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 Lucy Cooke When Frans de Waal was a psychology student at Nijmegen University (renamed in 2004 to Radboud University), in the Netherlands, he was tasked with looking after the department’s resident chimpanzees—Koos and Nozem. De Waal couldn’t help but notice how his charges became sexually aroused in the presence of his fellow female students. So, one day, de Waal decided to don a skirt, a pair of heels, and speak “in a high-pitched voice” to test their response. The chimps remained resolutely unstimulated by de Waal’s drag act, leading the young scientist to conclude there must be more to primate sexual discrimination than previously thought. De Waal died from stomach cancer on March 14 at his home in Georgia. He was 75. One of de Waal’s first forays into scientific experimentation demonstrates the playful curiosity and taboo-busting that underscored his extraordinary career as a primatologist. He was the recipient of numerous high-profile awards from the prestigious E.O. Wilson Literary Science Award to the Ig Nobel Prize—a satirical honor for research that makes people laugh and think. De Waal won the latter, with equal pride, for co-authoring a paper on chimpanzees’ tendency to recognize bums better than faces. It was this combination of humor, compassion, and iconoclastic thinking that drew me to his work. I first met him through his popular writing. The acclaimed primatologist was author of hundreds of peer-reviewed academic papers, but he was also that rare genius who could translate the complexities of his research into a highly digestible form, readily devoured by the masses. He was the author of 16 books, translated into over 20 languages. His public lectures were laced with deadpan humor, and a joy to attend. He saw no tension between being taken seriously as a pioneering scientist and hosting a Facebook page devoted to posting funny animal content. De Waal just loved watching animals. He was, by his own admission, a born naturalist. Growing up in a small town in southern Netherlands, he’d bred stickleback fish and raised jackdaw birds. So, it was only natural he’d wind up scrutinizing animal behavior for a career. What set de Waal’s observations apart was his ability to do so with fresh eyes. Where others could only see what they expected to see, de Waal managed to study primates outside of the accepted paradigms of the time. © 2024 NautilusNext Inc.,

Keyword: Evolution; Emotions
Link ID: 29208 - 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 Nora Bradford Early in her research, forensic anthropologist Alexandra Morton-Hayward came across a paper describing a 2,500-year-old brain preserved in a severed skull. The paper referenced another preserved brain. She found another. And another. By the time she’d reached 12, she noticed all of the papers described the brains as a unique phenomenon. She kept digging. Naturally preserved brains, it turns out, aren’t so rare after all, Morton-Hayward, of the University of Oxford, and colleagues report March 20 in Proceedings of the Royal Society B. The researchers have built an archive of 4,400 human brains preserved in the archaeological record, some dating back nearly 12,000 years. The archive includes brains from North Pole explorers, Inca sacrificial victims and Spanish Civil War soldiers. Because the brains have been described as exceptionally rare, little research has been done on them. “If they’re precious, one-of-a-kind materials, then you don’t want to analyze them or disturb them,” Morton-Hayward says. Less than 1 percent of the archive has been investigated. Matching where the brains were found with historical climate patterns hints at what might keep the brains from decaying. Over a third of the samples persisted because of dehydration; others were frozen or tanned. Depending on the conditions, the brains’ texture could be anywhere from dry and brittle to squishy and tofulike. © Society for Science & the Public 2000–2024.

Keyword: Brain imaging
Link ID: 29206 - Posted: 03.21.2024

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 Rachel Nuwer In 2011, archaeologists in the Netherlands discovered an ancient pit filled with 86,000 animal bones at a Roman-Era farmstead near the city of Utrecht. It fell to Martijn van Haasteren, an archaeozoologist at the Cultural Heritage Agency of the Netherlands, to sort through them. Deep into the cataloging process, Mr. van Haasteren was cleaning the mud from yet another bone when something unexpected happened: Hundreds of black specks the size of poppy seeds came pouring out from one end. The specks turned out to be seeds of black henbane, a potently poisonous member of the nightshade family that can be medicinal or hallucinogenic depending on the dosage. The bone — hollowed-out and sealed with a tar plug — was an ancient stash pouch that had kept the seeds safe for some 1,900 years. Researchers determined that the bone was deposited in the pit somewhere between A.D. 70 and 100 — a time when the Netherlands represented the Roman Empire’s northern border. Parts of the container were smooth, suggesting frequent handling. This “very special” discovery provides the first definitive evidence that Indigenous people living in such a far-flung Roman province had knowledge of black henbane’s powerful properties, said Maaike Groot, an archaeozoologist at the Free University of Berlin and a co-author of a paper published in the journal Antiquity last month describing the finding. At the time that the original owner stuffed the container full of seeds, the properties of black henbane were already well known in Rome. Writings by Pliny the Elder and others testify to the medicinal use of black henbane seeds and leaves, but warn that an overindulgence will result in mind-altering effects. The plant was mostly used during Roman times as an ointment for pain relief, although some sources also reference smoking its seeds or adding its leaves to wine. It seems its psychedelic effects came to the fore in the Middle Ages, when black henbane became associated “with witches and summoning demons,” said Mr. van Haasteren, who is a co-author of the paper. © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29204 - Posted: 03.21.2024

By Viviane Callier Biologists have often wondered what would happen if they could rewind the tape of life’s history and let evolution play out all over again. Would lineages of organisms evolve in radically different ways if given that opportunity? Or would they tend to evolve the same kinds of eyes, wings, and other adaptive traits because their previous evolutionary histories had already sent them down certain developmental pathways? A new paper published in Science this February describes a rare and important test case for that question, which is fundamental to understanding how evolution and development interact. A team of researchers at the University of California, Santa Barbara happened upon it while studying the evolution of vision in an obscure group of mollusks called chitons. In that group of animals, the researchers discovered that two types of eyes—eyespots and shell eyes—each evolved twice independently. A given lineage could evolve one type of eye or the other, but never both. Intriguingly, the type of eye that a lineage had was determined by a seemingly unrelated older feature: the number of slits in the chiton’s shell armor. This represents a real-world example of “path-dependent evolution,” in which a lineage’s history irrevocably shapes its future evolutionary trajectory. Critical junctures in a lineage act like one-way doors, opening up some possibilities while closing off other options for good. “This is one of the first cases [where] we’ve actually been able to see path-dependent evolution,” said Rebecca Varney, a postdoctoral fellow in Todd Oakley’s lab at UCSB and the lead author of the new paper. Although path-dependent evolution has been observed in some bacteria grown in labs, “showing that in a natural system was a really exciting thing to be able to do.” © 2024 NautilusNext Inc.,

Keyword: Vision; Evolution
Link ID: 29203 - 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 Sara Reardon For the past few decades, scientists studying candidate antidepressant drugs have had a convenient animal test: how long a rodent dropped in water keeps swimming. Invented in 1977, the forced swim test (FST) hinged on the idea that a depressed animal would give up quickly. It seemed to work: Antidepressants and electroconvulsive therapy often made the animal try harder. The test remains popular, appearing in about 600 papers per year. But researchers have recently begun to question the assumption that the test really gauges depression and is a good predictor of human responses to drugs. Opposition to the test is snowballing, driven in part by concerns it is unnecessarily cruel given its spotty results. This month, following similar moves by the Australian government, the United Kingdom’s Home Office announced it would require U.K. researchers to justify the use of the test and would encourage other U.K. ministries that regulate animal research to “completely eliminate” it. Such changes add urgency to efforts to develop better animal tests of psychiatric drugs’ effects. Neurobiologist Anne Mallien of Heidelberg University, who studies the effects of the FST on rodents’ well-being, says she would love to have other options. “The thing is that alternatives are somewhat missing.” In the FST, researchers put a mouse or rat in a container of water, usually for about 5 minutes, and time how long it exerts itself before giving up and simply floating. Rodents will often swim longer when treated with psychiatric drugs. “But does that mean something for [human medicine]?” says neuroscientist Carole Morel at the Icahn School of Medicine at Mount Sinai. The rodents’ high stress levels could complicate the results, and an intelligent animal quickly learns that researchers will rescue it once it gives up.

Keyword: Depression; Animal Rights
Link ID: 29201 - Posted: 03.21.2024

By Alex Traub Frans de Waal, who used his study of the inner lives of animals to build a powerful case that apes think, feel, strategize, pass down culture and act on moral sentiments — and that humans are not quite as special as many of us like to think — died on Thursday at his home in Stone Mountain, Ga. He was 75. The cause was stomach cancer, his wife, Catherine Marin, said. A psychologist at Emory University in Atlanta and a research scientist at the school’s Yerkes National Primate Research Center, Professor de Waal objected to the common usage of the word “instinct.” He saw the behavior of all sentient creatures, from crows to persons, existing on the same broad continuum of evolutionary adaptation. “Uniquely human emotions don’t exist,” he argued in a 2019 New York Times guest essay. “Like organs, the emotions evolved over millions of years to serve essential functions.” The ambition and clarity of his thought, his skills as a storyteller and his prolific output made him an exceptionally popular figure for a primatologist — or a serious scientist of any kind. Two of his books, “Are We Smart Enough to Know How Smart Animals Are?” (2016) and “Mama’s Last Hug: Animal Emotions and What They Tell Us About Ourselves” (2019), were best sellers. In the mid-1990s, when he was speaker of the House, Newt Gingrich put Professor de Waal’s first book, “Chimpanzee Politics” (1982), on a reading list for Republican House freshmen. The novelists Claire Messud and Sigrid Nunez both told The New York Times that they liked his writing. The actress Isabella Rossellini hosted a talk with him in Brooklyn last year. Major philosophers like Christine Korsgaard and Peter Singer wrote long, considered responses to his ideas. © 2024 The New York Times Company

Keyword: Evolution; Emotions
Link ID: 29200 - Posted: 03.21.2024

By Elizabeth Landau Electroconvulsive therapy has a public relations problem. The treatment, which sends electric currents through the brain to induce a brief seizure, has barbaric, inhumane connotations — for example, it was portrayed as a sadistic punishment in the film One Flew Over the Cuckoo’s Nest. But for patients with depression that does not improve with medications, electroconvulsive therapy (ECT) can be highly effective. Studies have found that some 50% to 70% of patients with major depressive disorder see their symptoms improve after a course of ECT. In comparison, medications aimed at altering brain chemistry help only 10% to 40% of depression patients. Still, even after many decades of use, scientists don’t know how ECT alters the brain’s underlying biology. Bradley Voytek, a neuroscientist at the University of California, San Diego, said a psychiatrist once told him that the therapy “reboots the brain” — an explanation he found “really unsatisfying.” Recently, Voytek and his collaborators paired their research into the brain’s electrical patterns with patient data to explore why inducing seizures has antidepressant effects. In two studies published last fall, the researchers observed that ECT and a related seizure therapy increased the unstructured background noise hiding behind well-defined brain waves. Neuroscientists call this background noise “aperiodic activity.” The authors suggested that induced seizures might help restore the brain’s balance of excitation and inhibition, which could have an overall antidepressant effect. “Every time that I talk to someone who’s not in this field about this work they’re like, ‘They still do that? They still use electroshock? I thought that was just in horror movies,’” said Sydney Smith, a graduate student in neuroscience in Voytek’s lab and the first author of the new studies. “Dealing with the stigma around it has become even more of a motivation to figure out how it works.” © 2024 Simons Foundation.

Keyword: Depression; Attention
Link ID: 29199 - Posted: 03.19.2024

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

By Gina Jiménez Being pregnant and giving birth changes a person’s brain, but the brain looks different depending on whether it’s examined during pregnancy or after a person gives birth, a recent study found. The research is helping disentangle some of the mysteries in the long-ignored field of maternal neuroscience. The study, published in January in Nature Neuroscience, followed more than 100 new mothers from near the end of their pregnancy until about three weeks on average after they had their baby. Previous research had examined birthing parents’ brain before they gave birth or during the postpartum period, but this study observed them both before and after birth, and it also took into account whether they had a vaginal birth or C-section. The findings reveal temporary changes in some brain regions and more permanent ones in a brain circuit that activates when people are not engaged in an active task and that is also involved in self-reflection and empathizing with others. The study has “ordered” some of the scientific disagreements in the field, says its senior author Susana Carmona, a neuroscience researcher now at Gregorio Marañón General University Hospital in Spain.* “It fills important gaps—that is why it’s novel,” says Joe Lonstein, a neuroscientist who studies animal parenting behaviors at Michigan State University but was not involved with the new paper. “There were things we just didn’t know about the timing of events.” Much of the scientific literature on pregnancy and postpartum neuroscience is only around a decade old. A 2016 study found that gray matter decreased in women after they had a baby for the first time, and the reductions persisted for at least six years after pregnancy. In contrast, other studies have observed that gray matter increases in the first weeks after people give birth. The new paper helps reconcile these results: the researchers found that women indeed lost gray matter during pregnancy and childbirth but got it back in most brain areas after they had their baby. © 2024 SCIENTIFIC AMERICAN,

Keyword: Sexual Behavior; Hormones & Behavior
Link ID: 29197 - Posted: 03.19.2024

By Julian E. Barnes New studies by the National Institutes of Health failed to find evidence of brain injury in scans or blood markers of the diplomats and spies who suffered symptoms of Havana syndrome, bolstering the conclusions of U.S. intelligence agencies about the strange health incidents. Spy agencies have concluded that the debilitating symptoms associated with Havana syndrome, including dizziness and migraines, are not the work of a hostile foreign power. They have not identified a weapon or device that caused the injuries, and intelligence analysts now believe the symptoms are most likely explained by environmental factors, existing medical conditions or stress. The lead scientist on one of the two new studies said that while the study was not designed to find a cause, the findings were consistent with those determinations. The authors said the studies are at odds with findings from researchers at the University of Pennsylvania, who found differences in brain scans of people with Havana syndrome symptoms and a control group Dr. David Relman, a prominent scientist who has had access to the classified files involving the cases and representatives of people suffering from Havana syndrome, said the new studies were flawed. Many brain injuries are difficult to detect with scans or blood markers, he said. He added that the findings do not dispute that an external force, like a directed energy device, could have injured the current and former government workers. The studies were published in The Journal of the American Medical Association on Monday alongside an editorial by Dr. Relman that was critical of the findings. © 2024 The New York Times Company

Keyword: Learning & Memory; Depression
Link ID: 29196 - Posted: 03.19.2024

By Heidi Ledford Two preliminary studies suggest that next-generation engineered immune cells show promise against one of the most feared forms of cancer. A pair of papers published on 13 March, one in Nature Medicine1 and the other in The New England Journal of Medicine2, describe the design and deployment of immune cells called chimeric antigen receptor T (CAR T) cells against glioblastoma, an aggressive and difficult-to-treat form of brain cancer. The average length of survival for people with this tumour is eight months. Both teams found early hints of progress using CAR T cells that target two proteins made by glioblastoma cells, thereby marking those cells for destruction. CAR T cells are currently approved for treating only blood cancers, such as leukaemia, and are typically engineered to home in on only one target. But these results add to mounting evidence that CAR T cells could be modified to treat a wider range of cancers. “It lends credence to the potential power of CAR T cells to make a difference in solid tumours, especially the brain,” says Bryan Choi, a neurosurgeon at Massachusetts General Hospital in Boston, and a lead author of the New England Journal of Medicine study. “It adds to the excitement that we might be able to move the needle.” Glioblastomas offer a formidable challenge. Fast-growing glioblastomas can mix with healthy brain cells, forming diffuse tumours that are difficult to remove surgically. Surgery, chemotherapy and radiation therapy are typically the only treatment options for these tumours, and tend to produce short-lived, partial responses. © 2024 Springer Nature Limited

Keyword: Neuroimmunology
Link ID: 29195 - Posted: 03.19.2024

By Elise Cutts In March 2019, on a train headed southwest from Munich, the neuroscientist Maximilian Bothe adjusted his careful grip on the cooler in his lap. It didn’t contain his lunch. Inside was tissue from half a dozen rattlesnake spinal cords packed in ice — a special delivery for his new research adviser Boris Chagnaud, a behavioral neuroscientist based on the other side of the Alps. In his lab at the University of Graz in Austria, Chagnaud maintains a menagerie of aquatic animals that move in unusual ways — from piranhas and catfish that drum air bladders to produce sound to mudskippers that hop around on land on two fins. Chagnaud studies and compares these creatures’ neuronal circuits to understand how new ways of moving might evolve, and Bothe was bringing his rattlesnake spines to join the endeavor. The ways that animals move are just about as myriad as the animal kingdom itself. They walk, run, swim, crawl, fly and slither — and within each of those categories lies a tremendous number of subtly different movement types. A seagull and a hummingbird both have wings, but otherwise their flight techniques and abilities are poles apart. Orcas and piranhas both have tails, but they accomplish very different types of swimming. Even a human walking or running is moving their body in fundamentally different ways. The tempo and type of movements a given animal can perform are set by biological hardware: nerves, muscle and bone whose functions are bound by neurological constraints. For example, vertebrates’ walking tempos are set by circuits in their spines that fire without any conscious input from the brain. The pace of that movement is dictated by the properties of the neuronal circuits that control them. For an animal to evolve a novel way of moving, something in its neurological circuitry has to change. Chagnaud wants to describe exactly how that happens. “In evolution, you don’t just invent the wheel. You take pieces that were already there, and you modify them,” he said. “How do you modify those components that are shared across many different species to make new behaviors?” © 2024 Simons Foundation.

Keyword: Evolution
Link ID: 29194 - Posted: 03.16.2024

By Esther Landhuis In January 2023, the US Food and Drug Administration (FDA) approved lecanemab — an antibody medication that decreases β-amyloid protein build-up in the brain — as a treatment for Alzheimer’s disease. Pivotal evidence came from a large, randomized trial of people with early-stage Alzheimer’s, which afflicts around 32 million people worldwide. By the end of that 18-month study1, patients in the placebo group scored on average 1.66 points worse than their performance at baseline on a standard dementia test, which assesses cognitive and functional changes over time through interviews with a patient and their caregiver. The mean score of treated participants, by comparison, worsened by 1.21 points — a 27% slowing of cognitive decline. But is this improvement meaningful for patients and their families? There are two major categories of drugs used to treat Alzheimer’s disease and other progressive conditions: symptomatic drugs, which treat the symptoms, and disease-modifying drugs, which target the root cause. Donepezil and rivastigmine, for example, are symptomatic drugs that boost the activity of chemicals in the brain to compensate for declines in cognitive and memory function caused by Alzheimer’s disease, but they cannot stop its progression. Lecanemab, developed jointly by Japanese pharmaceutical company Eisai and American biotechnology firm Biogen, targets the underlying issue of amyloid build-up in the brain, and in doing so, could fundamentally change the course of the disease. An important feature of disease-modifying drugs is that their benefits are cumulative. Studies of patients with multiple sclerosis, for example, have shown the benefits of starting disease-modifying drugs earlier in the course of the disease compared with later, including improved mortality rates and reduced disability in the long term. Being able to quantify how long a disease-modifying drug can delay or halt the progression of Alzheimer’s disease could change how researchers understand — and communicate — its benefits. © 2024 Springer Nature Limited

Keyword: Alzheimers
Link ID: 29193 - Posted: 03.16.2024

By Meghan Rosen Leakiness in the brain could explain the memory and concentration problems linked to long COVID. In patients with brain fog, MRI scans revealed signs of damaged blood vessels in their brains, researchers reported February 22 in Nature Neuroscience. In these people, dye injected into the bloodstream leaked into their brains and pooled in regions that play roles in language, memory, mood and vision. It’s the first time anyone’s shown that long COVID patients can have leaky blood brain barriers, says study coauthor Matthew Campbell, a geneticist at Trinity College Dublin in Ireland. That barrier, tightly knit cells lining blood vessels, typically keeps riffraff out of the brain, like bouncers guarding a nightclub. If the barrier breaks down, bloodborne viruses, cells and other interlopers can sneak into the brain’s tissues and wreak havoc, says Avindra Nath, a neurologist at the National Institutes of Health in Bethesda, Md. It’s too early to say definitively whether that’s happening in people with long COVID, but the new study provides evidence that “brain fog has a biological basis,” says Nath, who wasn’t involved with the work. That alone is important for patients, he says, because their symptoms may be otherwise discounted by physicians. For some people, brain fog can feel like a slowdown in thinking or difficulty recalling short-term memories, Campbell says. For example, “patients will go for a drive, and forget where they’re driving to.” That might sound trivial, he says, but it actually pushes people into panic mode. © Society for Science & the Public 2000–2024.

Keyword: Attention; Learning & Memory
Link ID: 29192 - Posted: 03.16.2024

By Jan Hoffman The death certificate for Ryan Bagwell, a 19-year-old from Mission, Texas, states that he died from a fentanyl overdose. His mother, Sandra Bagwell, says that is wrong. On an April night in 2022, he swallowed one pill from a bottle of Percocet, a prescription painkiller that he and a friend bought earlier that day at a Mexican pharmacy just over the border. The next morning, his mother found him dead in his bedroom. A federal law enforcement lab found that none of the pills from the bottle tested positive for Percocet. But they all tested positive for lethal quantities of fentanyl. “Ryan was poisoned,” Mrs. Bagwell, an elementary-school reading specialist, said. As millions of fentanyl-tainted pills inundate the United States masquerading as common medications, grief-scarred families have been pressing for a change in the language used to describe drug deaths. They want public health leaders, prosecutors and politicians to use “poisoning” instead of “overdose.” In their view, “overdose” suggests that their loved ones were addicted and responsible for their own deaths, whereas “poisoning” shows they were victims. “If I tell someone that my child overdosed, they assume he was a junkie strung out on drugs,” said Stefanie Turner, a co-founder of Texas Against Fentanyl, a nonprofit organization that successfully lobbied Gov. Greg Abbott to authorize statewide awareness campaigns about so-called fentanyl poisoning. “If I tell you my child was poisoned by fentanyl, you’re like, ‘What happened?’” she continued. “It keeps the door open. But ‘overdose’ is a closed door.” © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29191 - Posted: 03.16.2024

By Alejandra Manjarrez People wear gloves when making a snowman for a reason: Handling cold stuff can hurt. A new mouse study reveals what may be a key player in this response: a protein already known to enable sensory neurons in worms to detect cold. New evidence published this week in Nature Neuroscience confirms that this protein has the same function in mammals. “The paper is exciting,” says Theanne Griffith, a neuroscientist at the University of California, Davis who was not involved in the research. She notes that the protein, called GluK2, is found in the brain and has “traditionally been thought to play a major role in learning and memory.” The new work shows that elsewhere in the body, it has an unsuspected and “completely divergent role.” We perceive touch, pain, and temperature thanks to a system of nerves that extends throughout our bodies. Researchers have identified skin sensors that detect hot and warm stimuli. Cold sensors, though, have proved more challenging to find. Researchers have proposed various candidates but found limited and contradictory evidence for their function. An ion channel named TRPM8 is the exception. Famous for detecting the “cool” sensation of menthol, it also detects cold temperatures and helped earn its discoverers the Nobel Prize in Physiology or Medicine in 2021. “Nobody questions that TRPM8 is a cold sensor,” says sensory neurobiologist Félix Viana of the Institute for Neuroscience in Alicante, Spain. But it could not be the whole story. It works most efficiently at temperatures above roughly 10°C, and mice lacking the gene for TRPM8 can still detect very cold temperatures. A few years ago, University of Michigan neuroscientists Shawn Xu and Bo Duan and their colleagues found another candidate: a protein on certain sensory neurons in the tiny roundworm Caenorhabditis elegans that causes the animals to avoid temperatures between 17°C and 18°C, which are colder than their preferred temperatures. Preliminary data from that study hinted that the equivalent protein in mammals, GluK2, also allowed mice to sense cold.

Keyword: Pain & Touch
Link ID: 29190 - Posted: 03.16.2024