might hear, “Mental disorders are psychological, not biological,” and wonder, what does that mean, exactly? Experts have diverse opinions on the matter, with paper titles ranging from “Brain disorders? Not really,” to “Brain disorders? Precisely.” Even though a remarkable 21 percent of adults in the United States will experience a mood disorder at some point in their lives, we do not fully understand what causes them, and existing treatments do not work for everyone. How can we best move toward an impactful understanding of mood and mood disorders, with the longer-term goal of helping these people? What, if anything, makes mood fundamentally different from, say, memory? The answer turns out to be complex and nuanced—here, I hope to unpack it. I also ask brain and mind researchers with diverse perspectives to chime in. Among contemporary brain and mind researchers, I have yet to find any whose position is driven by the notion that some force in the universe beyond the brain, like a nonmaterial soul, gives rise to mood. Rather, the researchers generally agree that our brains mediate all mental function. If everyone agrees that both memory and mood disorders follow from things that happen in the brain, why would the former but not the latter qualify as “brain disorders”? © 2024 Simons Foundation

Keyword: Depression; Learning & Memory
Link ID: 29251 - Posted: 04.11.2024

By Helen Bradshaw Walk into a gas station in the United States, and you may see more than just boxes of cigarettes lining the back wall. Colorful containers containing delta-8, a form of the substance THC, are sold in gas stations and shops across the country, and teens are buying them. A recent survey of more than 2,000 U.S. high school seniors found that more than 11 percent of them had used delta-8 in the past year, researchers report March 12 in JAMA. This is the first year the Monitoring the Future study, one of the leading nationally representative surveys of drug use trends among adolescents in the United States, looked at delta-8 use. Because more than 1 in 10 senior students said they used the drug, the survey team plans to monitor delta-8 use every year going forward. “We don’t really want to see any kids being exposed to cannabis, because it potentially increases their risk for developmental harms … and some psychiatric reactions” such as suicidal thoughts, says Alyssa Harlow, a researcher on the survey and an epidemiologist at the University of Southern California Keck School of Medicine in Los Angeles. Despite its prevalence, especially in the South and the Midwest, delta-8 is still new to consumers and research. Science News talked with Harlow and addiction researcher Jessica Kruger of the University of Buffalo in New York to help explain the delta-8 craze and its effects on kids. What is delta-8-THC? Cannabis plants contain over 100 compounds known as cannabinoids. Delta-8 is one of them. The most well-known is delta-9-tetrahydrocannabinol, or delta-9-THC. © Society for Science & the Public 2000–2024.

Keyword: Drug Abuse
Link ID: 29248 - Posted: 04.11.2024

Jon Hamilton Sam and John Fetters, 19, are identical twins at opposite ends of the autism spectrum. Sam is a sophomore at Amherst College who plans to double major in history and political science. In his free time, he runs marathons. John attends a special school, struggles to form sentences, and likes to watch "Teletubbies" and "Sesame Street." Two brothers. Same genes. Different flavors of autism. To scientists, twins like Sam and John pose an important question: How can a disorder that is known to be highly genetic look so different in siblings who share the same genome? "That is one of the greatest mysteries right now in research on autism," says Dr. Stephanie Morris, a pediatric neurologist at the Kennedy Krieger Institute in Baltimore. Solving that mystery could help explain autism's odd mix of nature and nurture, Morris says. It also might help "modify the trajectory" of autistic children experiencing speech and language delays, or difficulty with social communication. Identical twins on separate paths Sam and John are spending the weekend with their mom, Kim Leaird, at the family's apartment in West Tisbury, a small town on Martha's Vineyard. The twins are crowded together on a couch. Even seated, they look tall. Standing, Sam is 6 feet five inches, his brother just an inch shorter. John lets Sam do most of the talking. He frequently touches his brother, who sometimes takes his hand. John has "a truly tremendous amount of empathy," Sam says. "He's able to be very supportive." © 2024 npr

Keyword: Autism; Genes & Behavior
Link ID: 29239 - Posted: 04.04.2024

by Alex Blasdel Patient One was 24 years old and pregnant with her third child when she was taken off life support. It was 2014. A couple of years earlier, she had been diagnosed with a disorder that caused an irregular heartbeat, and during her two previous pregnancies she had suffered seizures and faintings. Four weeks into her third pregnancy, she collapsed on the floor of her home. Her mother, who was with her, called 911. By the time an ambulance arrived, Patient One had been unconscious for more than 10 minutes. Paramedics found that her heart had stopped. After being driven to a hospital where she couldn’t be treated, Patient One was taken to the emergency department at the University of Michigan. There, medical staff had to shock her chest three times with a defibrillator before they could restart her heart. She was placed on an external ventilator and pacemaker, and transferred to the neurointensive care unit, where doctors monitored her brain activity. She was unresponsive to external stimuli, and had a massive swelling in her brain. After she lay in a deep coma for three days, her family decided it was best to take her off life support. It was at that point – after her oxygen was turned off and nurses pulled the breathing tube from her throat – that Patient One became one of the most intriguing scientific subjects in recent history. For several years, Jimo Borjigin, a professor of neurology at the University of Michigan, had been troubled by the question of what happens to us when we die. She had read about the near-death experiences of certain cardiac-arrest survivors who had undergone extraordinary psychic journeys before being resuscitated. Sometimes, these people reported travelling outside of their bodies towards overwhelming sources of light where they were greeted by dead relatives. Others spoke of coming to a new understanding of their lives, or encountering beings of profound goodness. Borjigin didn’t believe the content of those stories was true – she didn’t think the souls of dying people actually travelled to an afterworld – but she suspected something very real was happening in those patients’ brains. In her own laboratory, she had discovered that rats undergo a dramatic storm of many neurotransmitters, including serotonin and dopamine, after their hearts stop and their brains lose oxygen. She wondered if humans’ near-death experiences might spring from a similar phenomenon, and if it was occurring even in people who couldn’t be revived. © 2024 Guardian News & Media Limited

Keyword: Consciousness; Attention
Link ID: 29236 - Posted: 04.02.2024

By Paula Span The phone awakened Doug Nordman at 3 a.m. A surgeon was calling from a hospital in Grand Junction, Colo., where Mr. Nordman’s father had arrived at the emergency room, incoherent and in pain, and then lost consciousness. At first, the staff had thought he was suffering a heart attack, but a CT scan found that part of his small intestine had been perforated. A surgical team repaired the hole, saving his life, but the surgeon had some questions. “Was your father an alcoholic?” he asked. The doctors had found Dean Nordman malnourished, his peritoneal cavity “awash with alcohol.” The younger Mr. Nordman, a military personal finance author living in Oahu, Hawaii, explained that his 77-year-old dad had long been a classic social drinker: a Scotch and water with his wife before dinner, which got topped off during dinner, then another after dinner, and perhaps a nightcap. Having three to four drinks daily exceeds current dietary guidelines, which define moderate consumption as two drinks a day for men and one for women, or less. But “that was the normal drinking culture of the time,” said Doug Nordman, now 63. At the time of his 2011 hospitalization, though, Dean Nordman, a retired electrical engineer, was widowed, living alone and developing symptoms of dementia. He got lost while driving, struggled with household chores and complained of a “slipping memory.” He had waved off his two sons’ offers of help, saying he was fine. During that hospitalization, however, Doug Nordman found hardly any food in his father’s apartment. Worse, reviewing his father’s credit card statements, “I saw recurring charges from the Liquor Barn and realized he was drinking a pint of Scotch a day,” he said. Public health officials are increasingly alarmed by older Americans’ drinking. The annual number of alcohol-related deaths from 2020 through 2021 exceeded 178,000, according to recently released data from the Centers for Disease Control and Prevention: more deaths than from all drug overdoses combined. © 2024 The New York Times Company

Keyword: Drug Abuse; Alzheimers
Link ID: 29234 - Posted: 04.02.2024

By Markham Heid The human hand is a marvel of nature. No other creature on Earth, not even our closest primate relatives, has hands structured quite like ours, capable of such precise grasping and manipulation. But we’re doing less intricate hands-on work than we used to. A lot of modern life involves simple movements, such as tapping screens and pushing buttons, and some experts believe our shift away from more complex hand activities could have consequences for how we think and feel. “When you look at the brain’s real estate — how it’s divided up, and where its resources are invested — a huge portion of it is devoted to movement, and especially to voluntary movement of the hands,” said Kelly Lambert, a professor of behavioral neuroscience at the University of Richmond in Virginia. Dr. Lambert, who studies effort-based rewards, said that she is interested in “the connection between the effort we put into something and the reward we get from it” and that she believes working with our hands might be uniquely gratifying. In some of her research on animals, Dr. Lambert and her colleagues found that rats that used their paws to dig up food had healthier stress hormone profiles and were better at problem solving compared with rats that were given food without having to dig. She sees some similarities in studies on people, which have found that a whole range of hands-on activities — such as knitting, gardening and coloring — are associated with cognitive and emotional benefits, including improvements in memory and attention, as well as reductions in anxiety and depression symptoms. These studies haven’t determined that hand involvement, specifically, deserves the credit. The researchers who looked at coloring, for example, speculated that it might promote mindfulness, which could be beneficial for mental health. Those who have studied knitting said something similar. “The rhythm and repetition of knitting a familiar or established pattern was calming, like meditation,” said Catherine Backman, a professor emeritus of occupational therapy at the University of British Columbia in Canada who has examined the link between knitting and well-being. © 2024 The New York Times Company

Keyword: Learning & Memory; Stress
Link ID: 29231 - Posted: 04.02.2024

By Marta Zaraska The renowned Polish piano duo Marek and Wacek didn’t use sheet music when playing live concerts. And yet onstage the pair appeared perfectly in sync. On adjacent pianos, they playfully picked up various musical themes, blended classical music with jazz and improvised in real time. “We went with the flow,” said Marek Tomaszewski, who performed with Wacek Kisielewski until Wacek’s death in 1986. “It was pure fun.” The pianists seemed to read each other’s minds by exchanging looks. It was, Marek said, as if they were on the same wavelength. A growing body of research suggests that might have been literally true. Dozens of recent experiments studying the brain activity of people performing and working together — duetting pianists, card players, teachers and students, jigsaw puzzlers and others — show that their brain waves can align in a phenomenon known as interpersonal neural synchronization, also known as interbrain synchrony. “There’s now a lot of research that shows that people interacting together display coordinated neural activities,” said Giacomo Novembre, a cognitive neuroscientist at the Italian Institute of Technology in Rome, who published a key paper on interpersonal neural synchronization last summer. The studies have come out at an increasing clip over the past few years — one as recently as last week — as new tools and improved techniques have honed the science and theory. They’re finding that synchrony between brains has benefits. It’s linked to better problem-solving, learning and cooperation, and even with behaviors that help others at a personal cost. What’s more, recent studies in which brains were stimulated with an electric current hint that synchrony itself might cause the improved performance observed by scientists. © 2024 the Simons Foundation.

Keyword: Attention
Link ID: 29229 - Posted: 03.30.2024

By Jake Buehler Much like squirrels, black-capped chickadees hide their food, keeping track of many thousands of little treasures wedged into cracks or holes in tree bark. When a bird returns to one of their many food caches, a particular set of nerve cells in the memory center of their brains gives a brief flash of activity. When the chickadee goes to another stash, a different combination of neurons lights up. These neural combinations act like bar codes, and identifying them may give key insights into how episodic memories — accounts of specific past events, like what you did on your birthday last year or where you’ve left your wallet — are encoded and recalled in the brain, researchers report March 29 in Cell. This kind of memory is challenging to study in animals, says Selmaan Chettih, a neuroscientist at Columbia University. “You can’t just ask a mouse what memories it formed today.” But chickadees’ very precise behavior provides a golden opportunity for researchers. Every time a chickadee makes a cache, it represents a single, well-defined moment logged in the hippocampus, a structure in the vertebrate brain vital for memory. To study the birds’ episodic memory, Chettih and his colleagues built a special arena made of 128 small, artificial storage sites. The team inserted small probes into five chickadees’ brains to track the electrical activity of individual neurons, comparing that activity with detailed recordings of the birds’ body positions and behaviors. A black-capped chickadee stores sunflower seeds in an artificial arena made of 128 different perches and pockets. These birds excel at finding their hidden food stashes. The aim of the setup was to see how their brain stores and retrieves the memory of each hidey-hole. Researchers closely observed five chickadees, comparing their caching behavior with the activity from nerve cells in their hippocampus, the brain’s memory center. © Society for Science & the Public 2000–2024.

Keyword: Learning & Memory
Link ID: 29228 - Posted: 03.30.2024

By Saugat Bolakhe For desert ants, Earth’s magnetic field isn’t just a compass: It may also sculpt their brains. Stepping outside their nest for the first time, young ants need to learn how to forage. The ants train partly by walking a loop near their nests for the first three days. During this stroll, they repeatedly pause and then pirouette to gaze back at the nest entrance, learning how to find their way back home. But when the magnetic field around the nest entrance was disturbed, ant apprentices couldn’t figure out where to look, often gazing in random directions, researchers report in the Feb. 20 Proceedings of the National Academy of Sciences. What’s more, the altered magnetic field seemed to affect connections between neurons in the learning and memory centers in the young ants’ brains. The finding “may make it easier to better understand how magnetic fields are sensed [in animals]” as scientists now know one way that magnetic fields can influence brain development, says Robin Grob, a biologist at the Norwegian University of Science and Technology in Trondheim. For years, scientists have known that some species of birds, fishes, turtles, moths and butterflies rely on Earth’s magnetic field to navigate (SN: 4/3/18). In 2018, Grob and other scientists added desert ants to that list. Young ants first appeared to use the magnetic field as a reference while learning how to use landmarks and the sun as guides to orient themselves in the right direction to gaze back toward the nest with its small, hard-to-see entrance. However, knowing where in the brain magnetic cues are processed has proved challenging. © Society for Science & the Public 2000–2024.

Keyword: Animal Migration; Development of the Brain
Link ID: 29227 - Posted: 03.30.2024

By Angie Voyles Askham For Christopher Zimmerman, it was oysters: After a bout of nausea on a beach vacation, he could hardly touch the mollusks for months. For others, that gut-lurching trigger is white chocolate, margaritas or spicy cinnamon candy. Whatever the taste, most people know the feeling of not being able to stomach a food after it has caused—or seemed to cause—illness. That response helps us learn which foods are safe, making it essential for survival. But how the brain links an unpleasant gastric event to food consumed hours prior has long posed a mystery, says Zimmerman, who is a postdoctoral fellow in Ilana Witten’s lab at Princeton University. The time scale for this sort of conditioned food aversion is an order of magnitude different from other types of learning, which involve delays of only a few seconds, says Peter Dayan, director of computational neuroscience at the Max Planck Institute for Biological Cybernetics, who was not involved in the work. “You need to have something that bridges that gap in time” between eating and feeling ill, he says. A newly identified neuronal circuit can do just that. Neurons in the mouse brainstem that respond to drug-induced nausea reactivate a specific subset of cells in the animals’ central amygdala that encode information about a recently tasted food. And that reactivation happens with novel—but not familiar—flavors, according to work that Zimmerman presented at the annual COSYNE meeting in Lisbon last month. With new flavors, animals seem primed to recall a recent meal if they get sick, Zimmerman says. As he put it in his talk, “it suggests that the common phrase we associate with unexpected nausea, that ‘it must be something I ate,’ is literally built into the brain in the form of this evolutionarily hard-wired prior.” © 2024 Simons Foundation

Keyword: Learning & Memory; Evolution
Link ID: 29226 - Posted: 03.30.2024

By Catherine Offord Bone marrow transplants between mice can transmit symptoms and pathology associated with Alzheimer’s disease, according to a controversial study published today in Stem Cell Reports. Its authors found that healthy mice injected with marrow from a mouse strain carrying an extremely rare, Alzheimer’s-linked genetic mutation later developed cognitive problems and abnormal clumping of proteins in the brain. In claims that other scientists in the field have criticized as overstated, the team says its findings demonstrate “Alzheimer’s disease transmission” and support screening of human bone marrow, organ, and blood donors for mutations related to neurodegeneration. “The findings are not by any means conclusive,” says Lary Walker, a neuroscientist at Emory University. Although the team’s approach offers an interesting way to study potential causes of neurodegeneration, he says, “the mice do not have Alzheimer’s disease,” only certain symptoms that mimic those of the disorder and require further study. He and other scientists stress that the new findings should not deter people who medically need bone marrow or other transplants. Alzheimer’s is partly characterized by so-called plaques of beta amyloid, a fragment of a larger protein called APP, around cells in the brain. Although there are rare, early-onset versions of the disease driven by specific mutations in the gene coding for APP or related proteins, most cases arise in people over age 65 and don’t have a single known cause. Some research hints that in very unusual scenarios, Alzheimer’s could be transmitted via human tissue or medical equipment contaminated with disease-causing proteins. Earlier this year, for example, U.K. scientists described dementia and beta amyloid buildup in several people who had received injections of growth hormone from the brains of deceased donors. (The procedure was once a medical treatment for certain childhood disorders but was abandoned in the 1980s.)

Keyword: Alzheimers; Hormones & Behavior
Link ID: 29225 - Posted: 03.30.2024

By Max Kozlov Neurons (shown here in a coloured scanning electron micrograph) mend broken DNA during memory formation. Credit: Ted Kinsman/Science Photo Library When a long-term memory forms, some brain cells experience a rush of electrical activity so strong that it snaps their DNA. Then, an inflammatory response kicks in, repairing this damage and helping to cement the memory, a study in mice shows. The findings, published on 27 March in Nature1, are “extremely exciting”, says Li-Huei Tsai, a neurobiologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the work. They contribute to the picture that forming memories is a “risky business”, she says. Normally, breaks in both strands of the double helix DNA molecule are associated with diseases including cancer. But in this case, the DNA damage-and-repair cycle offers one explanation for how memories might form and last. It also suggests a tantalizing possibility: this cycle might be faulty in people with neurodegenerative diseases such as Alzheimer’s, causing a build-up of errors in a neuron’s DNA, says study co-author Jelena Radulovic, a neuroscientist at the Albert Einstein College of Medicine in New York City. This isn’t the first time that DNA damage has been associated with memory. In 2021, Tsai and her colleagues showed that double-stranded DNA breaks are widespread in the brain, and linked them with learning2. To better understand the part these DNA breaks play in memory formation, Radulovic and her colleagues trained mice to associate a small electrical shock with a new environment, so that when the animals were once again put into that environment, they would ‘remember’ the experience and show signs of fear, such as freezing in place. Then the researchers examined gene activity in neurons in a brain area key to memory — the hippocampus. They found that some genes responsible for inflammation were active in a set of neurons four days after training. Three weeks after training, the same genes were much less active. © 2024 Springer Nature Limited

Keyword: Learning & Memory; Genes & Behavior
Link ID: 29223 - Posted: 03.28.2024

By Ingrid Wickelgren You see a woman on the street who looks familiar—but you can’t remember how you know her. Your brain cannot attach any previous experiences to this person. Hours later, you suddenly recall the party at a friend’s house where you met her, and you realize who she is. In a new study in mice, researchers have discovered the place in the brain that is responsible for both types of familiarity—vague recognition and complete recollection. Both, moreover, are represented by two distinct neural codes. The findings, which appeared on February 20 in Neuron, showcase the use of advanced computer algorithms to understand how the brain encodes concepts such as social novelty and individual identity, says study co-author Steven Siegelbaum, a neuroscientist at the Mortimer B. Zuckerman Mind Brain Behavior Institute at Columbia University. The brain’s signature for strangers turns out to be simpler than the one used for old friends—which makes sense, Siegelbaum says, given the vastly different memory requirements for the two relationships. “Where you were, what you were doing, when you were doing it, who else [was there]—the memory of a familiar individual is a much richer memory,” Siegelbaum says. “If you’re meeting a stranger, there’s nothing to recollect.” The action occurs in a small sliver of a brain region called the hippocampus, known for its importance in forming memories. The sliver in question, known as CA2, seems to specialize in a certain kind of memory used to recall relationships. “[The new work] really emphasizes the importance of this brain area to social processing,” at least in mice, says Serena Dudek, a neuroscientist at the National Institute of Environmental Health Sciences, who was not involved in the study. © 2024 SCIENTIFIC AMERICAN,

Keyword: Attention; Learning & Memory
Link ID: 29222 - Posted: 03.28.2024

By Holly Barker Our understanding of memory is often summed up by a well-worn mantra: Neurons that fire together wire together. Put another way, when two brain cells simultaneously send out an impulse, their synapses strengthen, whereas connections between less active neurons slowly diminish. But there may be more to it, a new preprint suggests: To consolidate memories, synapses may also influence neighboring neurons by using a previously unknown means of communication. When synapses strengthen, they release a virus-like particle that weakens the surrounding cells’ connections, the new work shows. This novel form of plasticity may aid memory by helping some synapses to shout above the background neuronal hubbub, the researchers say. The mechanism involves the neuronal gene ARC, which is known to contribute to learning and memory and encodes a protein that assembles into virus-like capsids—protein shells that viruses use to package and spread their genetic material. ARC capsids enclose ARC messenger RNA and transfer it to nearby neurons, according to a 2018 study. This leads to an increase in ARC protein and, in turn, a decrease in the number of excitatory AMPA receptors at those cells’ synapses, the preprint shows. “ARC has this crazy virus-like biology,” says Jason Shepherd, associate professor of neurobiology at the University of Utah, who led the 2018 study and the new work. But how ARC capsids form and eject from neurons was unclear, he says. As it turns out, synaptic strengthening spurs ARC capsid release, according to the preprint. When neuronal connections strengthen, ARC capsids are packaged into vesicles, which then bubble out of neurons through their interactions with a protein called IRSp53. Surrounding cells absorb the vesicles containing ARC, which tamps down their synapses, the new work suggests. © 2024 Simons Foundation

Keyword: Learning & Memory
Link ID: 29209 - Posted: 03.23.2024

By Frances Vinall More than two-thirds of young children in Chicago could be exposed to lead-contaminated water, according to an estimate by the Johns Hopkins Bloomberg School of Public Health and the Stanford University School of Medicine. The research, published Monday in the journal JAMA Pediatrics, estimated that 68 percent of children under the age of 6 in Chicago are exposed to lead-contaminated drinking water. Of that group, 19 percent primarily use unfiltered tap water, which was associated with a greater increase in blood lead levels. “The extent of lead contamination of tap water in Chicago is disheartening — it’s not something we should be seeing in 2024,” lead author Benjamin Huynh, assistant professor of environmental health and engineering at the Johns Hopkins Bloomberg School of Public Health, said in a news release. The study suggested that residential blocks with predominantly Black and Hispanic populations were less likely to be tested for lead, but also disproportionately exposed to contaminated water. Gina Ramirez, Midwest regional lead of environmental health for the Natural Resources Defense Council, said she grew up in Chicago drinking bottled water, but now uses filtered water for her own family, because of a generational awareness of “not trusting my tap” to be safe. The study “confirmed my worst fears that children living in vulnerable populations in the city are the most impacted,” she said. “All children deserve to grow up in a healthy city, and to learn that something inside their home is impacting so many kids health and development is a huge wake-up call.”

Keyword: Neurotoxins; Development of the Brain
Link ID: 29207 - Posted: 03.23.2024

By Shaena Montanari When Nacho Sanguinetti-Scheck came across a seal study in Science in 2023, he saw it as confirmation of the “wild” research he had recently been doing himself. In the experiment, the researchers had attached portable, noninvasive electroencephalogram caps, custom calibrated to sense brain waves through blubber, to juvenile northern elephant seals. After testing the caps on five seals in an outdoor pool, the team attached the caps to eight seals free-swimming in the ocean. The results were striking: In the pool, the seals slept for six hours a day, but in the open ocean, they slept for just about two. And when seals were in REM sleep in the ocean, they flipped belly up and slowly spiraled downward, hundreds of meters below the surface. It was “one of my favorite papers of the past years,” says Sanguinetti-Scheck, a Harvard University neuroscience postdoctoral researcher who studies rodent behavior in the wild. “It’s just beautiful.” It was also the kind of experiment that needed to be done beyond the confines of a lab setting, he says. “You cannot see that in a pool.” Sanguinetti-Scheck is part of a growing cadre of researchers who champion the importance of studying animal behavior in the wild. Studying animals in the environment in which they evolved, these researchers say, can provide neuroscientific insight that is truly correlated with natural behavior. But not everyone agrees. In February, a group of about two dozen scientists and philosophers gathered in snowy, mountainous Terzolas, Italy, to wrestle with what, exactly, “natural behavior” means. “People don’t really think, ‘Well, what does it mean?’” says Mateusz Kostecki, a doctoral student at Nencki Institute of Experimental Biology in Poland. He helped organize the four-day workshop as “a good occasion to think critically about this trend.” © 2024 Simons Foundation

Keyword: Evolution; Sleep
Link ID: 29205 - Posted: 03.21.2024

By Claudia López Lloreda Loss of smell, headaches, memory problems: COVID-19 can bring about a troubling storm of neurological symptoms that make everyday tasks difficult. Now new research adds to the evidence that inflammation in the brain might underlie these symptoms. Not all data point in the same direction. Some new studies suggest that SARS-CoV-2, the virus that causes COVID-19, directly infects brain cells. Those findings bolster the hypothesis that direct infection contributes to COVID-19-related brain problems. But the idea that brain inflammation is key has gotten fresh support: one study, for example, has identified specific brain areas prone to inflammation in people with COVID-191. “The whole body of literature is starting to come together a little bit more now and give us some more concrete answers,” says Nicola Fletcher, a neurovirologist at University College Dublin. Immunological storm When researchers started looking for a culprit for the brain problems caused by COVID-19, inflammation quickly became a key suspect. That’s because inflammation — the flood of immune cells and chemicals that the body releases against intruders — has been linked to the cognitive symptoms caused by other viruses, such as HIV. SARS-CoV-2 stimulates a strong immune response throughout the body, but it was unclear whether brain cells themselves contributed to this response and, if so, how. Helena Radbruch, a neuropathologist at the Charité – Berlin University Medicine, and her colleagues looked at brain samples from people who’d died of COVID-19. They didn’t find any cells infected with SARS-CoV-2. But they did find these people had more immune activity in certain brain areas than did people who died from other causes. This unusual activity was noticeable in regions such as the olfactory bulb, which is involved in smell, and the brainstem, which controls some bodily functions, such as breathing. It was seen only in the brains of people who had died soon after catching the virus. © 2024 Springer Nature Limited

Keyword: Learning & Memory; Attention
Link ID: 29202 - Posted: 03.21.2024

By Tomasz Nowakowski, Karthik Shekhar Diverse neurons and their equally diverse circuits are the foundation of the brain’s remarkable ability to process information, store memories, regulate behavior and enable conscious thought. High-throughput, single-cell profiling technologies have made it possible to classify these cells more comprehensively than ever before, offering a 360-degree view of the sheer magnitude of neural diversity in the mammalian brain. A recent effort to define the complete set of transcriptomic cell types in the adult whole mouse brain, for example, defined roughly 5,000 distinct cell types distributed across dozens of brain areas. This landmark accomplishment is a critical step toward integrating information about function and connectivity, and extending similar efforts to the adult human brain. But this impressive gestalt conveys little, if any, information about how such diversity arises and develops in the first place. Single-cell atlases developed to date have been limited to a few points in time, focusing largely on the endpoint of neural development. How is this exquisite panoply of neurons generated and organized into precise and orderly circuits that last a lifetime? Providing the answer is the central task of developmental neuroscience. We want to understand the many transitions that unfold — where cells come from, the paths they take, and when terminal cell states emerge. The comprehensive nature of single-cell technologies offers tremendous promise for defining cell types and reconstructing the trajectories of gene expression that underlie their differentiation. Initial efforts to apply these technologies to development, including in the prenatal human brain, hint at the insights these approaches can bring. Single-cell transcriptomics has helped map the diversity of neural progenitor cells, for example, most notably identifying progenitors that are expanded in humans, and their associated molecular adaptations. Further insights into development will require methods that reveal the specific history of every neuron type, including those that can more densely sample brain cells’ trajectories over time and novel approaches for tracking fate transitions in individual cells. These discoveries will in turn help us to understand neurodevelopmental conditions, many of which are associated with genomic variation, and neurological disorders, such as brain tumors. © 2024 Simons Foundation

Keyword: Development of the Brain
Link ID: 29198 - Posted: 03.19.2024