By McKenzie Prillaman Wegovy, Ozempic and similar weight-loss drugs have become some of the most popular medications in the world. But legions of people are also quitting them. About two-thirds of those in the United States who started taking a drug of this class, known as GLP-1 agonists, in 2021 had stopped using them within a year, according to an industry analysis. Researchers and clinicians often view GLP-1 agonists as lifelong treatments. But myriad factors can force individuals off the medications. People might lose the means to pay for the costly drugs, experience brutal side effects, be affected by continuing shortages or be offered limited-term prescriptions. The UK National Health Service (NHS), for instance, provides only two years of coverage for people taking the drugs for weight loss. As the number of people with obesity continues to rise — the World Health Organization estimates that more than one billion people, or one-eighth of the global population, now have obesity — researchers have been answering a few key questions about what happens when people stop taking these medications for weight management. What happens to weight and health when people quit? Ozempic and Wegovy are both brand names for the drug semaglutide, which has been prescribed for several years to treat type 2 diabetes (Ozempic) and, since 2021, to those who are overweight or have obesity (Wegovy). The treatment’s aim is to reduce the risk of health complications posed by a large amount of excess body fat, such as heart and liver disease and certain cancers. The drug curbs hunger and food intake by mimicking a hormone, released by the gut after eating, that affects brain regions involved in appetite and reward. Research has shown what happens when people stop taking GLP-1 agonists. Many regain a substantial amount of what they lost with the help of the medications. The body naturally tries to stay around its own weight point, a pull that obesity specialist Arya Sharma likens to a taut rubber band. © 2024 Springer Nature Limited

Keyword: Obesity
Link ID: 29260 - Posted: 04.16.2024

Allison Aubrey Imagine if every moment is filled with a high-pitched buzz or ring that you can't turn off. More than 25 million adults in the U.S., have a condition called tinnitus, according to the American Tinnitus Association. It can be stressful, even panic-inducing and difficult to manage. Dozens of factors can contribute to the onset of tinnitus, including hearing loss, exposure to loud noise or a viral illness. There's no cure, but there are a range of strategies to reduce the symptoms and make it less bothersome, including hearing aids, mindfulness therapy, and one newer option – a device approved by the FDA to treat tinnitus using electrical stimulation of the tongue. The device has helped Victoria Banks, a singer and songwriter in Nashville, Tenn., who developed tinnitus about three years ago. "The noise in my head felt like a bunch of cicadas," Banks says. "It was terrifying." The buzz made it difficult for her to sing and listen to music. "It can be absolutely debilitating," she says. Banks tried taking dietary supplements, but those didn't help. She also stepped up exercise, but that didn't bring relief either. Then she read about a device called Lenire, which was approved by the FDA in March 2023. It includes a plastic mouthpiece with stainless steel electrodes that electrically stimulate the tongue. It is the first device of its kind to be approved for tinnitus. "This had worked for other people, and I thought I'm willing to try anything at this point," Banks recalls. She sought out audiologist Brian Fligor, who treats severe cases of tinnitus in the Boston area. Fligor was impressed by the results of a clinical trial that found 84% of participants who tried Lenire experienced a significant reduction in symptoms. He became one of the first providers in the U.S. to use the device with his patients. Fligor also served on an advisory panel assembled by the company who developed it. © 2024 npr

Keyword: Hearing
Link ID: 29259 - Posted: 04.16.2024

By Helen Bradshaw With its hairless silicone skin and blue complexion, Emo the robot looks more like a mechanical re-creation of the Blue Man Group than a regular human. Until it smiles. In a study published March 27 in Science Robotics, researchers detail how they trained Emo to smile in sync with humans. Emo can predict a human smile 839 milliseconds before it happens and smile back. Right now, in most humanoid robots, there’s a noticeable delay before they can smile back at a person, often because the robots are imitating a person’s face in real time. “I think a lot of people actually interacting with a social robot for the first time are disappointed by how limited it is,” says Chaona Chen, a human-robot interaction researcher at the University of Glasgow in Scotland. “Improving robots’ expression in real time is important.” Through synced facial expressions, future iterations of robots could be sources of connection in our loneliness epidemic, says Yuhang Hu, a roboticist at Columbia University who, along with colleagues, created Emo (SN: 11/7/23). Cameras in the robot’s eyes let it detect subtleties in human expressions that it then emulates using 26 actuators underneath its soft, blue face. To train Emo, the researchers first put it in front of a camera for a few hours. Like looking in a mirror would do for humans and their muscles, looking at itself in the camera while researchers ran random motor commands on the actuators helped Emo learn the relationships between activating actuators in its face and the expressions it created. “Then the robot knows, OK, if I want to make a smiley face, I should actuate these ‘muscles,’” Hu says. © Society for Science & the Public 2000–2024.

Keyword: Emotions; Robotics
Link ID: 29258 - Posted: 04.16.2024

By Carl Zimmer In the early 1900s, primatologists noticed a group of apes in central Africa with a distinctly slender build; they called them “pygmy chimpanzees.” But as the years passed, it became clear that those animals, now known as bonobos, were profoundly different from chimpanzees. Chimpanzee societies are dominated by males that kill other males, raid the territory of neighboring troops and defend their own ground with border patrols. Male chimpanzees also attack females to coerce them into mating, and sometimes even kill infants. Among bonobos, in contrast, females are dominant. Males do not go on patrols, form alliances or kill other bonobos. And bonobos usually resolve their disputes with sex — lots of it. Bonobos became famous for showing that nature didn’t always have to be red in tooth and claw. “Bonobos are an icon for peace and love, the world’s ‘hippie chimps,’” Sally Coxe, a conservationist, said in 2006. But these sweeping claims were not based on much data. Because bonobos live in remote, swampy rainforests, it has been much more difficult to observe them in the wild than chimpanzees. More recent research has shown that bonobos live a more aggressive life than their reputation would suggest. In a study based on thousands of hours of observations in the wild published on Friday, for example, researchers found that male bonobos commit acts of aggression nearly three times as often as male chimpanzees do. “There is no ‘hippie ape,’” said Maud Mouginot, a biological anthropologist at Boston University who led the analysis. As our closest living relatives, bonobos and chimpanzees can offer us clues about the roots of human behavior. We and the two species share a common ancestor that lived about 7 million years ago. About 5 million years later, bonobos split off from chimpanzees. © 2024 The New York Times Company

Keyword: Aggression; Evolution
Link ID: 29256 - Posted: 04.13.2024

By Bob Holmes Like many of the researchers who study how people find their way from place to place, David Uttal is a poor navigator. “When I was 13 years old, I got lost on a Boy Scout hike, and I was lost for two and a half days,” recalls the Northwestern University cognitive scientist. And he’s still bad at finding his way around. The world is full of people like Uttal — and their opposites, the folks who always seem to know exactly where they are and how to get where they want to go. Scientists sometimes measure navigational ability by asking someone to point toward an out-of-sight location — or, more challenging, to imagine they are someplace else and point in the direction of a third location — and it’s immediately obvious that some people are better at it than others. “People are never perfect, but they can be as accurate as single-digit degrees off, which is incredibly accurate,” says Nora Newcombe, a cognitive psychologist at Temple University who coauthored a look at how navigational ability develops in the 2022 Annual Review of Developmental Psychology. But others, when asked to indicate the target’s direction, seem to point at random. “They have literally no idea where it is.” While it’s easy to show that people differ in navigational ability, it has proved much harder for scientists to explain why. There’s new excitement brewing in the navigation research world, though. By leveraging technologies such as virtual reality and GPS tracking, scientists have been able to watch hundreds, sometimes even millions, of people trying to find their way through complex spaces, and to measure how well they do. Though there’s still much to learn, the research suggests that to some extent, navigation skills are shaped by upbringing. Nurturing navigation skills

Keyword: Learning & Memory
Link ID: 29255 - Posted: 04.13.2024

By Joanne Silberner In March, the sons of Gabriel García Márquez, the Nobel Prize-winning Colombian writer, published a posthumous novel against the specific wishes their father expressed before he died in 2014 at the age of 87. García Márquez had struggled through several versions of the book as dementia set in, and, perhaps stung by uncharacteristic negative reviews from his previous novel, didn’t want the new one published. “Until August,” the story of a woman who travels to her mother’s grave once a year and takes a new lover on each visit, got mixed reviews. Some were outright harsh. In The New York Times, Michael Greenberg wrote “It would be hard to imagine a more unsatisfying goodbye.” García Márquez’s decline, he continued, “seems to have been steep enough to prevent him from holding together the kind of imagined world that the writing of fiction demands.” Wendy Mitchell, who was an administrator with England’s National Health Service until her diagnosis of early-onset Alzheimer’s disease in 2014, recalled the moment she learned of the publication plans last year. “I type every day for fear of dementia snatching away that creative skill, which I see as my escape from dementia,” she wrote last October in The Guardian. “Maybe Márquez thought the same?” The novel’s publication raises some vital questions about living with an aging and perhaps ailing brain. What do mild cognitive impairment and dementia do to our creativity? How do these conditions affect our ability to use words, formulate sentences, and craft stories? Neuroscientists have been exploring these questions for several decades. First, a few definitions. People with mild cognitive impairment have lost more of their cognitive functioning than others their age, and often struggle to remember things. But they’re capable of managing daily activities like dressing, eating, bathing, and finding their way around. In dementia, cognitive difficulties have increased enough to interfere with daily life, and personality changes are more likely.

Keyword: Alzheimers
Link ID: 29254 - Posted: 04.13.2024

By McKenzie Prillaman It was hailed as a potentially transformative technique for measuring brain activity in animals: direct imaging of neuronal activity (DIANA), held the promise of mapping neuronal activity so fast that neurons could be tracked as they fired. But nearly two years on from the 2022 Science paper1, no one outside the original research group and their collaborators have been able to reproduce the results. Now, two teams have published a record of their replication attempts — and failures. The studies, published on 27 March in Science Advances2,3, suggest that the original results were due to experimental error or data cherry-picking, not neuronal activity after all. But the lead researcher behind the original technique stands by the results. “I’m also very curious as to why other groups fail in reproducing DIANA,” says Jang-Yeon Park, a magnetic resonance imaging (MRI) physicist at Sungkyunkwan University in Suwon, South Korea. Science said in an e-mail to Nature that, although it’s important to report the negative results, the Science Advances studies “do not allow a definitive conclusion” to be drawn about the original work, “because there were methodological differences between the papers”. In conventional functional MRI (fMRI), researchers monitor changes in blood flow to different brain regions to estimate activity. But this response lags by at least one second behind the activity of neurons, which send messages in milliseconds. Park and his co-authors said that DIANA could measure neuronal activity directly, which is an “extraordinary claim”, says Ben Inglis, a physicist at the University of California, Berkeley. © 2024 Springer Nature Limited

Keyword: Brain imaging
Link ID: 29253 - Posted: 04.11.2024

Matthew Farrer Parkinson’s disease is a neurodegenerative movement disorder that progresses relentlessly. It gradually impairs a person’s ability to function until they ultimately become immobile and often develop dementia. In the U.S. alone, over a million people are afflicted with Parkinson’s, and new cases and overall numbers are steadily increasing. There is currently no treatment to slow or halt Parkinson’s disease. Available drugs don’t slow disease progression and can treat only certain symptoms. Medications that work early in the disease, however, such as Levodopa, generally become ineffective over the years, necessitating increased doses that can lead to disabling side effects. Without understanding the fundamental molecular cause of Parkinson’s, it’s improbable that researchers will be able to develop a medication to stop the disease from steadily worsening in patients. Many factors may contribute to the development of Parkinson’s, both environmental and genetic. Until recently, underlying genetic causes of the disease were unknown. Most cases of Parkinson’s aren’t inherited but sporadic, and early studies suggested a genetic basis was improbable. Nevertheless, everything in biology has a genetic foundation. As a geneticist and molecular neuroscientist, I have devoted my career to predicting and preventing Parkinson’s disease. In our newly published research, my team and I discovered a new genetic variant linked to Parkinson’s that sheds light on the evolutionary origin of multiple forms of familial parkinsonism, opening doors to better understand and treat the disease. In the mid-1990s, researchers started looking into whether genetic differences between people with or without Parkinson’s might identify specific genes or genetic variants that cause the disease. In general, I and other geneticists use two approaches to map the genetic blueprint of Parkinson’s: linkage analysis and association studies. © 2010–2024, The Conversation US, Inc.

Keyword: Parkinsons; Genes & Behavior
Link ID: 29249 - Posted: 04.11.2024

Kimberly Rosvall Liz Aguilar The total solar eclipse on April 8, 2024, coincides with an exciting time for wild birds. Local birds are singing for mates and fighting for territories as they gear up for their once-a-year chance to breed. Tens of millions of migrating birds will be passing through the path of totality, and they mostly migrate at night. Because birds use light to match their behaviors to their environment, scientists like us have lots of questions about how they will respond to the eclipse. Will they pause their fighting and wooing and shift toward bedtime-like behaviors? How about a nocturnal animal like an owl or those nighttime migrants – will they start to rustle from their roosts before they realize it’s not night? As behavioral biologists at Indiana University, we research wild breeding birds, with a goal of understanding why animals behave the way that they do in response to environmental challenges and opportunities. For the 2024 eclipse, our team is launching a new project and developing an app. If everything goes as planned, we should end up with a large dataset after the eclipse, collected by community scientist volunteers across the country. On average, a total solar eclipse occurs in the same place only once every 375 years. Most wild animals, like most people, have never seen the sky quickly switch to night in the middle of the day. These rare events are a natural experiment that can help scientists like us understand how animals respond to an unusual sudden change in light. Most past research on animal behavior during total solar eclipses is anecdotal. Observers have reported that zoo animals acted distressed or went into their enclosures. Scientists have spotted spiders starting the nightly deconstruction of their webs in the middle of the day, and farmers have heard their roosters start to crow after totality, as if it’s once again dawn. Other reports suggest more subtle effects on animal behavior. © 2010–2024, The Conversation US, Inc.

Keyword: Biological Rhythms; Vision
Link ID: 29246 - Posted: 04.06.2024

By Matt Richtel Historically speaking, it’s not a bad time to be the liver of a teenager. Or the lungs. Regular use of alcohol, tobacco and drugs among high school students has been on a long downward trend. In 2023, 46 percent of seniors said that they’d had a drink in the year before being interviewed; that is a precipitous drop from 88 percent in 1979, when the behavior peaked, according to the annual Monitoring the Future survey, a closely watched national poll of youth substance use. A similar downward trend was observed among eighth and 10th graders, and for those three age groups when it came to cigarette smoking. In 2023, just 15 percent of seniors said that they had smoked a cigarette in their life, down from a peak of 76 percent in 1977. Illicit drug use among teens has remained low and fairly steady for the past three decades, with some notable declines during the Covid-19 pandemic. In 2023, 29 percent of high school seniors reported using marijuana in the previous year — down from 37 percent in 2017, and from a peak of 51 percent in 1979. There are some sobering caveats to the good news. One is that teen overdose deaths have sharply risen, with fentanyl-involved deaths among adolescents doubling from 2019 to 2020 and remaining at that level in the subsequent years. Dr. Nora Volkow has devoted her career to studying use of drugs and alcohol. She has been the director of the National Institute on Drug Abuse since 2003. She sat down with The New York Times to discuss changing patterns and the reasons behind shifting drug-use trends. What’s the big picture on teens and drug use? People don’t really realize that among young people, particularly teenagers, the rate of drug use is at the lowest risk that we have seen in decades. And that’s worth saying, too, for legal alcohol and tobacco. © 2024 The New York Times Company

Keyword: Drug Abuse
Link ID: 29243 - Posted: 04.06.2024

Jon Hamilton Sam and John Fetters, 19, are identical twins at opposite ends of the autism spectrum. Sam is a sophomore at Amherst College who plans to double major in history and political science. In his free time, he runs marathons. John attends a special school, struggles to form sentences, and likes to watch "Teletubbies" and "Sesame Street." Two brothers. Same genes. Different flavors of autism. To scientists, twins like Sam and John pose an important question: How can a disorder that is known to be highly genetic look so different in siblings who share the same genome? "That is one of the greatest mysteries right now in research on autism," says Dr. Stephanie Morris, a pediatric neurologist at the Kennedy Krieger Institute in Baltimore. Solving that mystery could help explain autism's odd mix of nature and nurture, Morris says. It also might help "modify the trajectory" of autistic children experiencing speech and language delays, or difficulty with social communication. Identical twins on separate paths Sam and John are spending the weekend with their mom, Kim Leaird, at the family's apartment in West Tisbury, a small town on Martha's Vineyard. The twins are crowded together on a couch. Even seated, they look tall. Standing, Sam is 6 feet five inches, his brother just an inch shorter. John lets Sam do most of the talking. He frequently touches his brother, who sometimes takes his hand. John has "a truly tremendous amount of empathy," Sam says. "He's able to be very supportive." © 2024 npr

Keyword: Autism; Genes & Behavior
Link ID: 29239 - Posted: 04.04.2024

By Tina Hesman Saey Atoosa Samani started learning about pigeon genetics at a young age. She grew up surrounded by pet pigeons in Isfahan, a city in central Iran famed for its pigeon towers. Her favorite was an all-white bird. But 6- or 7-year-old Samani noticed that this particular pigeon never fathered all-white offspring. She learned that white coloring is a recessive genetic trait — one that shows up only when an individual inherits two broken copies of a gene (SN: 2/7/22). In this case, the pigeon had two broken copies of a gene that normally makes pigment to color feathers, so his feathers were white. But his offspring inherited a normal, pigment-producing version of the gene from their mothers and had colored feathers. That early lesson in pigeon heredity stuck with Samani and fueled her desire to learn more about genetics. When she moved to the United States to study at the University of Utah in Salt Lake City, it seemed only natural to join Michael Shapiro’s lab to investigate why some pigeons (Columba livia) do backward somersaults (SN: 1/31/13). These roller pigeons come in two varieties: Flying rollers such as Birmingham rollers, which fly but do long tumbling runs toward the ground before resuming flight, and parlor rollers, which can’t fly but instead backflip along the ground. Many Persian poems say the pigeons perform the acrobatics because the birds are happy, but Samani says the truth is darker. “This is definitely a movement disorder, and it does not have any good aspects to it,” she says. The disorder is progressive, appearing soon after hatching and gradually getting worse until the birds can’t fly. © Society for Science & the Public 2000–2024.

Keyword: Movement Disorders; Genes & Behavior
Link ID: 29235 - Posted: 04.02.2024

Linda Geddes Science correspondent If you have wondered why your partner always beats you at tennis or one child always crushes the other at Fortnite, it seems there is more to it than pure physical ability. Some people are effectively able to see more “images per second” than others, research suggests, meaning they’re innately better at spotting or tracking fast-moving objects such as tennis balls. The rate at which our brains can discriminate between different visual signals is known as temporal resolution, and influences the speed at which we are able to respond to changes in our environment. Previous studies have suggested that animals with high visual temporal resolution tend to be species with fast-paced lives, such as predators. Human research has also suggested that this trait tends to decrease as we get older, and dips temporarily after intense exercise. However, it was not clear how much it varies between people of similar ages. One way of measuring this trait is to identify the point at which someone stops perceiving a flickering light to flicker, and sees it as a constant or still light instead. Clinton Haarlem, a PhD candidate at Trinity College Dublin, and his colleagues tested this in 80 men and women between the ages of 18 and 35, and found wide variability in the threshold at which this happened. The research, published in Plos One, found that some people reported a light source as constant when it was in fact flashing about 35 times a second, while others could still detect flashes at rates of greater than 60 times a second. © 2024 Guardian News & Media Limited

Keyword: Vision
Link ID: 29233 - Posted: 04.02.2024

By James Gaines A lethal, incurable malady similar to mad cow disease is sweeping across deer species in North America and starting to spread around the world. First identified in a single herd of captive mule deer in Colorado in 1967, chronic wasting disease — CWD — has now been found in captive and wild mule deer, white-tailed deer, elk, moose and reindeer. It’s been found in 32 states and has crossed international boundaries into Canada, South Korea and Norway, among other countries. The disease — caused by a rogue protein known as a prion — has not yet been shown to infect humans, though fears remain. But even if that never happens, CWD could kill off large numbers of deer and possibly wipe out individual populations. Wildlife management agencies may, in turn, introduce stricter hunting rules, and the fear of contaminated meat could scare away potential hunters, affecting the United States’ roughly $23 billion deer hunting industry. Since CWD’s emergence, scientists have been working to understand the disease and how it might be brought under control. Over the years, three potential mitigation strategies have emerged, but each has significant challenges. Nicholas Haley, a veterinary microbiologist at Midwestern University in Arizona, coauthored an overview of chronic wasting disease in the 2015 Annual Review of Animal Biosciences and has been working on the problem ever since. Knowable Magazine spoke with Haley about the options and whether we can ever contain the disease. What’s a prion disease? CWD isn’t caused by a bacterium or virus, but by a naturally occurring protein in our cells twisting out of shape.

Keyword: Prions
Link ID: 29232 - Posted: 04.02.2024

By Erin Blakemore More than three-quarters of sudden infant deaths involved multiple unsafe sleep practices, including co-sleeping, a recent analysis suggests. A study published in the journal Pediatrics looked at 7,595 sudden infant death cases in a Centers for Disease Control and Prevention registry between 2011 and 2020. The majority of deaths occurred in babies less than 3 months old. The statistics revealed that 59.5 percent of the infants who died suddenly were sharing a sleep surface at the time of death, and 75.9 percent were in an adult bed when they died. Though some demographic factors such as sex and length of gestation were not clinically significant, the researchers found that the babies sharing a sleep surface were more likely to be Black and publicly insured than those who didn’t share sleep surfaces. Soft bedding was common among all the infants who died, and 76 percent of the cases involved multiple unsafe practices. The analysis mirrors known risk factors for sudden infant death. Current recommendations direct parents and other caretakers to provide infants with firm, flat, level sleep surfaces that contain nothing but a fitted sheet. Though room sharing reduces the risk of sudden infant death, CDC officials discourage parents from sharing a sleep surface with their child. Exposure to cigarette smoke during pregnancy was more common among infants who shared surfaces when they died. Though most infants were supervised by an adult when they died, the supervisor was more likely to be impaired by drug and alcohol use among those who shared a sleeping surface.

Keyword: Sleep
Link ID: 29230 - Posted: 04.02.2024

By Jake Buehler Much like squirrels, black-capped chickadees hide their food, keeping track of many thousands of little treasures wedged into cracks or holes in tree bark. When a bird returns to one of their many food caches, a particular set of nerve cells in the memory center of their brains gives a brief flash of activity. When the chickadee goes to another stash, a different combination of neurons lights up. These neural combinations act like bar codes, and identifying them may give key insights into how episodic memories — accounts of specific past events, like what you did on your birthday last year or where you’ve left your wallet — are encoded and recalled in the brain, researchers report March 29 in Cell. This kind of memory is challenging to study in animals, says Selmaan Chettih, a neuroscientist at Columbia University. “You can’t just ask a mouse what memories it formed today.” But chickadees’ very precise behavior provides a golden opportunity for researchers. Every time a chickadee makes a cache, it represents a single, well-defined moment logged in the hippocampus, a structure in the vertebrate brain vital for memory. To study the birds’ episodic memory, Chettih and his colleagues built a special arena made of 128 small, artificial storage sites. The team inserted small probes into five chickadees’ brains to track the electrical activity of individual neurons, comparing that activity with detailed recordings of the birds’ body positions and behaviors. A black-capped chickadee stores sunflower seeds in an artificial arena made of 128 different perches and pockets. These birds excel at finding their hidden food stashes. The aim of the setup was to see how their brain stores and retrieves the memory of each hidey-hole. Researchers closely observed five chickadees, comparing their caching behavior with the activity from nerve cells in their hippocampus, the brain’s memory center. © Society for Science & the Public 2000–2024.

Keyword: Learning & Memory
Link ID: 29228 - Posted: 03.30.2024

By Max Kozlov Neurons (shown here in a coloured scanning electron micrograph) mend broken DNA during memory formation. Credit: Ted Kinsman/Science Photo Library When a long-term memory forms, some brain cells experience a rush of electrical activity so strong that it snaps their DNA. Then, an inflammatory response kicks in, repairing this damage and helping to cement the memory, a study in mice shows. The findings, published on 27 March in Nature1, are “extremely exciting”, says Li-Huei Tsai, a neurobiologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the work. They contribute to the picture that forming memories is a “risky business”, she says. Normally, breaks in both strands of the double helix DNA molecule are associated with diseases including cancer. But in this case, the DNA damage-and-repair cycle offers one explanation for how memories might form and last. It also suggests a tantalizing possibility: this cycle might be faulty in people with neurodegenerative diseases such as Alzheimer’s, causing a build-up of errors in a neuron’s DNA, says study co-author Jelena Radulovic, a neuroscientist at the Albert Einstein College of Medicine in New York City. This isn’t the first time that DNA damage has been associated with memory. In 2021, Tsai and her colleagues showed that double-stranded DNA breaks are widespread in the brain, and linked them with learning2. To better understand the part these DNA breaks play in memory formation, Radulovic and her colleagues trained mice to associate a small electrical shock with a new environment, so that when the animals were once again put into that environment, they would ‘remember’ the experience and show signs of fear, such as freezing in place. Then the researchers examined gene activity in neurons in a brain area key to memory — the hippocampus. They found that some genes responsible for inflammation were active in a set of neurons four days after training. Three weeks after training, the same genes were much less active. © 2024 Springer Nature Limited

Keyword: Learning & Memory; Genes & Behavior
Link ID: 29223 - Posted: 03.28.2024

By Dennis Normile By the time a person shows symptoms of Parkinson’s disease, neurons in a part of their brain key to movement have already quietly died. To learn how this process unfolds, identify warning signs, and test treatments, researchers have long wanted an animal model of the disease’s early stages. Now, they may have one: a cohort of transgenic marmosets, described at a conference on nonhuman primate models in Hong Kong last month. The animals, which neuroscientist Hideyuki Okano of Keio University and colleagues created using a mutated protein that seems to drive Parkinson’s in some people, closely mimic the disease’s onset and progression. And they have enabled Okano’s team to identify what could be an early, predictive sign of disease in brain imaging. The model could be “transformative” for Parkinson’s studies, says neurobiologist Peter Strick of the University of Pittsburgh, who attended the meeting, organized by the Hong Kong University of Science and Technology, Stanford University, and the University of California San Francisco. “We desperately need nonhuman primate models that recapitulate the natural onset and progression” of conditions like Parkinson’s, he says. Parkinson’s, which afflicts an estimated 8.5 million people, is thought to be triggered by a combination of genetic and environmental factors, such as exposure to toxic chemicals. It sets in as neurons that produce the chemical messenger dopamine in the substantia nigra, an area of the brain that controls movement, die off. Early symptoms include tremors, muscle stiffness, and hesitant motions. The disease can later affect cognition and lead to dementia. Researchers think one cause of neuronal death may be abnormal versions of a protein called alpha-synuclein that misfold and form toxic clumps in the brain years before symptoms emerge. © 2024 American Association for the Advancement of Science.

Keyword: Parkinsons; Genes & Behavior
Link ID: 29221 - Posted: 03.28.2024

Ian Sample Science editor Two nights of broken sleep are enough to make people feel years older, according to researchers, who said consistent, restful slumber was a key factor in helping to stave off feeling one’s true age. Psychologists in Sweden found that, on average, volunteers felt more than four years older when they were restricted to only four hours of sleep for two consecutive nights, with some claiming the sleepiness made them feel decades older. The opposite was seen when people were allowed to stay in bed for nine hours, though the effect was more modest, with participants in the study claiming to feel on average three months younger than their real age after ample rest. “Sleep has a major impact on how old you feel and it’s not only your long-term sleep patterns,” said Dr Leonie Balter, a psychoneuroimmunologist at the Karolinska Institute in Stockholm and first author on the study. “Even when you only sleep less for two nights that has a real impact on how you feel.” Beyond simply feeling more decrepit, the perception of being many years older may affect people’s health, Balter said, by encouraging unhealthy eating, reducing physical exercise, and making people less willing to socialise and engage in new experiences. The researchers ran two studies. In the first, 429 people aged 18 to 70 answered questions about how old they felt and on how many nights, if any, they had slept badly in the past month. Their sleepiness was also rated according to a standard scale used in psychology research. For each day of poor sleep the volunteers felt on average three months older, the scientists found, while those who reported no bad nights in the preceding month felt on average nearly six years younger than their true age. It was unclear, however, whether bad sleep made people feel older or vice versa. © 2024 Guardian News & Media Limited

Keyword: Sleep
Link ID: 29219 - Posted: 03.28.2024

By Robert D. Hershey Jr. Daniel Kahneman, who never took an economics course but who pioneered a psychologically based branch of that field that led to a Nobel in economic science in 2002, died on Wednesday. He was 90. His death was confirmed by his partner, Barbara Tversky. She declined to say where he died. Professor Kahneman, who was long associated with Princeton University and lived in Manhattan, employed his training as a psychologist to advance what came to be called behavioral economics. The work, done largely in the 1970s, led to a rethinking of issues as far-flung as medical malpractice, international political negotiations and the evaluation of baseball talent, all of which he analyzed, mostly in collaboration with Amos Tversky, a Stanford cognitive psychologist who did groundbreaking work on human judgment and decision-making. (Ms. Tversky, also a professor of psychology at Stanford, had been married to Professor Tversky, who died in 1996. She and Professor Kahneman became partners several years ago.) As opposed to traditional economics, which assumes that human beings generally act in fully rational ways and that any exceptions tend to disappear as the stakes are raised, the behavioral school is based on exposing hard-wired mental biases that can warp judgment, often with counterintuitive results. “His central message could not be more important,” the Harvard psychologist and author Steven Pinker told The Guardian in 2014, “namely, that human reason left to its own devices is apt to engage in a number of fallacies and systematic errors, so if we want to make better decisions in our personal lives and as a society, we ought to be aware of these biases and seek workarounds. That’s a powerful and important discovery.” © 2024 The New York Times Company

Keyword: Attention
Link ID: 29218 - Posted: 03.28.2024