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

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

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

Keyword: Miscellaneous
Link ID: 29693 - Posted: 03.05.2025

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

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

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

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

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

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

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

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

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

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

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

Keyword: Alzheimers
Link ID: 29687 - Posted: 03.01.2025

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

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

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

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

Vicki Hird Does a worm feel pain if it gets trodden on? Does a fly ache when its wings are pulled off? Is an ant happy when it finds a food source? If so, they may be sentient beings, which means they can “feel”, a bit or a lot, like we do. Invertebrate sentience is becoming an ever livelier topic of debate and with new science we are getting new insights. But Dr Andrew Crump at the Royal Veterinary College, who helped ensure that new UK laws recognising animal sentience were amended to include large cephalopod molluscs and decapod crustaceans – octopuses, lobsters, crabs to you and me – says this is not at all straightforward. Nervous systems are hugely complex, and identifying consciousness and sentience – and not just automatic pain reflexes – is hard. Are responses or reactions you see from an animal – be it a wolf or a wolf ant – feelings or just automatic reflexes? Crump and his colleagues found that bees, for example, were not simple stimulus-response robots, but reacted to stimuli in sophisticated, context-dependent ways. They were found to learn colour cues for their decisions on feeding – choosing painful overheated sugars they previously avoided when non-heated options had a low sugar concentration. So they made trade-offs by processing in the brain then modifying their behaviour. In fact, new research has shown that many responses in the larger invertebrates were complex, long-lasting, and pretty consistent with criteria for pain that had been produced initially for vertebrates such as rats. Octopuses, for example, can perform amazing feats of learning to avoid painful environments and choose painkilling environments. All this establishes and quantifies “feelings” in beings that are very different from us. The work of Crump and other scientists meant that the Animal Welfare (Sentience) Act 2022 recognised for the first time in UK law (vertebrate sentience was previously covered by EU regulation) that certain invertebrates can “feel”, requiring modifications to their treatment in areas such as farming and research. © 2025 Guardian News & Media Limited

Keyword: Pain & Touch; Evolution
Link ID: 29684 - Posted: 02.26.2025

By Ellen Barry The Food and Drug Administration has taken a crucial step toward expanding access to the antipsychotic medication clozapine, the only drug approved for treatment-resistant schizophrenia, among the most devastating of mental illnesses. The agency announced on Monday that it was eliminating a requirement that patients submit blood tests before their prescriptions can be filled. Clozapine, which was approved in 1989, is regarded by many physicians as the most effective available treatment for schizophrenia, and research shows that the drug significantly reduces suicidal behavior. Clozapine is also associated with a rare side effect called neutropenia, a drop in white blood cell counts that, in its most severe form, can be life-threatening. In 2015, federal regulators imposed a regimen known as risk evaluation and mitigation strategies, or REMS, that required patients to submit to weekly, biweekly and monthly blood tests that had to be uploaded onto a database and verified by pharmacists. Physicians have long complained that, as a result, clozapine is grossly underutilized. Dr. Frederick C. Nucifora, director of the Adult Schizophrenia Clinic at the Johns Hopkins School of Medicine, said he believed that around 30 percent of patients with schizophrenia would benefit from clozapine — far more than the 4 percent who currently take it. “I have had many patients who were doing terribly, who struggled to function outside the hospital, and cycled through many medications,” he said. “If they go on clozapine, they really tend to not be hospitalized again. I’ve had people go on to finish college and work. It’s quite remarkable.” © 2025 The New York Times Company

Keyword: Schizophrenia
Link ID: 29683 - Posted: 02.26.2025

By Lydia Denworth When Mala Murthy and Sebastian Seung of Princeton University saw high-resolution 2D electron microscope images in a 2018 Cell paper, they decided to try to build a fruit fly connectome with that dataset. Funded by the U.S. National Institutes of Health BRAIN Initiative, Murthy and Seung used the electron microscopy data to launch the work that resulted in FlyWire, a nine-paper package published in Nature in October 2024. The work made international headlines for its novelty and ambition. Not long ago, the length of the author list on the flagship FlyWire paper also would have been newsworthy: 46 researchers, including Murthy, Seung and first author Sven Dorkenwald. Neuroscience research has long been driven by individual labs and individual investigators, but today it is increasingly becoming a team sport similar to the FlyWire work—a 2024 preprint describing a study of hundreds of thousands of neuroscience papers published worldwide between 2001 and 2022 found a consistent rise in the number of authors per paper in nearly every country examined. There were 66 Nature Neuroscience papers in 2023 that had double-digit author counts, with the longest author list for that year comprising 209 names. The causes of this shift are related to technology breakthroughs that have allowed for the generation of massive datasets, as well as the general maturation of neuroscience, which is catching up with the large-scale, collaborative efforts put forth in other fields. The dual landmark papers in 2001 revealing the first draft of the Human Genome Project boasted 249 authors (in Nature) and 274 authors (in Science), and a fruit fly genome paper published in 2015 had more than 1,000. In physics, a 2015 paper providing an estimate of the mass of the Higgs boson listed more than 5,000 authors, thought to be a record. But researchers say long author lists are also raising questions about what kind of work is most productive for neuroscience and how to best parcel out credit. A stack of author names can diffuse “responsibility for what’s in the paper,” says neuroscientist J. Anthony Movshon of New York University. “We’re going to a place where it’s very hard to establish whose work you’re actually reading.” © 2025 Simons Foundation

Keyword: Miscellaneous
Link ID: 29682 - Posted: 02.26.2025

By Fred Schwaller Andrea West remembers the first time she heard about a new class of migraine medication that could end her decades of pain. It was 2021 and she heard a scientist on the radio discussing the promise of gepants, a class of drug that for the first time seemed to prevent migraine attacks. West followed news about these drugs closely, and when she heard last year that atogepant was approved for use in the United Kingdom, she went straight to her physician. West had endured migraines for 70 years. Since she started taking the drug, she hasn’t had one. “It’s marvellous stuff. It’s genuinely changed my life,” she says. For ages, the perception of migraine has been one of suffering with little to no relief. In ancient Egypt, physicians strapped clay crocodiles to people’s heads and prayed for the best. And as late as the seventeenth century, surgeons bored holes into people’s skulls — some have suggested — to let the migraine out. The twentieth century brought much more effective treatments, but they did not work for a significant fraction of the roughly one billion people who experience migraine worldwide. Now there is a new sense of progress running through the field, brought about by developments on several fronts. Medical advances in the past few decades — including the approval of gepants and related treatments — have redefined migraine as “a treatable and manageable condition”, says Diana Krause, a neuropharmacologist at the University of California, Irvine. At the same time, research is leading to a better understanding about the condition — and pointing to directions for future work. Studies have shown, for example, that migraine is a broad phenomenon that originates in the brain and can manifest in many debilitating symptoms, including light sensitivities and aura, brain fog and fatigue. “I used to think that disability travels with pain, and it’s only when the pain gets severe that people are impaired. That’s not only false, but we have treatments to do something about it,” says Richard Lipton, a neurologist at the Albert Einstein College of Medicine in New York City. © 2025 Springer Nature Limited

Keyword: Pain & Touch
Link ID: 29681 - Posted: 02.22.2025

Aaron Priester Traumatic brain injury is a leading cause of death and disability in the world. Blunt force trauma to the brain, often from a bad fall or traffic accident, accounts for the deaths of over 61,000 Americans each year. Over 80,000 will develop some long-term disability. While much of the physical brain damage occurs instantly – called the primary stage of injury – additional brain damage can result from the destructive chemical processes that arise in the body minutes to days to weeks following initial impact. Unlike the primary stage of injury, this secondary stage could potentially be prevented by targeting the molecules driving damage. I am a materials science engineer, and my colleagues and I are working to design treatments to neutralize the harm of secondary traumatic brain injury and reduce neurodegeneration. We designed a new material that could target and neutralize brain-damaging molecules in mice, improving their cognitive recovery and offering a potential new treatment for people. The primary stage of traumatic brain injury can severely damage and even destroy the blood-brain barrier – an interface protecting the brain by limiting what can enter it. Disruption of this barrier triggers damaged neurons or the immune system to release certain chemicals that result in destructive biochemical processes. One process called excitotoxicity occurs when too many calcium ions are allowed into neurons, activating enzymes that fragment DNA and damage cells, causing death. Another process, neuroinflammation, results from the activation of cells called microglia that can trigger inflammation in damaged areas of the brain. © 2010–2025, The Conversation US, Inc.

Keyword: Brain Injury/Concussion
Link ID: 29680 - Posted: 02.22.2025

By Bill Newsome What paper changed your life?: Activity of superior colliculus in behaving monkey. II. Effect of attention on neuronal responses. M.E. Goldberg and R.H. Wurtz Journal of Neurophysiology (1972) In 1972, Mickey Goldberg and Bob Wurtz published a quadrilogy of papers in the Journal of Neurophysiology—yes, you could do that in those days—on the physiological activity of single superior colliculus neurons in alert monkeys trained to perform simple eye fixation and eye movement tasks. The experiments revealed a rich variety of sensory and motor signals: Some neurons fired at the onset of a visual stimulus; others showed bursts of activity immediately prior to the eye movement. The researchers found that visually evoked activity differed depending on whether the monkey ultimately used the stimulus as a target for a saccadic eye movement. The neural response to the visual stimulus was stronger and continued until the time of the eye movement, forming a sort of temporal bridge between stimulus and evoked behavioral response. This bridge was alluring because it hinted at intermediate processes—perhaps the stuff of cognition—between sensory input and behavioral output. But it was also mysterious, in that no models existed for how such activity might be initiated and maintained until the behavioral response. These papers were revelatory to me because they pointed toward a mechanistic physiological understanding of such complex cognitive functions as attention. I was particularly fascinated by the second paper in the series of four, which dug into that mystery. Goldberg and Wurtz explicitly made a suggestive leap from physiology to psychology: “[Because] we can infer that the monkey attended to the stimulus when he made a saccade to it, the enhancement can be viewed as a neurophysiological event related to the psychological phenomenon of attention.” They also issued appropriate caveats, noting that “the unitary behavioral concept” of attention “may not have a single physiological mechanism.” h. © 2025 Simons Foundation

Keyword: Vision; Attention
Link ID: 29679 - Posted: 02.22.2025

Nell Greenfieldboyce Putting the uniquely human version of a certain gene into mice changed the way that those animals vocalized to each other, suggesting that this gene may play a role in speech and language. Mice make a lot of calls in the ultrasonic range that humans can't hear, and the high-frequency vocalizations made by the genetically altered mice were more complex and showed more variation than those made by normal mice, according to a new study in the journal Nature Communications. The fact that the genetic change produced differences in vocal behavior was "really exciting," says Erich Jarvis, a scientist at Rockefeller University in New York who worked on this research. Still, he cautioned, "I don't think that one gene is going to be responsible — poof! — and you've got spoken language." For years, scientists have been trying to find the different genes that may have been involved in the evolution of speech, as language is one of the key features that sets humans apart from the rest of the animal kingdom. "There are other genes implicated in language that have not been human-specific," says Robert Darnell, a neuroscientist and physician at Rockefeller University, noting that one gene called FOXP2 has been linked to speech disorders. He was interested in a different gene called NOVA1, which he has studied for over two decades. NOVA1 is active in the brain, where it produces a protein that can affect the activity of other genes. NOVA1 is found in living creatures from mammals to birds, but humans have a unique variant. Yoko Tajima, a postdoctoral associate in Darnell's lab, led an effort to put this variant into mice, to see what effect it would have. © 2025 npr

Keyword: Language; Genes & Behavior
Link ID: 29678 - Posted: 02.19.2025

By Moises Velasquez-Manoff When President Trump announced plans to impose tariffs on Mexico and Canada, one of his stated rationales was to force those countries to curb the flow of fentanyl into the United States. In fiscal year 2024, United States Customs and Border Protection seized nearly 22,000 pounds of pills, powders and other products containing fentanyl, down from 27,000 pounds in the previous fiscal year. More than 105,000 people died from overdoses, three-quarters of them from fentanyl and other opioids, in 2023. It doesn’t take much illicit fentanyl — said to be about 50 times as powerful as heroin and 100 times as powerful as morphine — to cause a fatal overdose. In my article for the magazine, I note that one of the many tragedies of the opioid epidemic is that a proven treatment for opioid addiction, a drug called buprenorphine, has been available in the United States for more than two decades yet has been drastically underprescribed. Tens of thousands of lives might have been saved if it had been more widely used earlier. In his actions and rhetoric, Trump seems to emphasize the reduction of supply as the answer to the fentanyl crisis. But Mexico’s president, Claudia Sheinbaum, has pointed to American demand as a driver of the problem. Indeed, if enough opioid users in the United States ended up receiving buprenorphine and other effective medication-based treatments, perhaps that demand for illicit opioids like fentanyl could be reduced. Devastating losses. Drug overdose deaths, largely caused by the synthetic opioid drug fentanyl, reached record highs in the United States in 2021. Here’s what you should know to keep your loved ones safe: Understand fentanyl’s effects. Fentanyl is a potent and fast-acting drug, two qualities that also make it highly addictive. A small quantity goes a long way, so it’s easy to suffer an overdose. With fentanyl, there is only a short window of time to intervene and save a person’s life during an overdose. Stick to licensed pharmacies. Prescription drugs sold online or by unlicensed dealers marketed as OxyContin, Vicodin and Xanax are often laced with fentanyl. Only take pills that were prescribed by your doctor and came from a licensed pharmacy. © 2025 The New York Times Company

Keyword: Drug Abuse
Link ID: 29677 - Posted: 02.19.2025

By Laura Sanders Depression can affect not just the mind, but the body, too. Inner experiences of mental struggles are private. But in this episode, Jon Nelson and another volunteer, Amanda, let listeners in. Woven into their stories is a brief history of deep brain stimulation, the experimental treatment that involves permanent brain implants. You’ll hear how that research — with its ups and downs — carried the experiments to where they are today. Laura Sanders: This episode deals with mental illness, depression, and suicide. Please listen with care. Previously on The Deep End: Support Science Today. Barbara: He would be up in bed with the lights out or watching like endless hours of television and it was very unpredictable and then there’s a whole life going on downstairs. Jon: That isolation, there’s a little bit of lying involved because you just wanna get out of things, right? Mayberg: I think part of why this kind of treatment resistant depression is so painful and so associated with high rates of suicide, is that you’re suffering. You know exactly what you’re trying to get away from and you can’t move. And if you do move, it follows you. There’s no relief. Jon: I’d be the one standing up in front of everybody leading the champagne toast, and then I’d be driving home and wanting to slam my car into a tree. Sanders: Today we’re going to get into some heavy stuff, but there’s light at the end, I promise. We’re going to pull back the curtain on what depression can do to the body and to the brain. Maybe you know that feeling firsthand. If you don’t, you probably know somebody who does. You’ll also hear the backstory of some people who volunteered for the experiment and the backstory of the science itself. I’m Laura Sanders. Welcome to The Deep End. © Society for Science & the Public 2000–2025.

Keyword: Depression
Link ID: 29676 - Posted: 02.19.2025

Jon Hamilton People who inherit one very rare gene mutation are virtually guaranteed to develop Alzheimer's before they turn 50. Except for Doug Whitney. "I'm 75 years old, and I think I'm functioning fairly well," says Whitney, who lives near Seattle. "I'm still not showing any of the symptoms of Alzheimer's." Now a team of scientists is trying to understand how Whitney's brain has defied his genetic destiny. "If we are able to learn what is causing the protection here, then we could translate that to therapeutic approaches and apply that to the more common forms of the disease," says Dr. Jorge Llibre-Guerra, an assistant professor of neurology at Washington University School of Medicine in St. Louis. One possibility is high levels of heat shock proteins found in Whitney's brain, the team reports in the journal Nature Medicine. There are hints that these proteins can prevent the spread of a toxic protein that is one of the hallmarks of Alzheimer's, Llibre-Guerra says. A genetic surprise Early-onset Alzheimer's is everywhere in Whitney's family. His mother and 11 of her 13 siblings all had the disease by about age 50. "None of them lasted past 60," Whitney says. Whitney's wife, Ione, saw this up close. "We went home for Thanksgiving, and his mom couldn't remember the pumpkin pie recipe," she says. "A year later when we went back, she was already wandering off and not finding her way back home." © 2025 npr

Keyword: Alzheimers; Genes & Behavior
Link ID: 29675 - Posted: 02.19.2025