By Lauren J. Young Kimberly Chauche, a corporate secretary in Lincoln, Neb., says she’s always been overweight. When she was as young as five years old, her doctors started trying to figure out why. Since then her life has involved nutritionists and personal trainers, and eventually she sought therapists to treat her compulsive eating and weight-related anxiety. Yet answers never arrived, and solutions never lasted. At 43, Chauche was prescribed a weight-loss medi­cation called Wegovy—one of a new class of drugs that mimic a hormone responsible for insulin pro­duction. She took her first dose in March 2024, in­jecting it into herself with a needle. Within a couple of months she had lost almost 20 pounds, and that felt great. But the weight loss seemed like a bonus com­pared with a startling change in how she reacted to food. She noticed the shift almost immediately: One day her son was eating popcorn, a snack she could never resist, and she walked right past the bowl. “All of a sudden it was like some part of my brain that was always there just went quiet,” she says. Her eating habits improved, and her anxiety eased. “It felt almost surreal to put an injector against my leg and have happen in 48 hours what decades of intervention could not ac­complish,” she says. “If I had lost almost no weight, just to have my brain working the way it’s working, I would stay on this medication forever.” Chauche is hardly alone in her effusive descriptions of how Wegovy vanquished her intrusive thoughts about food—an experience increasingly referred to as the “quieting of food noise.” Researchers—some of whom ushered in the development of these blockbuster drugs—want to understand why. Among them is biochemist Svetlana Mojsov of the Rockefeller University, who has spent about 50 years investigating gut hormones that could be key to regulating blood glucose levels. In seeking potential treatments for type 2 diabetes, Mojsov ultimately focused on one hormone: glucagonlike peptide 1, or GLP-1. Her sequence of the protein in the 1980s became the initial template for drugs like Wegovy. The medications, called GLP-1 receptor agonists, use a synthetic version of the natural substance to activate the hormone’s receptors. The first ones arrived in 2005. In 2017 the U.S. Food and Drug Administration approved semaglutide—now widely known as Ozempic. © 2024 SCIENTIFIC AMERICAN,

Keyword: Obesity; Hormones & Behavior
Link ID: 29373 - Posted: 06.26.2024

By Meghan Rosen Float like a butterfly, sniff out cancer like a bee? Honeybees can detect the subtle scents of lung cancer in the lab — and even the faint aroma of disease that can waft from a patient’s breath. Inspired by the insects’ exquisite olfactory abilities, scientists hooked the brains of living bees up to electrodes, passed different scents under the insects’ antennae and then recorded their brain signals. “It’s very clear — like day and night — whether [a bee] is responding to a chemical or not,” says Debajit Saha, a neural engineer at Michigan State University in East Lansing. Different odors sparked recognizable brain activity patterns, a kind of neural fingerprint for scent, Saha and colleagues report June 4 in Biosensors and Bioelectronics. One day, he says, doctors might be able to use honeybees in cancer clinics as living sensors for early disease detection. Electronic noses, or e-noses, and other types of mechanical odor-sensing equipment exist, but they’re not exactly the bee’s knees. When it comes to scent, Saha says, “biology has this ability to differentiate between very, very similar mixtures, which no other engineered sensors can do.” Scent is an important part of how many insect species communicate, says chemical ecologist Flora Gouzerh of the French National Research Institute for Sustainable Development in Montpellier. For them, “it’s a language,” she says. The idea that animal senses can get a whiff of disease is nothing new; doctors reported a case of a border collie and a Doberman sniffing out their owner’s melanoma in 1989. More recently, scientists have shown that dogs can detect COVID-19 cases by smelling people’s sweat (SN: 6/1/22). A lot of insects probably have disease-detecting abilities, too, Gouzerh says. Ants, for instance, can be trained to pick out the smell of cancer cells grown in a lab dish. But until now, bees’ abilities haven’t been quite so clear, she says. © Society for Science & the Public 2000–2024.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29372 - Posted: 06.26.2024

By Charles Q. Choi The largest-yet single-cell genomics analysis reveals new details of the molecular pathways and cell types that are altered in the cortex in people with autism. The work, published last month in Science, also hints at how genes linked to the condition contribute to these brain differences. The findings are part of a package of 14 new papers from PsychENCODE, a multi-institution consortium launched in 2015 to study the molecular basis of neuropsychiatric conditions. The initiative’s latest phase of research analyzed human brains at the single-cell level instead of relying on bulk tissue samples as in previous efforts. “Single-cell analysis gives you the ability to really understand a condition in terms of cell-cell interactions, and how a condition might affect different cell types in very different ways,” says PsychENCODE chair Daniel Geschwind, professor of human genetics, neurology and psychiatry at the University of California, Los Angeles, who led the new autism study. Past work by Geschwind and others identified a “molecular signature” in tissue samples of autism brains, characterized by increased expression of immune signaling genes, decreased activity of synaptic and neuronal genes, and a reduction in the regional gene-expression patterns typically seen across the cortex. The first single-cell analysis—involving cells from 15 autistic and 16 non-autistic people, and published in 2019—hinted at a role for microglia and excitatory neurons in layer 2/3 of the cortex. The new study confirms these previous findings and expands autism’s molecular signature to include a subtype of interneurons and layer 5/6 excitatory neurons, which project to other cortical areas. It also adds gene-expression changes, such as heightened immune responses in oligodendrocytes, cells that help produce the myelin sheath insulating the central nervous system. “That suggests there may be something going on broadly with connectivity in autism,” Geschwind says. © 2024 Simons Foundation

Keyword: Autism; Epigenetics
Link ID: 29371 - Posted: 06.26.2024

By Dana G. Smith In July 2016, a heat wave hit Boston, with daytime temperatures averaging 92 degrees for five days in a row. Some local university students who were staying in town for the summer got lucky and were living in dorms with central air-conditioning. Other students, not so much — they were stuck in older dorms without A.C. Jose Guillermo Cedeño Laurent, a Harvard researcher at the time, decided to take advantage of this natural experiment to see how heat, and especially heat at night, affected the young adults’ cognitive performance. He had 44 students perform math and self-control tests five days before the temperature rose, every day during the heat wave, and two days after. “Many of us think that we are immune to heat,” said Dr. Cedeño, now an assistant professor of environmental and occupational health and justice at Rutgers University. “So something that I wanted to test was whether that was really true.” It turns out even young, healthy college students are affected by high temperatures. During the hottest days, the students in the un-air-conditioned dorms, where nighttime temperatures averaged 79 degrees, performed significantly worse on the tests they took every morning than the students with A.C., whose rooms stayed a pleasant 71 degrees. A heat wave is once again blanketing the Northeast, South and Midwest. High temperatures can have an alarming effect on our bodies, raising the risk for heart attacks, heatstroke and death, particularly among older adults and people with chronic diseases. But heat also takes a toll on our brains, impairing cognition and making us irritable, impulsive and aggressive. Numerous studies in lab settings have produced similar results to Dr. Cedeño’s research, with scores on cognitive tests falling as scientists raised the temperature in the room. One investigation found that just a four-degree increase — which participants described as still feeling comfortable — led to a 10 percent average drop in performance across tests of memory, reaction time and executive functioning. © 2024 The New York Times Company

Keyword: Aggression
Link ID: 29370 - Posted: 06.26.2024

Jon Hamilton About 170 billion cells are in the brain, and as they go about their regular tasks, they produce waste — a lot of it. To stay healthy, the brain needs to wash away all that debris. But how exactly it does this has remained a mystery. Now, two teams of scientists have published three papers that offer a detailed description of the brain's waste-removal system. Their insights could help researchers better understand, treat and perhaps prevent a broad range of brain disorders. The papers, all published in the journal Nature, suggest that during sleep, slow electrical waves push the fluid around cells from deep in the brain to its surface. There, a sophisticated interface allows the waste products in that fluid to be absorbed into the bloodstream, which takes them to the liver and kidneys to be removed from the body. One of the waste products carried away is amyloid, the substance that forms sticky plaques in the brains of patients with Alzheimer's disease. This illustration demonstrates how the thin film of sensors could be applied to the brain during surgery. There's growing evidence that in Alzheimer's disease, the brain's waste-removal system is impaired, says Jeffrey Iliff, who studies neurodegenerative diseases at the University of Washington but was not a part of the new studies. The new findings should help researchers understand precisely where the problem is and perhaps fix it, Iliff says. "If we restore drainage, can we prevent the development of Alzheimer's disease?" he asks. The new studies come more than a decade after Iliff and Dr. Maiken Nedergaard, a Danish scientist, first proposed that the clear fluids in and around the brain are part of a system to wash away waste products. The scientists named it the glymphatic system, a nod to the body's lymphatic system, which helps fight infection, maintain fluid levels and filter out waste products and abnormal cells. © 2024 npr

Keyword: Sleep
Link ID: 29369 - Posted: 06.26.2024

By Miryam Naddaf Researchers have developed a four-dimensional model of spinal-cord injury in mice, which shows how nearly half a million cells in the spinal cord respond over time to injuries of varying severity. The model, known as a cell atlas, could help researchers to resolve outstanding questions and develop new treatments for people with spinal-cord injury (SCI). “If you know what every single cell on the spinal cord is doing in response to injury, you could use that knowledge to develop tailor-made and mechanism-based therapies,” says Mark Anderson, a neurobiologist at the Swiss Federal Institute of Technology in Geneva, Switzerland, who worked on the atlas. “Things don’t need to be a shot in the dark.” Anderson and his colleagues used machine-learning algorithms to build the atlas by mapping data from RNA sequencing and other cell-biology techniques. They described the work in a Nature paper published today1 and have made the entire atlas available through an online platform. The atlas is a valuable resource for testing hypotheses about SCI, says Binhai Zheng, who studies spinal-cord regeneration at the University of California, San Diego. “There are a lot of hidden treasures.” The researchers examined sections of the spinal cord, sampled from 52 injured and uninjured mice at 1, 4, 7, 14, 30 and 60 days after injury. Their analysis involved 18 experimental SCI conditions, including different types of injury and levels of severity. They used RNA-sequencing tools to explore how 482,825 cells responded to injury over time. © 2024 Springer Nature Limited

Keyword: Brain imaging; Brain Injury/Concussion
Link ID: 29368 - Posted: 06.26.2024

Hannah Devlin Science correspondent A UK teenager with severe epilepsy has become the first person in the world to be fitted with a brain implant aimed at bringing seizures under control. Oran Knowlson’s neurostimulator sits under the skull and sends electrical signals deep into the brain, reducing his daytime seizures by 80%. His mother, Justine, said that her son had been happier, chattier and had a much better quality of life since receiving the device. “The future looks hopeful, which I wouldn’t have dreamed of saying six months ago,” she said. Martin Tisdall, a consultant paediatric neurosurgeon who led the surgical team at Great Ormond Street hospital (Gosh) in London, said: “For Oran and his family, epilepsy completely changed their lives and so to see him riding a horse and getting his independence back is absolutely astounding. We couldn’t be happier to be part of their journey.” Oran, who is 13 and lives in Somerset, had the surgery in October as part of a trial at Gosh in partnership with University College London, King’s College hospital and the University of Oxford. Oran has Lennox-Gastaut syndrome, external, a treatment-resistant form of epilepsy which he developed at the age of three. Between then and having the device fitted, he hasn’t had a single day without a seizure and sometimes suffered hundreds in a day. He often lost consciousness and would stop breathing, needing resuscitation. This means Oran needed round-the-clock care, as seizures could happen at any time of day, and he was at a significantly increased risk of sudden unexpected death in epilepsy (Sudep). © 2024 Guardian News & Media Limited

Keyword: Epilepsy; Robotics
Link ID: 29367 - Posted: 06.24.2024

By Claire Yuan Men and women experience pain differently, and until now, scientists didn’t know why. New research says it may be in part due to differences in male and female nerve cells. Pain-sensing nerve cells from male and female animal tissues responded differently to the same sensitizing substances, researchers report June 3 in Brain. The results suggest that at the cellular level, pain is produced differently between the sexes. The results might allow researchers “to come up with drugs that would be specific to treat female patients or male patients,” says Katherine Martucci, a neuroscientist who studies chronic pain at Duke University School of Medicine and was not involved in the study. “There’s no debate about it. They’re seeing these differences in the cells.” Some types of chronic and acute pain appear more often in one sex, but it’s unclear why. For instance, about 50 million adults in the United States suffer from chronic pain conditions, many of which are more common in women (SN: 5/22/23). Similar disparities exist for acute conditions. Such differences prompted pain researcher Frank Porreca of the University of Arizona Health Sciences in Tucson and colleagues to study nerve cells called nociceptors, which can act like alarm sensors for the body. The cells’ pain sensors, found in skin, organs and elsewhere in the body, can detect potentially dangerous stimuli and send signals to the brain, which then interprets the information as pain. In some cases, the nerve cells can become more sensitive to outside stimulation, registering even gentle sensations — like a shirt rubbing sunburned skin — as pain. © Society for Science & the Public 2000–2024.

Keyword: Pain & Touch; Sexual Behavior
Link ID: 29366 - Posted: 06.24.2024

By Sara Reardon Specific nerve cells on the penis and clitoris detect vibrations and then become activated, causing sexual behaviours such as erections, a study in mice has revealed1. The findings could lead to new treatments for conditions such as erectile dysfunction, or for restoring sexual function in people with lower-body paralysis. Krause corpuscles — nerve endings in tightly wrapped balls located just under the skin — were first discovered in human genitals more than 150 years ago. The structures are similar to touch-activated corpuscles found on people’s fingers and hands, which respond to vibrations as the skin moves across a textured surface. But there is little research into how the genital corpuscles work and how they are involved in sex, probably because the topic is sometimes considered taboo. “It’s been hard to get people to work on this because some people have a hard time talking about it,” says David Ginty, a sensory neurobiologist at Harvard Medical School in Boston, Massachusetts, who led the team that conducted the latest research. “But I don’t, because the biology is so interesting.” Ginty and other sensory biologists have long wanted to study these mysterious neuron balls. But activating and tracking specific neurons was nearly impossible until advanced molecular techniques emerged in the past 20 years. In a 19 June paper in Nature1, Ginty and his collaborators activated the Krause corpuscles in both male and female mice using various mechanical and electrical stimuli. The neurons fired in response to low-frequency vibrations in the range of 40–80 hertz. Ginty notes that these frequencies are generally used in many sex toys; humans, it seems, realized that this was the best way to stimulate Krause corpuscles before any official experiments were published. © 2024 Springer Nature Limited

Keyword: Sexual Behavior; Pain & Touch
Link ID: 29365 - Posted: 06.24.2024

By Dennis Normile For several decades, evidence has accumulated that animals turn to medicinal plants to relieve their ailments. Chimpanzees (and some other species) swallow leaves to mechanically clear the gut of parasites. Chimps also rely on the ingested pith of an African relative of the daisy, Vernonia amygdalina, to rid themselves of intestinal worms. Dolphins rub against antibacterial corals and sponges to treat skin infections. And recently, a male Sumatran orangutan was observed chewing the leaves of Fibraurea tinctoria, a South Asian plant with antibacterial and anti-inflammatory properties, and dabbing the juice onto a wound. These instances of animals playing doctor with therapeutic plants have typically been identified one by one. Today, in PLOS ONE, a multinational team proposes adding 17 samples from 13 plant species to the chimpanzee pharmacopia. “The paper provides important new findings about self-medication behavior in wild chimpanzees,” a topic that’s still relatively unknown, says Isabelle Laumer, a cognitive biologist at the Max Planck Institute of Animal Behavior and lead author on the orangutan self-medication paper who was not involved in the new chimp research. Observers with the team behind today's paper spent 4 months with each of two chimp communities habituated to human observers in Uganda’s Budongo Forest. The researchers supplemented their own observations with historical data. From the 170 chimps in the two communities, the observers zeroed in on 51 individuals suffering bacterial infections and inflammation as indicated by abnormal urine composition, diarrhea, traces of parasites, or apparent wounds. For 10 hours a day they followed the sick chimps through the forest, noting which plants they ate and when, and watching in particular to see whether the animals went out of their way to find and consume plants not part of their usual diet. In one example, researchers observed an individual suffering from diarrhea very briefly venture outside the group’s safe home territory to eat a small amount of dead wood from Alstonia boonei, a tree in the dogbane family. Chimps rarely eat dead wood, which is not nutritious for them, the team says.

Keyword: Evolution
Link ID: 29364 - Posted: 06.24.2024

By Scott Sayare As a boy, Les Milne carried an air of triumph about him, and an air of sorrow. Les was a particularly promising and energetic young man, an all-Scottish swim champion, head boy at his academy in Dundee, a top student bound for medical school. But when he was young, his father died; his mother was institutionalized with a diagnosis of manic depression, and he and his younger brother were effectively left to fend for themselves. His high school girlfriend, Joy, was drawn to him as much by his sadness as his talents, by his yearning for her care. “We were very, very much in love,” Joy, now a flaxen-haired 72-year-old grandmother, told me recently. In a somewhat less conventional way, she also adored the way Les smelled, and this aroma of salt and musk, accented with a suggestion of leather from the carbolic soap he used at the pool, formed for her a lasting sense of who he was. “It was just him,” Joy said, a steadfast marker of his identity, no less distinctive than his face, his voice, his particular quality of mind. Listen to this article, read by Robert Petkoff Joy’s had always been an unusually sensitive nose, the inheritance, she believes, of her maternal line. Her grandmother was a “hyperosmic,” and she encouraged Joy, as a child, to make the most of her abilities, quizzing her on different varieties of rose, teaching her to distinguish the scent of the petals from the scent of the leaves from the scent of the pistils and stamens. Still, her grandmother did not think odor of any kind to be a polite topic of conversation, and however rich and enjoyable and dense with information the olfactory world might be, she urged her granddaughter to keep her experience of it to herself. Les only learned of Joy’s peculiar nose well after their relationship began, on a trip to the Scandinavian far north. Joy would not stop going on about the creamy odor of the tundra, or what she insisted was the aroma of the cold itself. Joy planned to go off to university in Paris or Rome. Faced with the prospect of tending to his mother alone, however, Les begged her to stay in Scotland. He trained as a doctor, she as a nurse; they married during his residency. He was soon the sort of capable young physician one might hope to meet, a practitioner of uncommon enthusiasm, and shortly after his 30th birthday, he was appointed consultant anesthesiologist at Macclesfield District General Hospital, outside Manchester, in England, the first in his graduating class to make consultant. © 2024 The New York Times Company

Keyword: Parkinsons; Chemical Senses (Smell & Taste)
Link ID: 29363 - Posted: 06.15.2024

By Lauren Leffer Noland Arbaugh has a computer chip embedded in his skull and an electrode array in his brain. But Arbaugh, the first user of the Neuralink brain-computer interface, or BCI, says he wouldn’t know the hardware was there if he didn’t remember going through with the surgery. “If I had lost my memory, and I woke up, and you told me there was something implanted in my brain, then I probably wouldn’t believe you,” says the 30-year-old Arizona resident, who has been paralyzed below the middle of his neck since a 2016 swimming accident. “I have no sensation of it—no way of telling it’s there unless someone goes and physically pushes on it.” The Neuralink chip may be physically unobtrusive, but Arbaugh says it’s had a big impact on his life, allowing him to “reconnect with the world.” He underwent robotic surgery in January to receive the N1 Implant, also called “the Link,” in Neuralink’s first approved human trial. BCIs have existed for decades. But because billionaire technologist Elon Musk owns Neuralink, the company has received outsize attention. It’s brought renewed public interest to a technology that could significantly improve the life of those living with quadriplegia, such as Arbaugh, as well as people with other disabilities or neurodegenerative diseases. BCIs record electrical activity in the brain and translate those data into output actions, such as opening and closing a robotic hand or clicking a computer mouse. They vary in their design, level of invasiveness and the resolution of the information they capture. Some detect neurons’ electrical activity with entirely external electroencephalogram (EEG) arrays placed over a subject’s head. Others use electrodes placed on the brain’s surface to track neural activity. Then there are intracortical devices, which use electrodes implanted directly into brain tissue, to get as close as possible to the targeted neurons. Neuralink’s implant falls into this category. © 2024 SCIENTIFIC AMERICAN,

Keyword: Robotics; Movement Disorders
Link ID: 29362 - Posted: 06.15.2024

By Esther Landhuis Last month, researchers discovered cells in the brainstem that regulate inflammation throughout the body. In response to an injury, these nerve cells not only sense inflammatory molecules, but also dial their circulating levels up and down to keep infections from harming healthy tissues. The discovery adds control of the immune system to the brainstem’s core functions — a list that also includes monitoring heart rate, breathing and aspects of taste — and suggests new potential targets for treating inflammatory disorders like arthritis and inflammatory bowel disease. During an intense workout or high-stakes exam, your brain can sense the spike in your heart rate and help restore a normal rhythm. Likewise, the brain can help stabilize your blood pressure by triggering chemical signals that widen or constrict blood vessels. Such feats often go unnoticed, but they illustrate a fundamental concept of physiology known as homeostasis — the capacity of organisms to keep their internal systems working smoothly and stably amid shifting circumstances. Now, in a paper published on May 1 in Nature, researchers describe how homeostatic control extends even to the sprawl of cells and tissues that comprise our immune system. The team applied a clever genetic approach in mice to identify cells in the brainstem that adjust immune reactions to pathogens and other outside triggers. These neurons operate like a “volume controller” that keeps the animals’ inflammatory responses within a physiological range, said paper author Hao Jin, a neuroimmunologist at the National Institute of Allergy and Infectious Diseases. © 2024 Simons Foundation.

Keyword: Miscellaneous
Link ID: 29361 - Posted: 06.15.2024

By Shaena Montanari Five years ago, while working to develop a tool to label neurons active during seizures in mice, Quynh Anh Nguyen noticed something she had not seen before. “There was a particular region in the brain that seemed to light up really prominently,” she says. Nguyen, assistant professor of pharmacology at Vanderbilt University, had induced seizures in the animals by injecting kainic acid into the hippocampus—a common strategy to model temporal lobe epilepsy. The condition often involves hyperactivity in the anterior and middle regions of the hippocampus, but Nguyen’s mice also showed the activation in a tiny posterior part of the hippocampus that she was not familiar with. Nguyen brought the data to her then-supervisor Ivan Soltesz, professor of neurosciences and neurosurgery at Stanford University. Together they realized that these neurons were in an area called the fasciola cinereum—a subregion of the hippocampus so understudied, Soltesz says, that when Nguyen first asked him what it was, he had “no idea.” Despite the subregion’s obscurity, it looks to be an important and previously overlooked contributor to epilepsy in people who do not respond to anti-seizure medications or tissue ablation in the hippocampus, Nguyen and her colleagues say. Fasciola cinereum neurons were active during seizures in six people with drug-resistant epilepsy, the team reported in April. © 2024 Simons Foundation

Keyword: Epilepsy
Link ID: 29360 - Posted: 06.15.2024

By Susan Dominus About a year ago, a friend of mine started evading my invitations to grab a drink. It was only when we caught up for a walk that she explained she wasn’t putting me off for any personal reason — it was just that she had stopped drinking. She wasn’t a heavy drinker — she had a glass of wine with dinner, the occasional Aperol spritz — but she’d been hearing on podcasts and reading in the news that even a small amount of alcohol was much worse for her health than had previously been understood. Listen to this article, read by Kirsten Potter My friend was picking up on a swing in the public-health messaging around alcohol. For many years, she might have felt that she was making a healthy choice in having a glass of wine or a beer with dinner. Right around the time when she came of legal age to drink, the early 1990s, some prominent researchers were promoting, and the media helped popularize, the idea that moderate drinking — for women, a drink a night; for men, two — was linked to greater longevity. The cause of that association was not clear, but red wine, researchers theorized, might have anti-inflammatory properties that extended life and protected cardiovascular health. Major health organizations and some doctors always warned that alcohol consumption was linked to higher cancer risk, but the dominant message moderate drinkers heard was one of not just reassurance but encouragement. More recently, though, research has piled up debunking the idea that moderate drinking is good for you. Last year, a major meta-analysis that re-examined 107 studies over 40 years came to the conclusion that no amount of alcohol improves health; and in 2022, a well-designed study found that consuming even a small amount brought some risk to heart health. That same year, Nature published research stating that consuming as little as one or two drinks a day (even less for women) was associated with shrinkage in the brain — a phenomenon normally associated with aging. © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29359 - Posted: 06.15.2024

By Max Kozlov A crucial brain signal linked to long-term memory falters in rats when they are deprived of sleep — which might help to explain why poor sleep disrupts memory formation1. Even a night of normal slumber after a poor night’s sleep isn’t enough to fix the brain signal. These results, published today in Nature, suggest that there is a “critical window for memory processing”, says Loren Frank, a neuroscientist at the University of California, San Francisco, who was not involved with the study. “Once you’ve lost it, you’ve lost it.” In time, these findings could lead to targeted treatments to improve memory, says study co-author Kamran Diba, a computational neuroscientist at the University of Michigan Medical School in Ann Arbor. Neurons in the brain seldom act alone; they are highly interconnected and often fire together in a rhythmic or repetitive pattern. One such pattern is the sharp-wave ripple, in which a large group of neurons fire with extreme synchrony, then a second large group of neurons does the same and so on, one after the other at a particular tempo. These ripples occur in a brain area called the hippocampus, which is key to memory formation. The patterns are thought to facilitate communication with the neocortex, where long-term memories are later stored. One clue to their function is that some of these ripples are accelerated re-runs of brain-activity patterns that occurred during past events. For example, when an animal visits a particular spot in its cage, a specific group of neurons in the hippocampus fires in unison, creating a neural representation of that location. Later, these same neurons might participate in sharp-wave ripples — as if they were rapidly replaying snippets of that experience. © 2024 Springer Nature Limited

Keyword: Learning & Memory; Sleep
Link ID: 29358 - Posted: 06.13.2024

Jon Hamilton A flexible film bristling with tiny sensors could make surgery safer for patients with a brain tumor or severe epilepsy. The experimental film, which looks like Saran wrap, rests on the brain’s surface and detects the electrical activity of nerve cells below. It’s designed to help surgeons remove diseased tissue while preserving important functions like language and memory. “This will enable us to do a better job,” says Dr. Ahmed Raslan, a neurosurgeon at Oregon Health and Science University who helped develop the film. The technology is similar in concept to sensor grids already used in brain surgery. But the resolution is 100 times higher, says Shadi Dayeh, an engineer at the University of California, San Diego, who is leading the development effort. In addition to aiding surgery, the film should offer researchers a much clearer view of the neural activity responsible for functions including movement, speech, sensation, and even thought. “We have these complex circuits in our brains,” says John Ngai, who directs the BRAIN Initiative at the National Institutes of Health, which has funded much of the film’s development. “This will give us a better understanding of how they work.” Mapping an ailing brain The film is intended to improve a process called functional brain mapping, which is often used when a person needs surgery to remove a brain tumor or tissue causing severe epileptic seizures. © 2024 npr

Keyword: Brain imaging; Epilepsy
Link ID: 29357 - Posted: 06.13.2024

By Olivia Gieger Three pioneers in face-perception research have won the 2024 Kavli Prize in Neuroscience. Nancy Kanwisher, professor of cognitive neuroscience at the Massachusetts Institute of Technology; Winrich Freiwald, professor of neurosciences and behavior at Rockefeller University; and Doris Tsao, professor of neurobiology at the University of California, Berkeley, will share the $1 million Kavli Prize for their discoveries of the regions—in both the human and monkey brains—responsible for identifying and recognizing faces. “This is work that’s very classic and very elegant, not only in face-processing and face-recognition work, but the impact it’s had on how we think about brain organization in general is huge,” says Alexander Cohen, assistant professor of neurology at Harvard Medical School, who studies face recognition in autistic people. The Norwegian Academy of Science and Letters awards the prize every two years. Kanwisher says she long suspected that something special happens in the brain when we look at faces, because people with prosopagnosia—the inability to recognize faces—maintain the ability to recognize nearly all other objects. What’s more, it is harder to recognize an upside-down face than most other inverted objects, studies have shown. To get to the root of face processing, Kanwisher spent hours as a young researcher lying still in an MRI machine as images of faces and objects flashed before her. A spot in the bottom right of the cerebral cortex lit up when she and others looked at faces, according to functional MRI (fMRI) scans, she and her colleagues reported in a seminal 1997 paper. They called the region the fusiform face area. © 2024 Simons Foundation

Keyword: Attention
Link ID: 29356 - Posted: 06.13.2024

By Erin Garcia de Jesús Chronic wasting disease has been spreading among deer in the United States, which has raised concerns that the fatal neurological illness might make the leap to people. But a recent study suggests that the disease has a tough path to take to get into humans. The culprit behind chronic wasting disease, or CWD, isn’t a virus or bacterium but a misfolded brain protein called a prion. A new study using miniature, lab-grown organs called organoids supports previous work, showing that CWD prions don’t infect human brain tissue. Brain organoids exposed to high doses of prions from white-tailed deer, mule deer and elk remained infection-free for the duration of the study, or 180 days, researchers report in the June 2024 Emerging Infectious Diseases. However, organoids exposed to human prions that cause a related condition, Creutzfeldt-Jakob disease, quickly became infected. The finding suggests that a substantial species barrier prevents CWD from making the jump from deer to humans. “This was a model that could really help tell us … whether or not it was a real risk,” says Bradley Groveman, a biologist at the National Institutes of Health’s Rocky Mountain Laboratories in Hamilton, Mont. But brain organoids aren’t a perfect mimic of the real thing and may lack features that would make them susceptible to infection. And new prion strains can appear, perhaps including some that might help deer prions lock onto healthy brain proteins in humans. © Society for Science & the Public 2000–2024.

Keyword: Prions
Link ID: 29355 - Posted: 06.11.2024

By Gina Kolata and Pam Belluck A committee of independent advisers to the Food and Drug Administration voted unanimously on Monday that the benefits outweigh the risks of the newest experimental drug for Alzheimer’s disease. Alzheimer’s afflicts more than six million Americans. It has no cure, and there is no treatment or lifestyle modification that can restore memory loss or reverse cognitive decline. The drug, made by Eli Lilly, is donanemab. It modestly slowed cognitive decline in patients in the early stages of the disease but also had significant safety risks, including swelling and bleeding in the brain. The committee concluded, though, that the consequences of Alzheimer’s are so dire that even a modest benefit can be worthwhile. The F.D.A. usually follows the advice of the agency’s advisory committees but not always. The drug is based on a long-held hypothesis that Alzheimer’s disease begins when rough hard balls of amyloid, a protein, pile up in patients’ brains, followed by a cascade of reactions leading to the death of neurons. The idea is to treat Alzheimer’s by attacking amyloid, clearing it from the brain. Two similar amyloid-fighting drugs were approved recently: Leqembi, made by Eisai and Biogen, was approved last year. That drug’s risks and modest benefits are similar to those of donanemab. Aduhelm, made by Biogen, is the other drug and was approved in 2021 but was discontinued because there was insufficient evidence that it could benefit patients. Donanemab was expected to be approved earlier this year, but in March, the F.D.A. decided that, instead, it would require donanemab to undergo the scrutiny of an independent advisory committee, a surprise to Eli Lilly. © 2024 The New York Times Company

Keyword: Alzheimers
Link ID: 29354 - Posted: 06.11.2024