Robin McKie, Science Editor People in Britain could benefit from a key medical breakthrough next year. They may be given access to the first drugs ever developed to slow the impact of Alzheimer’s disease. The first of these medicines – lecanemab – was recently approved in the US and Japan, where treatments using it have already been launched. A second drug, donanemab, is expected to follow soon, and next year it is anticipated that the UK medical authorities will consider both of them for approval in Britain. The prospect has raised hopes that, after years of effort, scientists may be closing in on ways to directly tackle the UK’s dementia crisis. About a million people are living with the condition in this country, and this is expected to rise to about 1.7 million by 2040 – with potentially grim consequences. Last year dementia took the lives of 66,000 people in England and Wales, and it is now the leading cause of death in Britain, with Alzheimer’s accounting for two-thirds of cases. Until now doctors have only been able to prescribe medicines that help patients manage their symptoms, so the arrival of the first drugs that treat the actual cause of the condition has been welcomed – although experts have warned that their use should be treated with some caution. “The new drugs slow down the development of Alzheimer’s by six months to a year and are useful only for those in the early stages of the condition, so they are certainly not miracle medicines,” said David Thomas, head of policy at Alzheimer’s Research UK. “However, after decades of research, they are the first to improve patients’ lives directly, and that is a justifiable cause for excitement. If nothing else, they suggest we are probably on the right road to tackling Alzheimer’s.” © 2023 Guardian News & Media Limited

Keyword: Alzheimers
Link ID: 29056 - Posted: 12.19.2023

By Mark MacNamara The notion of boxing as the “sweet science” is often thought to have been coined in 1956 by the great New Yorker writer A.J. Liebling. He used the term as the title of his definitive book on the sport, but he took it—with much appreciation—from a British sportswriter, Pierce Egan. In 1813, Egan wrote about the “sweet science of bruising” in his master work, Boxiana. The book is a collection of magazine pieces set in a bloody, bare-knuckled world opposite Jane Austen’s. As for the “sweet science,” no one ever really defines it. A carefully thrown knockout punch to a sweet spot on the chin is one possible derivation. There’s also the play on a science with so little apparent sweetness. But that’s not it. The sweet science Liebling and Egan describe had more to do with British principles of “stoic virtues,” “generosity,” and “true courage”—altogether, life in a contradictory place. It’s a square ring, after all, where sometimes hope transcends the specter of an awful inevitability. Or so I’ve come to think, on a journey I’ve begun in the past year, exploring how the sweet science can be used as a treatment for Parkinson’s disease—that increasingly common degenerative disorder of the nervous system, tied to a loss of the brain chemical dopamine, which is involved in movement, memory, motivation, and cognition. Someone told her she moved like a wavy wind sock outside a used car lot. “Exactly how I feel,” she said. In October 2022, a longtime tennis partner noticed something “strange” in my stride, along with a noisy shuffle. “Fatigue,” I replied with pique. The truth is I’m 75 and had known something might not be right for years, particularly the ominous hand tremors, as well as the night-of-the-living-dead gait and a facial expression to match. Add severe anxiety in public places and bizarre nightmares, some quite disturbing. © 2023 NautilusNext Inc.,

Keyword: Parkinsons
Link ID: 29055 - Posted: 12.19.2023

By Sandra G. Boodman His plane was coming in for a landing at Philadelphia International Airport when Allen M. Weiss, a marketing professor at the University of Southern California, felt a spasm of pain pierce his left cheek near his nose. “It was really weird,” recalled Weiss, then director of Mindful USC, a group of meditation-based programs at the Los Angeles university. “My face froze up.” Within minutes the pain disappeared and the final leg of Weiss’s December 2015 trip home to California was uneventful. But over the next few months the sensation recurred in the same spot. At first the unpredictable pain was fairly mild and merely bothersome; later it became an excruciating daily torment. Several years after the pain first occurred Weiss, who had consulted dentists, oral pain experts and an otolaryngologist, was given a diagnosis that ended up being correct. But his complicated medical history, a radiology report that failed to describe an important finding and a cryptic warning by one of his doctors delayed effective treatment for three more years. “It was completely confusing,” Weiss said. In June 2023 he underwent surgery that has significantly reduced his pain and improved the quality of his life. N. Nicole Moayeri, the Santa Barbara, Calif., neurosurgeon who operated on Weiss, said a protracted search for a diagnosis and treatment is not unusual for those suffering from Weiss’s uncommon malady. “I commonly see people who’ve had multiple dental procedures for years” when the problem was not in their mouths, Moayeri said. “It’s really shocking to me that so many people suffer” with this for so long. After three months of intermittent pain following the flight, Weiss consulted his internist. For reasons that are unclear, the doctor told Weiss the cause was probably psychological, not physical, and that it wasn’t serious. He sent Weiss to an ear, nose and throat specialist whom he saw in March 2016. She performed an exam and ordered a CT scan that revealed a deviated septum, a typically painless condition estimated to affect up to 80 percent of the population in which the bone or cartilage that divides the nostrils is off-center. A moderate or severe deviation can contribute to the development of sinus infections, headaches and breathing problems. But Weiss had none of these. And a deviated septum didn’t explain the spasms of pain.

Keyword: Pain & Touch
Link ID: 29054 - Posted: 12.19.2023

By Carl Zimmer Neanderthals were morning people, a new study suggests. And some humans today who like getting up early might credit genes they inherited from their Neanderthal ancestors. The new study compared DNA in living humans with genetic material retrieved from Neanderthal fossils. It turns out that Neanderthals carried some of the same clock-related genetic variants as do people who report being early risers. Since the 1990s, studies of Neanderthal DNA have exposed our species’ intertwined history. About 700,000 years ago, our lineages split apart, most likely in Africa. While the ancestors of modern humans largely stayed in Africa, the Neanderthal lineage migrated into Eurasia. About 400,000 years ago, the population split in two. The hominins who spread west became Neanderthals. Their cousins to the east evolved into a group known as Denisovans. The two groups lived for hundreds of thousands of years, hunting game and gathering plants, before disappearing from the fossil record about 40,000 years ago. By then, modern humans had expanded out of Africa, sometimes interbreeding with Neanderthals and Denisovans. And today, fragments of their DNA can be found in most living humans. Research carried out over the past few years by John Capra, a geneticist at the University of California, San Francisco, and other scientists suggested that some of those genes passed on a survival advantage. Immune genes inherited from Neanderthals and Denisovans, for example, might have protected them from new pathogens they had not encountered in Africa. Dr. Capra and his colleagues were intrigued to find that some of the genes from Neanderthals and Denisovans that became more common over generations were related to sleep. For their new study, published in the journal Genome Biology and Evolution, they investigated how these genes might have influenced the daily rhythms of the extinct hominins. © 2023 The New York Times Company

Keyword: Biological Rhythms; Evolution
Link ID: 29052 - Posted: 12.16.2023

By Joseph Howlett Garter snakes have something in common with elephants, orcas, and naked mole rats: They form social groups that center around females. The snakes have clear “communities” composed of individuals they prefer hanging out with, and females act as leaders that tie the groups together and guide their members’ movements, according to the most extensive field study of snake sociality ever carried out. “This is an important first step in understanding how a community of snakes is organized in the wild,” says Gordon Burghardt, an ecologist at the University of Tennessee, Knoxville, who was not involved in the research. Other experts agree: “This is a big deal,” says integrative biologist Robert Mason of Oregon State University. “It’s a whole new avenue of research that I don’t think people have really given any thought to.” Ecologists had long assumed snakes are antisocial loners that hang out together only for core functions such as mating and hibernation. However, in 2020, Morgan Skinner, a behavioral ecologist at Wilfrid Laurier University, and collaborators showed in laboratory experiments that captive garter snakes have “friends”—specific snakes whose company they prefer over others. Still, studies of wild snakes were lacking “because they’re so secretive and difficult to find,” Skinner says. Then he learned that the Ontario Ministry of Transportation had funded an unprecedented long-term study of a huge population of Butler’s garter snakes (Thamnophis butleri) in Windsor, Canada. Ecologists began to monitor the flute-size slitherers in 2009 to keep them safe from nearby road construction. They regularly captured snakes in the 250-hectare study area, using identifying markings to track more than 3000 individuals over a 12-year span—about the lifetime of a garter snake. “We were mainly monitoring the population after they were relocated, to make sure they were thriving,” says Megan Hazell, a biologist with the consulting firm WSP, who led the field research as a graduate student at Queen’s University.

Keyword: Evolution; Sexual Behavior
Link ID: 29050 - Posted: 12.16.2023

By Oshan Jarow Sometimes when I’m looking out across the northern meadow of Brooklyn’s Prospect Park, or even the concrete parking lot outside my office window, I wonder if someone like Shakespeare or Emily Dickinson could have taken in the same view and seen more. I don’t mean making out blurry details or more objects in the scene. But through the lens of their minds, could they encounter the exact same world as me and yet have a richer experience? One way to answer that question, at least as a thought experiment, could be to compare the electrical activity inside our brains while gazing out upon the same scene, and running some statistical analysis designed to actually tell us whose brain activity indicates more richness. But that’s just a loopy thought experiment, right? Not exactly. One of the newest frontiers in the science of the mind is the attempt to measure consciousness’s “complexity,” or how diverse and integrated electrical activity is across the brain. Philosophers and neuroscientists alike hypothesize that more complex brain activity signifies “richer” experiences. The idea of measuring complexity stems from information theory — a mathematical approach to understanding how information is stored, communicated, and processed —which doesn’t provide wonderfully intuitive examples of what more richness actually means. Unless you’re a computer person. “If you tried to upload the content onto a hard drive, it’s how much memory you’d need to be able to store the experience you’re having,” Adam Barrett, a professor of machine learning and data science at the University of Sussex, told me. Another approach to understanding richness is to look at how it changes in different mental states. Recent studies have found that measures of complexity are lowest in patients under general anesthesia, higher in ordinary wakefulness, and higher still in psychedelic trips, which can notoriously turn even the most mundane experiences — say, my view of the parking lot outside my office window — into profound and meaningful encounters.

Keyword: Consciousness
Link ID: 29049 - Posted: 12.16.2023

By Tosin Thompson Last month saw the first-ever approval of a gene therapy that uses the CRISPR–Cas9 gene-editing tool, a treatment for the blood conditions sickle-cell disease and β-thalassaemia that works by precisely cutting out a faulty gene in people’s stem cells. Now, researchers in search of new treatments for Alzheimer’s disease are hoping to deploy similar strategies against forms of the disease that are caused by genetic mutations. Although there are now some treatments that slow the progression of Alzheimer’s, these often don’t benefit people who are in the later stages or who have mutations that raise the risk of the disease. “CRISPR therapies could potentially be a one-and-done cure, which no other drug can match,” says Subhojit Roy, a neuroscientist at the University of California, San Diego. But he adds that there is a long way to go before these therapies could be deployed against such a complex condition. “Cutting and pasting a gene is much harder to do in the brain using current technology.” Alzheimer’s is the most common form of dementia, a health issue of global concern. More than 55 million people are affected by dementia, and this figure is projected to nearly triple by 2050. “We do not fully understand how the brain works, which makes the challenge of understanding and treating brain diseases like Alzheimer’s very difficult,” says Tara Spires-Jones, who studies neurodegeneration at the University of Edinburgh, UK. Much of Alzheimer’s research is driven by the amyloid hypothesis, the idea that the build-up of amyloid-β proteins in the brain, which eventually form clumps called plaques, is the main cause of the disease. Amyloid plaques trigger another brain protein, called tau, to clump together and spread inside neurons. It is usually well into this process that symptoms such as memory loss start to appear. Usually, the more tau is present, the more severe the symptoms are. © 2023 Springer Nature Limited

Keyword: Alzheimers; Genes & Behavior
Link ID: 29046 - Posted: 12.13.2023

By Gina Kolata Dr. Edward Lewis, a pediatrician in Rochester, N.Y., has seen hundreds of children with obesity over the years in his medical practice. He finally may have a treatment for their medical condition — the powerful weight loss drug Wegovy. But that does not mean Dr. Lewis is prescribing it. Nor are most other pediatricians. “I am reluctant to prescribe medications we don’t use on a day-to-day basis,” Dr. Lewis said. And, he added, he is disinclined to use “a medicine that is a relative newcomer to the scene in kids.” Regulators and medical groups have all said that these drugs are appropriate for children as young as 12. But like Dr. Lewis, many pediatricians hesitate to prescribe Wegovy to young people, fearful that too little is known about long term effects, and mindful of past cases when problems emerged years after a drug was approved. Twenty-two percent of adolescents age 12 to 19 have obesity. Research shows that most are unlikely to ever overcome the condition — advice to diet and exercise usually has not helped. The reason, obesity researchers say, is that obesity is not caused by a lack of will power. Instead, it is a chronic disease characterized by an overwhelming desire to eat. Of particular concern to doctors are the 6 percent of children and adolescents with severe obesity, which is defined as having a body mass index at or above 120 percent of the 95th percentile for height and weight. “We are not talking about kids who are mildly overweight,” said Susan Yanovski, co-director of the office of obesity research at the National Institute of Diabetes and Digestive and Kidney Diseases. Such extreme obesity in adolescents, she said, often has “a really severe course.” These teenagers develop diabetes, heart disease, high blood pressure, kidney failure and eye damage much earlier than adults with obesity. “It is terrifying,” Dr. Yanovski added. The seriousness of health outcomes for obese teenagers motivated the American Academy of Pediatrics to recommend weight loss drugs like Wegovy for adolescents in January, after the Food and Drug Administration approved it for people age 12 and older. When that happened, experts in obesity medicine were elated, knowing full well the scope of the problem. “We said, Wow, we finally have something we can offer,” Dr. Yanovski said. Still, drugs like Wegovy are new, and the impediments to using them are snowballing. Doctors also worry about the dearth of data on long-term safety. And those who want to prescribe Wegovy say that they are beset by roadblocks put up by health insurers along with severe and continuing drug shortages. © 2023 The New York Times Company

Keyword: Obesity
Link ID: 29044 - Posted: 12.13.2023

By Yasemin Saplakoglu Erin Calipari comes from a basketball family. Her father, John Calipari, has coached college and professional basketball since 1998, leading six teams to the NCAA Final Four, and her brother coaches men’s basketball at Vanderbilt University in Nashville, Tennessee, where she now works. But when she joined her college team as an undergraduate, she realized her strengths lay elsewhere. “I was fine. I wasn’t great,” she said. “It was pretty clear to me a couple years in that it was not a career path.” Off the court, as a biology major she gravitated toward hormones and neurotransmitters. She grew fascinated with the neurobiology of how and why drugs such as cocaine and opioids are addictive, as she learned about the effects of ecstasy on the serotonin system. “I thought drugs were so cool because they hijack the brain,” she said. “Drugs essentially take the normal systems we have in our body and drive them in a way that makes you want to take drugs again.” After pursuing graduate work in neuroscience, in 2017 Calipari set up her lab at Vanderbilt to explore how addiction is connected to the ways the brain learns and makes decisions. “Deciding what to do and what not to do is really fundamental to everything we do,” Calipari said. “You put your hand on a hot stove, you learn really quickly not to do that again.” Addiction can diminish a person’s ability to learn that drug use is hurting them, and also their ability to learn anything at all. Her world still collides with sports, for instance when she gives talks to athletes about the dangers of substance use. Athletes can be vulnerable to addiction when they are prescribed pain medicines, such as opioids, for injuries. There is a risk of dependence if opioids are taken for long periods of time, even when patients follow doctors’ orders — a fact that has led to a nationwide public health emergency. Tennessee is an epicenter of the opioid epidemic. In 2022, Nashville had the second-highest rate of overdose deaths in the country. All Rights Reserved © 2023

Keyword: Drug Abuse
Link ID: 29039 - Posted: 12.09.2023

By Amitha Kalaichandran In May, I was invited to take part in a survey by the National Academies of Sciences, Engineering, and Medicine to better delineate how long Covid is described and diagnosed as part of The National Research Action Plan on Long Covid. The survey had several questions around definitions and criteria to include, such as “brain fog” often experienced by those with long Covid. My intuition piqued, and I began to wonder about the similarities between these neurological symptoms and those experienced by people with attention-deficit/hyperactivity disorder, or ADHD. As a medical journalist with clinical and epidemiological experience, I found the possible connection and its implications impossible to ignore. We know that three years of potential exposure to SARS-CoV-2, in combination with the shift in social patterns (including work-from-home and social isolation), has impacted several aspects of neurocognition, as detailed in a recent report from the Substance Abuse and Mental Health Services Administration. A 2021 systematic review found persistent neuropsychiatric symptoms in Covid-19 survivors, and a 2021 paper in the journal JAMA Network Open found that executive functioning, processing speed, memory, and recall were impacted in patients hospitalized with Covid-19. Long Covid may indeed be linked to developing chronic neurocognitive issues, and even dementia may be accelerated. The virus might impact the frontal lobe, the area that governs executive function — which involves how we make decisions and plan, use our working memory, and control impulses. In October, a paper in Cell reported that long Covid brain fog could be traced to serotonin depletion driven by immune system proteins called viral-associated interferons. Similarly, the symptoms of attention-deficit/hyperactivity disorder, or ADHD, are believed to be rooted structurally in the frontal lobe and possibly from a naturally low level of the neurotransmitter dopamine, with contributions from norepinephrine, serotonin, and GABA. This helps explain why people with ADHD, who experience inattention, hyperactivity, and impulsivity, among other symptoms, may seek higher levels of stimulation: to activate the release of dopamine. However, a deficit in serotonin can also trigger ADHD. The same neurotransmitter, when depleted, may be responsible for brain fog in long Covid.

Keyword: ADHD
Link ID: 29038 - Posted: 12.09.2023

By Amanda Gefter On a February morning in 1935, a disoriented homing pigeon flew into the open window of an unoccupied room at the Hotel New Yorker. It had a band around its leg, but where it came from, or was meant to be headed, no one could say. While management debated what to do, a maid rushed to the 33rd floor and knocked at the door of the hotel’s most infamous denizen: Nikola Tesla. The 78-year-old inventor quickly volunteered to take in the homeless pigeon. “Dr. Tesla … dropped work on a new electrical project, lest his charge require some little attention,” reported The New York Times. “The man who recently announced the discovery of an electrical death-beam, powerful enough to destroy 10,000 airplanes at a swoop, carefully spread towels on his window ledge and set down a little cup of seed.” Nikola Tesla—the Serbian-American scientist famous for designing the alternating current motor and the Tesla coil—had, for years, regularly been spotted skulking through the nighttime streets of midtown Manhattan, feeding the birds at all hours. In the dark, he’d sound a low whistle, and from the gloom, hordes of pigeons would flock to the old man, perching on his outstretched arms. He was known to keep baskets in his room as nests, along with caches of homemade seed mix, and to leave his windows perpetually open so the birds could come and go. Once, he was arrested for trying to lasso an injured homing pigeon in the plaza of St. Patrick’s Cathedral, and, from his holding cell in the 34th Street precinct, had to convince the officers that he was—or had been—one of the most famous inventors in the world. It had been years since he’d produced a successful invention. He was gaunt and broke—living off of debt and good graces—having been kicked out of a string of hotels, a trail of pigeon droppings and unpaid rent in his wake. He had no family or close friends, except for the birds. © 2023 NautilusNext Inc.,

Keyword: Consciousness
Link ID: 29034 - Posted: 12.09.2023

Saga Briggs Trauma is not merely a phenomenon of the mind but also a condition physically embedded in the body, often eluding our conscious awareness and affecting our overall health. That was the main argument in psychiatrist Bessel van der Kolk’s 2014 bestseller The Body Keeps the Score, which quickly became a modern classic among trauma researchers, clinicians, and survivors. The book shifted how many in the West view psychiatric illness, which was often viewed solely through a psychological or neurochemical lens, and it sparked new interest in more holistic treatments for trauma that had long been considered alternative: yoga, eye movement desensitization and reprocessing therapy (EMDR), the performing arts, and psychedelics, to name a few. But what does it really mean for the body to “keep the score”? Is it biologically possible for the viscera to actually store and release trauma? In his book, van der Kolk writes: “The body keeps the score. If the memory of trauma is encoded in the viscera, in heartbreaking and gut-wrenching emotions, in autoimmune disorders and skeletal/muscular problems, and if mind/brain/visceral communication is the royal road to emotion regulation, this demands a radical shift in our therapeutic assumptions.” Can the body “keep score”? Recently, neuroscientists have expressed skepticism over the notion that the body can “keep score” of anything. In a 2023 Big Think video, Lisa Feldman Barrett argued that everything, including trauma, is in our heads, and that “the brain keeps the score and the body is the scorecard.” In her view, everything we experience is constructed by the brain, which learns to predict how we will feel based on past experiences, issues, and sensations that seem to come from our body but actually come from our brain. “When you feel your heart beating, you are not feeling it in your chest, you are feeling it in your brain,” she said. “Your body is always sending sensory signals to the brain, of course, but emotions are made in the brain, not in the body. They are experienced in the brain, like everything else you experience, not in the body. If you experience a trauma, you experience it in your brain.”

Keyword: Emotions; Stress
Link ID: 29031 - Posted: 12.06.2023

By Jake Buehler Nesting chinstrap penguins take nodding off to the extreme. The birds briefly dip into a slumber many thousands of times per day, sleeping for only seconds at a time. The penguins’ breeding colonies are noisy and stressful places, and threats from predatory birds and aggressive neighbor penguins are unrelenting. The extremely disjointed sleep schedule may help the penguins to protect their young while still getting enough shut-eye, researchers report in the Dec. 1 Science. The findings add to evidence “that avian sleep can be very different from the sleep of land mammals,” says UCLA neuroscientist Jerome Siegel. Nearly a decade ago, behavioral ecologist Won Young Lee of the Korea Polar Research Institute in Incheon noticed something peculiar about how chinstrap penguins (Pygoscelis antarcticus) nesting on Antarctica’s King George Island were sleeping. They would seemingly doze off for very short periods of time in their cacophonous colonies. Then in 2018, Lee learned about frigate birds’ ability to steal sleep while airborne on days-long flights. Lee teamed up with sleep ecophysiologist Paul-Antoine Libourel of the Lyon Neuroscience Research Center in France and other researchers to investigate the penguins’ sleep. In 2019, the team studied the daily sleep patterns of 14 nesting chinstrap penguins using data loggers mounted on the birds’ backs. The devices had electrodes surgically implanted into the penguins’ brains for measuring brain activity. Other instruments on the data loggers recorded the animals’ movements and location. Nesting penguins had incredibly fragmented sleep patterns, taking over 600 “microsleeps” an hour, each averaging only four seconds, the researchers found. At times, the penguins slept with only half of their brain; the other half stayed awake. All together, the oodles of snoozes added up, providing over 11 hours of sleep for each brain hemisphere across more than 10,000 brief sleeps each day. © Society for Science & the Public 2000–2023.

Keyword: Sleep; Evolution
Link ID: 29028 - Posted: 12.02.2023

By Catherine Offord As millions in the United States settle down to Thanksgiving dinner this week, few will be pondering a major question in neuroscience: Why, when so much of life across the animal kingdom revolves around finding and consuming food, do we ever stop eating? Scientists have identified brain regions and even specific cells involved in terminating meals. But exactly how this process is coordinated remains murky. Now, using brain recordings from mice tucking into food, researchers have for the first time identified how specific neurons in a region called the caudal nucleus of the solitary tract (cNTS) switch on during a meal to slow down and eventually end eating. “Nobody has really been able to [do this] in awake, behaving animals” before, says Nicholas Betley, a neuroscientist at the University of Pennsylvania who was not involved in the work. The findings, published today in Nature, suggest the brain manages a coordinated sequence of behavioral responses to food as it travels from the mouth through the gastrointestinal tract, and could provide new insight into humans’ eating behaviors and disorders, he adds. Previous research on what causes animals to stop eating has largely focused on two types of cells located in the cNTS. One is prolactin-releasing hormone (PRLH) neurons, which have been linked to many functions, including the inhibition of feeding behavior. The other is GCG neurons, which produce glucagon-like peptide-1—the appetite-suppressing hormone mimicked by newly popular weight loss drugs such as Wegovy. Studies of anesthetized animals have found that both neuron types become active in response to the stomach filling, which researchers mimic by inflating a balloon in the stomach or by directly infusing food. But such techniques are a poor proxy for what happens in real life, says Zachary Knight, a neurobiologist and Howard Hughes Medical Institute investigator at the University of California, San Francisco (UCSF). “You don’t really have any sense of what’s happening dynamically.”

Keyword: Obesity
Link ID: 29023 - Posted: 11.26.2023

Nell Greenfieldboyce If you've got itchy skin, it could be that a microbe making its home on your body has produced a little chemical that's directly acting on your skin's nerve cells and triggering the urge to scratch. That's the implication of some new research that shows how a certain bacteria, Staphylococcus aureus, can release an enzyme that generates an itchy feeling. What's more, a drug that interferes with this effect can stop the itch in laboratory mice, according to a new report in the journal Cell. "That's exciting because it's a drug that's already approved for another condition, but maybe it could be useful for treating itchy skin diseases like eczema," says Isaac Chiu, a scientist at Harvard Medical School who studies interactions between microbes and nerve cells. He notes that eczema or atopic dermatitis is actually pretty common, affecting about 20% of children and 10% of adults. In the past, says Chiu, research on itchy skin conditions has focused on the role of the immune response and inflammation in generating the itch sensation. People with eczema often take medications aimed at immune system molecules. But scientists have also long known that people with eczema frequently have skin that's colonized by Staphylococcus aureus, says Chiu, even though it's never been clear what role the bacteria might play in this condition. Chiu's previous lab work had made him realize that bacteria can directly act on nerve cells to cause pain. "So this made us ask: Could certain microbes like Staphylococcus aureus also particularly be in some way linked to itch?" says Chiu. "Is there a role for microbes in talking to itch neurons?" He and his colleagues first found that putting this bacteria on the skin of mice resulted in vigorous scratching by these animals, leading to damaged skin that spread beyond the original exposure site. © 2023 npr

Keyword: Pain & Touch
Link ID: 29022 - Posted: 11.26.2023

By Hannah Docter-Loeb Paxlovid can prevent severe illness from COVID-19, but it comes with a price: In many users, the antiviral drug leaves a weird, metallic aftertaste that can last for days—a condition nicknamed “Paxlovid mouth.” Now, researchers say they’ve figured out why. A component of Paxlovid activates one of the tongue’s bitter taste receptors even at low levels, which may draw out the yuck factor, the team reports this month in Biochemical and Biophysical Research Communications. The work could lead to ways to alleviate the unpleasant side effect. The study is a “good first step” in teasing apart the mechanism behind Paxlovid mouth, says Alissa Nolden, a sensory scientist at the University of Massachusetts Amherst who was not involved with the research. But she says more work will be needed to truly understand why the metallic taste lingers for so long. Paxlovid is composed of two antivirals: nirmatrelvir and ritonavir. Nirmatrelvir blocks a key protein that SARS-CoV-2 needs to replicate. Ritonavir helps maintain the level of nirmatrelvir in the blood. Scientists have suspected that ritonavir is the primary culprit behind Paxlovid mouth. It was originally used in HIV medications and was known to directly taste bitter. A recent study also demonstrated that the compound acts on several tongue receptors that respond to bitter taste. However, ritonavir’s bitterness is short-lived, says Peihua Jiang, a molecular biologist at the Monell Chemical Senses Center, an independent research institute. So in the new study, he and colleagues looked more closely at nirmatrelvir. They added the antiviral to various groups of cells, each collection with a different member of the 25 human bitter taste receptors. They then identified the receptors that responded most vigorously to the compound by changes in a fluorescence marker in the cells. Nirmatrelvir seemed to hone in on TAS2R1, one of the primary receptors responsible for the bitter aftertaste of antiviral medicines, the researchers found. The compound activated the receptor even when its concentration was relatively low, which could explain why Paxlovid causes a persistent bitter taste.

Keyword: Chemical Senses (Smell & Taste)
Link ID: 29016 - Posted: 11.22.2023

By Annie Roth A few years ago, Nicolas Fasel, a biologist at the University of Lausanne in Switzerland, and his colleagues developed a fascination with the penises of serotine bats, a species found in woodlands and the attics of old buildings across Europe and Asia. Serotine bats sport abnormally long penises with wide, heart-shaped heads. When erect, the members are around seven times longer than the female’s vagina, and their bulbous heads are seven times wider than the female’s vaginal opening. “We wondered: How does that work? How can they use that for copulation?” Dr. Fasel recalled. What they discovered has overturned an assumption about mammalian reproduction, namely that procreation must always involve penetration. In a study, published Monday in the journal Current Biology, Dr. Fassel and his colleagues presented evidence that serotine bats mate without penetration, making them the first mammals known to do so. Instead of using their penises to penetrate their partners, the scientists found, the male bats use them to push their partner’s tail membrane out of the way so they can align their openings and engage in contact mating, a behavior similar to one found in birds and known as “cloacal kissing.” To learn how these bats overcome their substantial genital size difference, Dr. Fasel and his colleagues analyzed nearly 100 videos of serotine bats mating. The videos were provided by a bat rehabilitation center in Ukraine and a citizen scientist filming bats in the attic of a church in the Netherlands. The footage revealed a mating strategy unlike any other used by mammals. While the two bats hang upside down, the male climbs on the female’s back and grasps the nape of her neck. Once he has a firm hold, the male will use his erect penis to push the female’s tail membrane to the side and probe between her legs until he has located her vulva. The male then presses the heart-shaped head of his penis to the female’s vulva and holds it there until the deed is done. While this process took less than an hour for most of the couples the researchers observed, one pair went at it for nearly 13 hours. “It’s a really weird reproductive strategy, but bats are weird and have a lot of weird reproductive strategies,” said Patty Brennan, a biologist at Mount Holyoke College in Massachusetts who studies the evolution of genital morphology but was not involved in the study. © 2023 The New York Times Company

Keyword: Sexual Behavior; Evolution
Link ID: 29014 - Posted: 11.22.2023

Jon Hamilton MICHEL MARTIN, HOST: If you are thinking about brining that turkey for Thanksgiving - and full disclosure here, I will be doing that - here is something to consider. Food and drinks that are really salty can be appealing one day and off-putting the next. And scientists think they've figured out why. NPR's Jon Hamilton reports on a study that found two separate brain circuits that affect the taste for salt. JON HAMILTON, BYLINE: Our relationship with salt is complicated. Yuki Oka, a scientist at Caltech, says sodas, sports drinks and even tap water all contain a little salt, also known as sodium chloride. YUKI OKA: You enjoy low-sodium water, but if you imagine very high concentration of sodium, like ocean water, you really hate it. HAMILTON: Unless your body is really low on salt. That's pretty rare in people these days, but Oka says experiments with animals show that when salt levels plummet, the tolerance for salty water goes up. OKA: If your body needs sodium, then animals immediately start liking ocean water. HAMILTON: They crave sodium, and they can tolerate it in high concentrations they would normally avoid. Oka wanted to know how this system works in the brain, so he and a team of scientists studied mice. They showed that one set of neurons toward the back of the brain regulates the craving for salt. OKA: If you stimulate these neurons, then animals run to sodium source and then start eating. HAMILTON: Another group of neurons toward the front of the brain normally sets an upper limit on salt tolerance, but when salt levels get low enough, Oka says, these neurons get switched off. OKA: This means that the sodium craving and the sodium tolerance are controlled by completely different types of neurons. HAMILTON: The finding, which appears in the journal Cell, is part of a growing field of study called interoception. It deals with internal sensations like hunger and pain. Stephen Liberles, a cell biologist at Harvard Medical School, says scientists already know a lot about how the brain deals with sensory information coming from the eyes, ears, nose and skin. © 2023 npr

Keyword: Obesity
Link ID: 29013 - Posted: 11.22.2023

By Carl Zimmer Sign up for Science Times Get stories that capture the wonders of nature, the cosmos and the human body. Get it sent to your inbox. If a troop of baboons encounters another troop on the savanna, they may keep a respectful distance or they may get into a fight. But human groups often do something else: They cooperate. Tribes of hunter-gatherers regularly come together for communal hunts or to form large-scale alliances. Villages and towns give rise to nations. Networks of trade span the planet. Human cooperation is so striking that anthropologists have long considered it a hallmark of our species. They have speculated that it emerged thanks to the evolution of our powerful brains, which enable us to use language, establish cultural traditions and perform other complex behaviors. But a new study, published in Science on Thursday, throws that uniqueness into doubt. It turns out that two groups of apes in Africa have regularly mingled and cooperated with each other for years. “To have extended, friendly, cooperative relationships between members of other groups who have no kinship ties is really quite extraordinary,” said Joan Silk, a primatologist at Arizona State University who was not involved in the study. The new research comes from long-term observations of bonobos, an ape species that lives in the forests of the Democratic Republic of Congo. A century ago, primatologists thought bonobos were a slender subspecies of chimpanzee. But the two species are genetically distinct and behave in some remarkably different ways. Among chimpanzees, males hold a dominant place in society. They can be extremely violent, even killing babies. In bonobo groups, however, females dominate, and males have never been observed to commit infanticide. Bonobos often defuse conflict with sex, a strategy that primatologists have not observed among chimpanzees. Scientists made most of their early observations of bonobos in zoos. But in recent years they’ve conducted long-term studies of the apes in the wild. © 2023 The New York Times Company

Keyword: Evolution; Aggression
Link ID: 29011 - Posted: 11.18.2023

By Emily Cataneo It’s 1922. You’re a scientist presented with a hundred youths who, you’re told, will grow up to lead conventional adult lives — with one exception. In 40 years, one of the one hundred is going to become impulsive and criminal. You run blood tests on the subjects and discover nothing that indicates that one of them will go off the rails in four decades. And yet sure enough, 40 years later, one bad egg has started shoplifting and threatening strangers. With no physical evidence to explain his behavior, you conclude that this man has chosen to act out of his own free will. Now, imagine the same experiment starting in 2022. This time, you use the blood samples to sequence everyone’s genome. In one, you find a mutation that codes for something called tau protein in the brain and you realize that this individual will not become a criminal in 40 years out of choice, but rather due to dementia. It turns out he did not shoplift out of free will, but because of physical forces beyond his control. Now, take the experiment a step further. If a man opens fire in an elementary school and kills scores of children and teachers, should he be held responsible? Should he be reviled and punished? Or should observers, even the mourning families, accept that under the right circumstances, that shooter could have been them? Does the shooter have free will while the man with dementia does not? Can you explain why? These provocative, even disturbing questions about similar scenarios underlie two new books about whether humans have control over our personalities, opinions, actions, and fates. “Free Agents: How Evolution Gave Us Free Will,” by professor of genetics and neuroscience Kevin J. Mitchell, and “Determined: A Science of Life Without Free Will,” by biology and neurology professor Robert M. Sapolsky, both undertake the expansive task of using the tools of science to probe the question of whether we possess free will, a question with stark moral and existential implications for the way we structure human society.

Keyword: Consciousness
Link ID: 29009 - Posted: 11.18.2023