By Tomas Weber Trinian Taylor, a 52-year-old car dealer, pushed his cart through the aisles of a supermarket as I pretended not to follow him. It was a bright August day in Northern California, and I had come to the store to meet Emily Auerbach, a relationship manager at Mattson, a food-innovation firm that creates products for the country’s largest food and beverage companies: McDonald’s and White Castle, PepsiCo and Hostess. Auerbach was trying to understand the shopping behavior of Ozempic users, and Taylor was one of her case studies. She instructed me to stay as close as I could without influencing his route around the store. In her experience of shop-alongs, too much space, or taking photos, would be a red flag for the supermarket higher-ups, who might figure out we were not here to shop. “They’d be like, ‘You need to exit,’” she said. Auerbach watched in silence as Taylor, who was earning $150 in exchange for being tailed, propelled his cart through snack aisles scattered with products from Mattson’s clients. He took us straight past the Doritos and the Hostess HoHos, without a side glance at the Oreos or the Cheetos. We rushed past the Pop-Tarts and the Hershey’s Kisses, the Lucky Charms and the Lay’s — they all barely registered. Clumsily, close on his heels, Auerbach and I stumbled right into what has become, under the influence of the revolutionary new diet drug, Taylor’s happy place: the produce section. He inspected the goods. “I’m on all of these,” he told us. “I eat a lot of pineapple. A lot of pineapple, cucumber, ginger. Oh, a lot of ginger.” Taylor, who lives in Hayward, Calif., used to nurse a sugar addiction, he said, but he can no longer stomach Hostess treats. A few days earlier, his daughter fed him some candy. “I just couldn’t,” he said. “It was so sweet it choked me.” His midnight snack used to be cereal, but now he stirs at night with strange urges. Salads. Chicken. He has sworn off canned sodas and fruit juices and infuses his water with lemon and cucumber. He dropped a heavy bag of lemons into the cart and sauntered over to the leafy vegetables. “I love Swiss chard,” he said. “I eat a lot of kale.” For decades, Big Food has been marketing products to people who can’t stop eating, and now, suddenly, they can. The active ingredient in Ozempic, as in Wegovy, Zepbound and several other similar new drugs, mimics a natural hormone, called glucagon-like peptide-1 (GLP-1), that slows digestion and signals fullness to the brain. Around seven million Americans now take a GLP-1 drug, and Morgan Stanley estimates that by 2035 the number of U.S. users could expand to 24 million. © 2024 The New York Times Company

Keyword: Obesity
Link ID: 29569 - Posted: 11.20.2024

Ian Sample Science editor Losing weight can be a frustrating game: after months of successful slimming, the kilos may soon pile on again, leaving people back where they started. No one factor drives the yo-yo effect, but new research points to fatty tissue as a leading culprit. Fat “remembers” past obesity and resists attempts to lose weight, scientists found. Researchers identified the biological memory after examining fat tissue from people with obesity before and after they lost weight after bariatric surgery. The tissues were further compared with fat from healthy individuals who had never been obese. The analysis showed that fat cells were affected by obesity in a way that altered how they responded to food, potentially for years. In tests, the cells grew faster than others by absorbing nutrients more swiftly. Prof Ferdinand von Meyenn, a senior author on the study at the Federal Institute of Technology in Zurich, said: “Our study indicates that one reason maintaining body weight after initial weight loss is difficult is that the fat cells remember their prior obese state and likely aim to return to this state. “The memory seems to prepare cells to respond quicker, and maybe also in unhealthy ways, to sugars or fatty acids.” Further work on mouse cells traced the biological memory to chemical modifications on DNA or the proteins DNA is wrapped around. These epigenetic changes alter gene activity and metabolism. Writing in Nature, the scientists describe how formerly obese mice gained weight faster than others when put on a high-fat diet, suggesting a shift in metabolism that made it easier for them to gain weight. The memory of obesity in fat cells was not solely to blame, however. The scientists suspect a similar memory exists in brain cells that affects how much food animals consume and how much energy they expend. © 2024 Guardian News & Media Limited

Keyword: Obesity
Link ID: 29568 - Posted: 11.20.2024

By Joanne Silberner To describe the destructive effects of intense health anxiety to his young doctors in training at Columbia University Irving Medical Center in New York City, psychiatrist Brian Fallon likes to quote 19th-century English psychiatrist Henry Maudsley: “The sorrow which has no vent in tears may make other organs weep.” That weeping from other parts of the body may come in the form of a headache that, in the mind of its sufferer, is flagging a brain tumor. It may be a rapid heartbeat a person wrongly interprets as a brewing heart attack. The fast beats may be driven by overwhelming, incapacitating anxiety. Hal Rosenbluth, a businessman in the Philadelphia area, says he used to seek medical care for the slightest symptom. In his recent book Hypochondria, he describes chest pains, breathing difficulties and vertigo that came on after he switched from a daily diabetes drug to a weekly one. He ended up going to the hospital by ambulance for blood tests, multiple electrocardiograms, a chest x-ray, a cardiac catheterization and an endoscopy, all of which were normal. Rosenbluth’s worries about glucose levels had led him to push for the new diabetes drug, and its side effects were responsible for many of his cardiac symptoms. His own extreme anxiety had induced doctors to order the extra care. Hypochondria can, in extreme cases, leave people unable to hold down a job or make it impossible for them to leave the house, cook meals, or care for themselves and their families. Recent medical research has shown that hypochondria is as much a real illness as depression and post-traumatic stress disorder. This work, scientists hope, will convince doctors who believed the disorder was some kind of character flaw that their patients are truly ill—and in danger. A study published just last year showed that people with hypochondria have higher death rates than similar but nonafflicted people, and the leading nonnatural cause of death was suicide. It was relatively rare, but the heightened risk was clear.

Keyword: Stress; Attention
Link ID: 29567 - Posted: 11.20.2024

By Laura Sanders Growing up, Roberto S. Luciani had hints that his brain worked differently than most people. He didn’t relate when people complained about a movie character looking different than what they’d pictured from the book, for instance. But it wasn’t until he was a teenager that things finally clicked. His mother had just woken up and was telling him about a dream she had. “Movielike,” is how she described it. “Up until then, I assumed that cartoon depictions of imagination were exaggerated,” Luciani says, “I asked her what she meant and quickly realized my visual imagery was not functioning like hers.” That’s because Luciani has a condition called aphantasia — an inability to picture objects, people and scenes in his mind. When he was growing up, the term didn’t even exist. But now, Luciani, a cognitive scientist at the University of Glasgow in Scotland, and other scientists are getting a clearer picture of how some brains work, including those with a blind mind’s eye. In a recent study, Luciani and colleagues explored the connections between the senses, in this case, hearing and seeing. In most of our brains, these two senses collaborate. Auditory information influences activity in brain areas that handle vision. But in people with aphantasia, this connection isn’t as strong, researchers report November 4 in Current Biology. While in a brain scanner, blindfolded people listened to three sound scenes: A forest full of birds, a crowd of people, and a street bustling with traffic. In 10 people without aphantasia, these auditory scenes create reliable neural hallmarks in parts of the visual cortex. But in 23 people with aphantasia, these hallmarks were weaker. © Society for Science & the Public 2000–2024.

Keyword: Attention
Link ID: 29566 - Posted: 11.20.2024

By Miryam Naddaf Humans have evolved disproportionately large brains compared with our primate relatives — but this neurological upgrade came at a cost. Scientists exploring the trade-off have discovered unique genetic features that show how human brain cells handle the stress of keeping a big brain working. The work could inspire new lines of research to understand conditions such as Parkinson’s disease and schizophrenia. The study, which was posted to the bioRxiv preprint server on 15 November1, focuses on neurons that produce the neurotransmitter dopamine, which is crucial for movement, learning and emotional processing. By comparing thousands of laboratory-grown dopamine neurons from humans, chimpanzees, macaques and orangutans, researchers found that human dopamine neurons express more genes that boost the activity of damage-reducing antioxidants than do those of the other primates. The findings, which are yet to be peer-reviewed, are a step towards “understanding human brain evolution and all the potentially negative and positive things that come with it”, says Andre Sousa, a neuroscientist at the University of Wisconsin–Madison. “It's interesting and important to really try to understand what's specific about the human brain, with the potential of developing new therapies or even avoiding disease altogether in the future.” Just as walking upright has led to knee and back problems, and changes in jaw structure and diet resulted in dental issues, the rapid expansion of the human brain over evolutionary time has created challenges for its cells, says study co-author Alex Pollen, a neuroscientist at the University of California, San Francisco. “We hypothesized that the same process may be occurring, and these dopamine neurons may represent vulnerable joints.” © 2024 Springer Nature Limited

Keyword: Development of the Brain; Stress
Link ID: 29565 - Posted: 11.20.2024

By Sara Manning Peskin Seven Deadly Sins: The Biology of Being Human Guy Leschziner William Collins (2024) There is no food in sight in Alex’s house. Even the rubbish bin is fastened closed. The kitchen is like a bank vault, hidden behind a locked door from which staff members bring out portioned meals for Alex and her six housemates, all of whom have a genetic disorder called Prader–Willi syndrome. Although Alex was born underweight, by early adulthood she could eat three servings in a sitting, had gorged on cat food and carried 110 kilograms on her small frame. Her ‘gluttony’, writes neurologist Guy Leschziner in Seven Deadly Sins, is the result of a condition that instils such a voracious appetite that some people have eaten to the point of bursting their stomachs. Whereas marketers of diet programmes have conventionally coupled obesity to a lack of willpower, Leschziner uses Alex’s case to argue that body size is driven less by moralistic factors and more by genetics, hormones and gut microorganisms. Similar themes run throughout the book, as the author examines lust, envy and other supposed infractions, gathering examples of people who exhibit these traits because of neurological disorders. Like his earlier books about sleep and the senses, Seven Deadly Sins educates as much as it entertains, turning complex neuroscientific topics into fodder for cocktail-party conversations. The biology of behaviour Exploring wrath, Leschziner introduces two men with epilepsy. One lurches into rages in the wake of his seizures and finds himself surrounded by shards of broken dishes afterwards. Another, a “gentle giant”, has anger outbursts because of a medication prescribed to control his disease. © 2024 Springer Nature Limited

Keyword: Emotions
Link ID: 29564 - Posted: 11.20.2024

By Claudia López Lloreda Fear memories serve a purpose: A mouse in the wild learns to fear the sound of footsteps, which helps it avoid predators. But in certain situations, those fear memories can also tinge neutral memories with fear, resulting in maladaptive behavior. A mouse or person, for instance, may learn to fear stimuli that should presumably be safe. This shift can occur when an existing fear memory broadens—either by recruiting inappropriate neurons into the cell ensemble that contains it or by linking up to a previously neutral memory, according to two new studies in mice, one published today and another last week. Memories are embodied in the brain through sparse ensembles of neurons, called engrams, that activate when an animal forms a new memory or recalls it later. These ensembles were thought to be “stable and permanent,” says Denise Cai, associate professor of neuroscience at the Icahn School of Medicine at Mount Sinai, who led one of the studies. But the new findings reveal how, during times of fear and stress, memories can become malleable, either as they are brought back online or as the neurons that encode them expand. There is “this really powerful ability of stress to look back and change memories for neutral experiences that have come before by pulling them into the same neural representation or by exciting them more during offline periods,” says Elizabeth Goldfarb, assistant professor of psychiatry at the Yale School of Medicine, who was not involved in the studies. That challenges the previous dogma, Cai says. “We’ve learned that these memory ensembles are actually quite dynamic.” © 2024 Simons Foundation

Keyword: Learning & Memory; Stress
Link ID: 29563 - Posted: 11.16.2024

By Ann Gibbons As the parent of any teenager knows, humans need a long time to grow up: We take about twice as long as chimpanzees to reach adulthood. Anthropologists theorize that our long childhood and adolescence allow us to build comparatively bigger brains or learn skills that help us survive and reproduce. Now, a study of an ancient youth’s teeth suggests a slow pattern of growth appeared at least 1.8 million years ago, half a million years earlier than any previous evidence for delayed dental development. Researchers used state-of-the art x-ray imaging methods to count growth lines in the molars of a member of our genus, Homo, who lived 1.77 million years ago in what today is Dmanisi, Georgia. Although the youth developed much faster than children today, its molars grew as slowly as a modern human’s during the first 5 years of life, the researchers report today in Nature. The finding, in a group whose brains are hardly larger than chimpanzees, could provide clues to why humans evolved such long childhoods. “One of the main questions in paleoanthropology is to understand when this pattern of slow development evolves in [our genus] Homo,” says Alessia Nava, a bioarchaeologist at the Sapienza University of Rome who is not part of the study. “Now, we have an important hint.” Others caution that although the teeth of this youngster grew slowly, other individuals, including our direct ancestors, might have developed faster. Researchers have known since the 1930s that humans stay immature longer than other apes. Some posit our ancestors evolved slow growth to allow more time and energy to build bigger brains, or to learn how to adapt to complex social interactions and environments before they had children. To pin down when this slow pattern of growth arose, researchers often turn to teeth, especially permanent molars, because they persist in the fossil record and contain growth lines like tree rings. What’s more, the dental growth rate in humans and other primates correlates with the development of the brain and body.

Keyword: Evolution; Sexual Behavior
Link ID: 29562 - Posted: 11.16.2024

Ari Daniel The birds of today descended from the dinosaurs of yore. Researchers have known relatively little, however, about how the bird's brain took shape over tens of millions of years. "Birds are one of the most intelligent groups of living vertebrate animals," says Daniel Field, a vertebrate biologist at the University of Cambridge. "They really rival mammals in terms of their relative brain size and the complexity of their behaviors, social interactions, breeding displays." Now, a newly discovered fossil provides the most complete glimpse to date of the brains of the ancestral birds that once flew above the dinosaurs. The species was named Navaornis hestiae, and it's described in the journal Nature. Piecing together how bird brains evolved has been a challenge. First, most of the fossil evidence dates back to tens of millions of years before the end of the Cretaceous period when dinosaurs went extinct and birds diversified. In addition, the fossils of feathered dinosaurs that have turned up often have a key problem. "They're beautiful, but they're all like roadkill," says Luis Chiappe, a paleontologist and curator at the Natural History Museum of Los Angeles County. "They're all flattened and there are aspects that you're never going to be able to recover from those fossils." The shape and three-dimensional structure of the brain are among those missing aspects. But in 2016, Brazilian paleontologist William Nava discovered a remarkably well-preserved fossil in São Paulo state. It came from a prehistoric bird that fills in a crucial gap in understanding of how modern bird brains evolved. © 2024 npr

Keyword: Evolution; Development of the Brain
Link ID: 29561 - Posted: 11.16.2024

By Elena Renken Small may be mightier than we think when it comes to brains. This is what neuroscientist Marcella Noorman is learning from her neuroscientific research into tiny animals like fruit flies, whose brains hold around 140,000 neurons each, compared to the roughly 86 billion in the human brain. Nautilus Members enjoy an ad-free experience. Log in or Join now . In work published earlier this month in Nature Neuroscience, Noorman and colleagues showed that a small network of cells in the fruit fly brain was capable of completing a highly complex task with impressive accuracy: maintaining a consistent sense of direction. Smaller networks were thought to be capable of only discrete internal mental representations, not continuous ones. These networks can “perform more complex computations than we previously thought,” says Noorman, an associate at the Howard Hughes Medical Institute. The scientists monitored the brains of fruit flies as they walked on tiny rotating foam balls in the dark, and recorded the activity of a network of cells responsible for keeping track of head direction. This kind of brain network is called a ring attractor network, and it is present in both insects and in humans. Ring attractor networks maintain variables like orientation or angular velocity—the rate at which an object rotates—over time as we navigate, integrating new information from the senses and making sure we don’t lose track of the original signal, even when there are no updates. You know which way you’re facing even if you close your eyes and stand still, for example. After finding that this small circuit in fruit fly brains—which contains only about 50 neurons in the core of the network—could accurately represent head direction, Noorman and her colleagues built models to identify the minimum size of a network that could still theoretically perform this task. Smaller networks, they found, required more precise signaling between neurons. But hundreds or thousands of cells weren’t necessary for this basic task. As few as four cells could form a ring attractor, they found. © 2024 NautilusNext Inc.,

Keyword: Development of the Brain; Vision
Link ID: 29560 - Posted: 11.16.2024

By Tim Vernimmen Few people are fond of earwigs, with their menacing abdominal pincers — whether they’re skittering across your floor, getting comfy in the folds of your camping tent or minding their own business. Scientists, too, have given them short shrift, compared with the seemingly endless attention they have lavished on social insects like ants and bees. Yet there are a handful of exceptions. Some researchers have made conscious career decisions to dig into the hidden, underground world where earwigs reside, and have found the creatures to be surprisingly interesting and social, if still not exactly endearing. Work in the 1990s and early 2000s focused on earwig courtship. These often-intricate performances of attraction and repulsion — in which pincers and antennae play prominent roles — can last hours, and the mating itself as long as 20 hours, at least in one Papua New Guinea species, Tagalina papua. The females usually decide when they’ve had enough, though males of some species use their pincers to restrain the object of their desire. Males of the bone-house earwig Marava arachidis (often found in bone meal plants and slaughterhouses) are particularly coercive, says entomologist Yoshitaka Kamimura of Keio University in Japan, who has studied earwig mating for 25 years. “They bite the female’s antennae and use a little hook on their genitalia to lock them inside her reproductive tract.” Size matters

Keyword: Sexual Behavior; Evolution
Link ID: 29559 - Posted: 11.16.2024

By Angie Voyles Askham Engrams, the physical circuits of individual memories, consist of more than just neurons, according to a new study published today in Nature. Astrocytes, too, shape how some memories are stored and retrieved, the work shows. The results represent “a fundamental change” in how the neuroscience field should think about indexing memories, says lead researcher Benjamin Deneen, professor of neurosurgery at Baylor College of Medicine. “We need to reconsider the cellular, physical basis of how we store memories.” When mice form a new memory, a specific set of neurons becomes active and expresses the immediate early gene c-FOS, past work has found. Reactivating that ensemble of neurons, the engram, causes the mice to recall that memory. Interactions between neurons and astrocytes are critical for the formation of long-term memory, according to a spatial transcriptomics study from February, and both astrocytes and oligodendrocytes are involved in memory formation, other work has shown. Yet engram studies have largely ignored the activity of non-neuronal cells, says Sheena Josselyn, senior scientist at the Hospital for Sick Children, who was not involved in the new study. But astrocytes are also active alongside neurons as memories are formed and recalled, and disrupting the star-shaped cells’ function interferes with these processes, the new work reveals. The study does not dethrone neurons as the lead engram stars, according to Josselyn. “It really shows that, yes, neurons are important. But there are also other players that we’re just beginning to understand the importance of,” she says. “It’ll help broaden our focus.” © 2024 Simons Foundation

Keyword: Learning & Memory; Glia
Link ID: 29558 - Posted: 11.13.2024

By Fred Schwaller Scott Imbrie still remembers the first time that physicians switched on the electrodes sitting on the surface of his brain. He felt a tingling, poking sensation in his hand, like “reaching into an evergreen bush”, he says. “It was like I was decorating a Christmas tree.” Back in 1985, a car crash shattered three of Imbrie’s vertebrae and severed 70% of his spinal cord, leaving him with very limited sensation or mobility in parts of his body. Now, thanks to an implanted brain–computer interface (BCI), Imbrie can operate a robotic arm, and receive sensory information related to what that arm is doing. Imbrie spends four days a week, three hours at a time, testing, refining and tuning the device with a team of researchers at the University of Chicago in Illinois. Scientists have been trying to restore mobility for people with missing or paralysed limbs for decades. The aim, historically, was to give people the ability to control prosthetics with commands from the nervous system. But this motor-first approach produced bionic limbs that were much less helpful than hoped: devices were cumbersome and provided only rudimentary control of a hand or leg. What’s more, they just didn’t feel like they were part of the body and required too much concentration to use. Scientists gradually began to realize that restoring full mobility meant restoring the ability to sense touch and temperature, says Robert Gaunt, a bioengineer at the University of Pittsburgh in Pennsylvania. Gaunt says that this realization has led to a revolution in the field. A landmark study1 came in 2016, when a team led by Gaunt restored tactile sensations in a person with upper-limb paralysis using a computer chip implanted in a region of the brain that controls the hand. Gaunt then teamed up with his Pittsburgh colleague, bioengineer Jennifer Collinger, to integrate a robotic arm with the BCI, allowing the individual to feel and manipulate objects. © 2024 Springer Nature Limited

Keyword: Robotics; Pain & Touch
Link ID: 29557 - Posted: 11.13.2024

Terry Gross We've all had bug bites, or dry scalp, or a sunburn that causes itch. But what if you felt itchy all the time — and there was no relief? Journalist Annie Lowrey suffers from primary biliary cholangitis (PBC), a degenerative liver disease in which the body mistakenly attacks cells lining the bile ducts, causing them to inflame. The result is a severe itch that doesn't respond to antihistamines or steroids. "It feels like being trapped inside your own body," Lowrey says of the disease. "I always describe it as being like a car alarm. Like, you can't stop thinking about it." PBC is impacts approximately 80,000 people in the U.S., the majority of whom are women. At its worst, Lowrey says, the itch caused her to dig holes in her skin and scalp. She's even fantasized about having limbs amputated to escape the itch. Lowrey writes about living with PBC in the Atlantic article, "Why People Itch and How to Stop It." She says a big part of her struggle is coming to terms with the fact that she may never feel fully at ease in her skin. "I talked to two folks who are a lot older than I was, just about like, how do you deal with it? How do you deal with the fact that you might itch and never stop itching? … And both of them were kind of like, 'You put up with it, stop worrying about it and get on with your life,'" she says. "I think I was mentally trapped ... and sometimes it's like, OK, ... go do something else. Life continues on. You have a body. It's OK." © 2024 npr

Keyword: Pain & Touch
Link ID: 29556 - Posted: 11.13.2024

By Kim Tingley There are two opposite paths to achievement in science. The first is straightforward: Identify a problem and set about solving it. The second is rather unscientific-sounding and perhaps more faith-based: Study in obscurity and hope serendipity strikes. In 1980, a young gastroenterologist named Jean-Pierre Raufman wound up taking the latter road through the digestive-diseases branch of the National Institutes of Health. His goal there was to gain research experience. While doing so, he chanced to meet the lead chemist of another laboratory, John Pisano, who had a passion for seeking out new and interesting examples of a specific kind of hormone, called a peptide, in animal venoms. Pisano regularly appealed to local insect and reptile enthusiasts in the classified pages of The Washington Post; in response, they would show up at his office door carrying plastic bags wriggling with possibility. Pisano offered some venom samples to Raufman for his meandering analyses. Over the following month, Raufman experimented with them to see if they stimulated pancreatic cells harvested from guinea pigs. The venom with the biggest effect by far came from a desert reptile that Raufman had never heard of: the Gila monster. Gila monsters — sluggish, thick-tailed ground dwellers — are native to southern Arizona and northern Mexico. They have blunt noses and bumpy black skin with tan, pink or orange squiggles. They spend 95 percent of their lives underground. Like their cousins to the south, Mexican beaded lizards, they are one of the very few lizard species that produces venom, which they excrete from mouth glands into grooves in their serrated teeth. The strength of their jaws is typically enough to subdue their prey (chicks, frogs, worms and the like). But if threatened and unable to escape or hide, they may bite a predator. Whenever they clamp down, piercing the skin, venom enters the victim’s bloodstream. This causes intense pain and can initiate a cascade of other symptoms that, in people, includes vomiting, dizziness, rapid heart rate, low blood pressure and, in rare circumstances, death. © 2024 The New York Times Company

Keyword: Neurotoxins; Obesity
Link ID: 29555 - Posted: 11.13.2024

Denis Campbell Health policy editor Hundreds of thousands of smokers will be given a pill that increases people’s chances of quitting, in a move that NHS bosses believe will save thousands of lives. About 85,000 people a year in England will be offered the chance to use varenicline, a once-a-day tablet that experts say is as effective as vapes at helping people to kick the habit. Amanda Pritchard, the chief executive of NHS England, hailed the pill as a potential “gamechanger” in the fight to tackle smoking and the huge harm to health it causes. The drug helps people to quit by reducing their cravings for nicotine and ensuring that it cannot affect the brain in its usual way. It has also been found to reduce the side-effects smokers can experience when they stop using tobacco, such as trouble sleeping and irritability. The NHS in England will give varenicline as part of its efforts to keep driving down the number of people who smoke. A decline in smoking rates over the past 20 years means that only 11.6% of adults in England still have the habit – about 6 million people. Health service bosses hope its use will lead to 9,500 fewer smoking-related deaths over the next five years. The drug – known at the time as Champix – began being used in 2006 and was taken by about 85,800 people a year until July 2021. It then became unavailable after the Medicines and Healthcare products Regulatory Agency (MHRA), which regulates drugs, found impurities in it. That problem has now been addressed to the MHRA’s satisfaction and it has recently approved a generic version of the drug, which NHS England will use. It cited research by University College London that found it would save £1.65 in healthcare costs for every £1 it spent on the pill. © 2024 Guardian News & Media Limited

Keyword: Drug Abuse
Link ID: 29554 - Posted: 11.13.2024

By Christina Caron In high school, Sophie Didier started falling behind. She found it difficult to concentrate on her schoolwork, felt restless in class and often got in trouble for talking too much. “I had a teacher that used to give me suckers so that I would shut up,” she said. At 15, a doctor diagnosed her with attention deficit hyperactivity disorder. Medication helped, but she discovered that having a demanding schedule was also important. In both high school and college, her grades improved when she was juggling lacrosse and other extracurricular activities with her classes. Being so busy forced her to stick to a routine. “I felt more organized then,” recalled Ms. Didier, now 24 and living in Kansas City, Mo. “Like I had a better handle on things.” Research has shown that A.D.H.D. symptoms can change over time, improving and then worsening again or vice versa. And according to a recently published study, having additional responsibilities and obligations is associated with periods of milder A.D.H.D. This might mean that staying busy had been beneficial, researchers said. It could also just mean that people with milder symptoms had been able to handle more demands, they added. Oftentimes, people with A.D.H.D. “seem to do best when there’s an urgent deadline or when the stakes are high,” said Margaret Sibley, who is a professor of psychiatry and behavioral sciences at the University of Washington School of Medicine in Seattle and who led the study. The study, published online in October in the Journal of Clinical Psychiatry, tracked 483 patients in the United States and Canada who each had a combination of inattentive and hyperactive-impulsive A.D.H.D. symptoms. The researchers followed the participants for 16 years, starting at an average age of 8. They found that about three-quarters of the patients experienced fluctuations in their symptoms, generally beginning around age 12, which included either a full or partial remission of symptoms. © 2024 The New York Times Company

Keyword: ADHD
Link ID: 29553 - Posted: 11.13.2024

By Erin Garcia de Jesús The first detailed structure of an infectious prion that causes chronic wasting disease, or CWD, reveals features that could help guide vaccine development or explain why the illness hasn’t yet made the leap to people, researchers report October 24 in Acta Neuropathologica. One such feature is a 180-degree twist between two sections of the prion. In versions engineered to infect rodents in order to study the disease, that twist doesn’t exist. Like the prion illness Creutzfeldt-Jakob disease in people, CWD prions in deer, elk and moose transform a healthy brain protein called PrP into misshapen versions that clump together and cause symptoms such as listlessness, drastic weight loss and lack of fear. While no person has contracted the disease and studies in mice and primates suggest that the risk to humans is extremely low, CWD’s spread among animals that people eat has raised concerns that it one day could jump to people (SN: 6/10/24). Understanding how deer prions misfold could help reveal why CWD doesn’t easily spread to humans. But “prions are messy,” says Byron Caughey, a biochemist at the National Institutes of Health’s Rocky Mountain Laboratories in Hamilton, Mont. Because the proteins “are very sticky and they tend to cling together,” researchers have a tough time getting a clear picture of what diseased prions look like. Previous studies looking at other prions, including rodent-adapted versions originally from sheep, showed that the proteins stack together like plates. Using hundreds of thousands of electron microscopy images, Caughey and colleagues found that a natural prion from the brain tissue of a white-tailed deer stacks in a similar way, but with some potentially key differences. © Society for Science & the Public 2000–2024.

Keyword: Prions
Link ID: 29552 - Posted: 11.13.2024

By Miryam Naddaf When a dog shakes water off its fur, the action is not just a random flurry of movements — nor a deliberate effort to drench anyone standing nearby. This instinctive reflex is shared by many furry mammals including mice, cats, squirrels, lions, tigers and bears. The move helps animals to remove water, insects or other irritants from hard-to-reach places. But underlying the shakes is a complex — and previously mysterious — neurological mechanism. Now, researchers have identified the neural circuit that triggers characteristic ‘wet dog’ shaking behaviour in mice — which involves a specific class of touch receptors, and neurons that connect the spinal cord to the brain. Their findings were published in Science on 7 November1. “The touch system is so complex and rich that [it] can distinguish a water droplet from a crawling insect from the gentle touch of a loved one,” says Kara Marshall, a neuroscientist at Baylor College of Medicine in Houston, Texas. “It’s really remarkable to be able to link a very specific subset of touch receptors to this familiar and understandable behaviour.” The hairy skin of mammals is packed with more than 12 types of sensory neuron, each with a unique function to detect and interpret various sensations. Study co-author Dawei Zhang, a neuroscientist then at Harvard Medical School in Boston, Massachusetts, and his colleagues focused on a type of ultra-sensitive touch detecting receptors called C-fibre low-threshold mechanoreceptors (C-LTMRs), which wrap around hair follicles. In humans, these receptors are associated with pleasant touch sensations, such as a soft hug or a soothing stroke. But in mice and other animals, they serve a protective role: alerting them to the presence of something on their skin, whether it’s water, dirt or a parasite. When these stimuli cause hairs on the skin to bend it activates the C-LTMRs, says Marshall, “extending the sensibility of the skin beyond just the surface”. © 2024 Springer Nature Limited

Keyword: Pain & Touch; Evolution
Link ID: 29551 - Posted: 11.09.2024

By Shaena Montanari In the Sterling Hall of Medicine at Yale University, a sign on a walk-in refrigerator door tells people to keep their voices down. Inside, about 250 ground squirrels are hibernating, each surrounded by shredded paper fluff and curled up in a clear plastic box. Shelves lined with these makeshift nests are bathed in red light that only the researchers can see, leaving the motionless animals in complete darkness. From about September to April—roughly the hibernation season for these thirteen-lined ground squirrels, which have stripes reminiscent of a chipmunk—the temperature inside the homemade hibernaculum is set at 4 degrees Celsius. The tiny rodents’ body temperature is the same as the chilly air, and their breathing and heart rates slow to just a handful of breaths and beats per minute—an energy-conserving response known as torpor. Scientists have studied this extreme physiological state for more than a century, says Elena Gracheva, whose bustling lab sits just outside the silent hibernaculum. But to date, they have focused mainly on physiological changes in individual peripheral organs that help an animal survive in cold temperatures. It is still unknown how the central nervous system regulates the process, she says. “We know a lot about physiology, but we don’t know the molecular basis.” Gracheva, professor of physiology and neuroscience at Yale University, is part of a small cadre of scientists who have set their sights on revealing those neural hibernation controls, using advanced tools to explore how the brain and other organ systems work together to maintain homeostasis. Their efforts are opening a “new era” in hibernation research, says Shona Wood, associate professor of Arctic chronobiology and physiology at the Arctic University of Norway. © 2024 Simons Foundation

Keyword: Sleep
Link ID: 29550 - Posted: 11.09.2024