Tijl Grootswagers Genevieve L Quek Manuel Varlet You are standing in the cereal aisle, weighing up whether to buy a healthy bran or a sugary chocolate-flavoured alternative. Your hand hovers momentarily before you make the final grab. But did you know that during those last few seconds, while you’re reaching out, your brain is still evaluating the pros and cons – influenced by everything from your last meal, the health star rating, the catchy jingle in the ad, and the colours of the letters on the box? Our recently published research shows our brains do not just think first and then act. Even while you are reaching for a product on a supermarket shelf, your brain is still evaluating whether you are making the right choice. Read news coverage based on evidence, not tweets Further, we found measuring hand movements offers an accurate window into the brain’s ongoing evaluation of the decision – you don’t have to hook people up to expensive brain scanners. What does this say about our decision-making? And what does it mean for consumers and the people marketing to them? There has been debate within neuroscience on whether a person’s movements to enact a decision can be modified once the brain’s “motor plan” has been made. Our research revealed not only that movements can be changed after a decision – “in flight” – but also the changes matched incoming information from a person’s senses. To study how our decisions unfold over time, we tracked people’s hand movements as they reached for different options shown in pictures – for example, in response to the question “is this picture a face or an object?” Put simply, reaching movements are shaped by ongoing thinking and decision-making. © 2010–2024, The Conversation US, Inc.

Keyword: Consciousness
Link ID: 29387 - Posted: 07.11.2024

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

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

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

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

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

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

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

Keyword: Prions
Link ID: 29355 - Posted: 06.11.2024

Leyland Cecco in Toronto A leading federal scientist in Canada has alleged he was barred from investigating a mystery brain illness in the province of New Brunswick and said he fears more than 200 people affected by the condition are experiencing unexplained neurological decline. The allegations, made in leaked emails to a colleague seen by the Guardian, have emerged two years after the eastern province closed its investigation into a possible “cluster” of cases. “All I will say is that my scientific opinion is that there is something real going on in [New Brunswick] that absolutely cannot be explained by the bias or personal agenda of an individual neurologist,” wrote Michael Coulthart, a prominent microbiologist. “A few cases might be best explained by the latter, but there are just too many (now over 200).” New Brunswick health officials warned in 2021 that more than 40 residents were suffering from a possible unknown neurological syndrome, with symptoms similar to those of the degenerative brain disorder Creutzfeldt-Jakob disease. Those symptoms were varied and dramatic: some patients started drooling and others felt as though bugs were crawling on their skin. A year later, however, an independent oversight committee created by the province determined that the group of patients had most likely been misdiagnosed and were suffering from known illnesses such as cancer and dementia. The committee and the New Brunswick government also cast doubt on the work of neurologist Alier Marrero, who was initially referred dozens of cases by baffled doctors in the region, and subsequently identified more cases. The doctor has since become a fierce advocate for patients he feels have been neglected by the province. © 2024 Guardian News & Media Limited

Keyword: Alzheimers; Depression
Link ID: 29342 - Posted: 06.04.2024

By Matthew Hutson ChatGPT and other AI tools are upending our digital lives, but our AI interactions are about to get physical. Humanoid robots trained with a particular type of AI to sense and react to their world could lend a hand in factories, space stations, nursing homes and beyond. Two recent papers in Science Robotics highlight how that type of AI — called reinforcement learning — could make such robots a reality. “We’ve seen really wonderful progress in AI in the digital world with tools like GPT,” says Ilija Radosavovic, a computer scientist at the University of California, Berkeley. “But I think that AI in the physical world has the potential to be even more transformational.” The state-of-the-art software that controls the movements of bipedal bots often uses what’s called model-based predictive control. It’s led to very sophisticated systems, such as the parkour-performing Atlas robot from Boston Dynamics. But these robot brains require a fair amount of human expertise to program, and they don’t adapt well to unfamiliar situations. Reinforcement learning, or RL, in which AI learns through trial and error to perform sequences of actions, may prove a better approach. “We wanted to see how far we can push reinforcement learning in real robots,” says Tuomas Haarnoja, a computer scientist at Google DeepMind and coauthor of one of the Science Robotics papers. Haarnoja and colleagues chose to develop software for a 20-inch-tall toy robot called OP3, made by the company Robotis. The team not only wanted to teach OP3 to walk but also to play one-on-one soccer. “Soccer is a nice environment to study general reinforcement learning,” says Guy Lever of Google DeepMind, a coauthor of the paper. It requires planning, agility, exploration, cooperation and competition. © Society for Science & the Public 2000–2024.

Keyword: Robotics
Link ID: 29328 - Posted: 05.29.2024

By Christina Jewett Just four months ago, Noland Arbaugh had a circle of bone removed from his skull and hair-thin sensor tentacles slipped into his brain. A computer about the size of a small stack of quarters was placed on top and the hole was sealed. Paralyzed below the neck, Mr. Arbaugh is the first patient to take part in the clinical trial of humans testing Elon Musk’s Neuralink device, and his early progress was greeted with excitement. Working with engineers, Mr. Arbaugh, 30, trained computer programs to translate the firing of neurons in his brain into the act of moving a cursor up, down and around. His command of the cursor was soon so agile that he could challenge his stepfather at Mario Kart and play an empire-building video game late into the night. But as weeks passed, about 85 percent of the device’s tendrils slipped out of his brain. Neuralink’s staff had to retool the system to allow him to regain command of the cursor. Though he needed to learn a new method to click on something, he can still skate the cursor across the screen. Neuralink advised him against a surgery to replace the threads, he said, adding that the situation had stabilized. The setback became public earlier this month. And although the diminished activity was initially difficult and disappointing, Mr. Arbaugh said it had been worth it for Neuralink to move forward in a tech-medical field aimed at helping people regain their speech, sight or movement. “I just want to bring everyone along this journey with me,” he said. “I want to show everyone how amazing this is. And it’s just been so rewarding. So I’m really excited to keep going.” From a small desert town in Arizona, Mr. Arbaugh has emerged as an enthusiastic spokesman for Neuralink, one of at least five companies leveraging decades of academic research to engineer a device that can help restore function in people with disabilities or degenerative diseases. © 2024 The New York Times Company

Keyword: Robotics
Link ID: 29320 - Posted: 05.23.2024

By Meghan Willcoxon In the summer of 1991, the neuroscientist Vittorio Gallese was studying how movement is represented in the brain when he noticed something odd. He and his research adviser, Giacomo Rizzolatti, at the University of Parma were tracking which neurons became active when monkeys interacted with certain objects. As the scientists had observed before, the same neurons fired when the monkeys either noticed the objects or picked them up. But then the neurons did something the researchers didn’t expect. Before the formal start of the experiment, Gallese grasped the objects to show them to a monkey. At that moment, the activity spiked in the same neurons that had fired when the monkey grasped the objects. It was the first time anyone had observed neurons encode information for both an action and another individual performing that action. Those neurons reminded the researchers of a mirror: Actions the monkeys observed were reflected in their brains through these peculiar motor cells. In 1992, Gallese and Rizzolatti first described the cells in the journal Experimental Brain Research and then in 1996 named them “mirror neurons” in Brain. The researchers knew they had found something interesting, but nothing could have prepared them for how the rest of the world would respond. Within 10 years of the discovery, the idea of a mirror neuron had become the rare neuroscience concept to capture the public imagination. From 2002 to 2009, scientists across disciplines joined science popularizers in sensationalizing these cells, attributing more properties to them to explain such complex human behaviors as empathy, altruism, learning, imitation, autism, and speech. Then, nearly as quickly as mirror neurons caught on, scientific doubts about their explanatory power crept in. Within a few years, these celebrity cells were filed away in the drawer of over-promised, under-delivered discoveries. © 2024 NautilusNext Inc.,

Keyword: Attention; Vision
Link ID: 29316 - Posted: 05.21.2024

Ian Sample Science editor A device that stimulates the spinal nerves with electrical pulses appears to boost how well people recover from major spinal cord injuries, doctors say. An international trial found that patients who had lost some or all use of their hands and arms after a spinal cord injury regained strength, control and sensation when the stimulation was applied during standard rehabilitation exercises. The improvements were small but were described by doctors and patients as life-changing because of the impact they had on the patients’ daily routines and quality of life. “It actually makes it easier for people to move, including people who have complete loss of movement in their hands and arms,” said Prof Chet Moritz, in the department of rehabilitation medicine at the University of Washington in Seattle. “The benefits accumulate gradually over time as we pair this spinal stimulation with intensive therapy of the hands and arms, such that there are benefits even when the stimulator is turned off.” Rather than being implanted, the Arc-Ex device is worn externally and uses electrodes that are placed on the skin near the section of the spinal cord responsible for controlling a particular movement or function. The researchers believe that electrical stimulation helps nerves that remain intact after the injury to send signals and ultimately partially restore some communication between the brain and paralysed body part. More than half of patients who suffer spinal cord injuries still have some intact nerves that cross the injury site. © 2024 Guardian News & Media Limited

Keyword: Robotics; Movement Disorders
Link ID: 29315 - Posted: 05.21.2024

By Kermit Pattison Since the Stone Age, hunters have brought down big game with spears, atlatls, and bows and arrows. Now, a new study reveals traditional societies around the globe also relied on another deadly but often-overlooked weapon: our legs. According to a report published today in Nature Human Behaviour, running down big game such as antelope, moose, and even kangaroos was far more widespread than previously recognized. Researchers documented nearly 400 cases of endurance pursuits—a technique in which prey are chased to exhaustion—by Indigenous peoples around the globe between the 16th and 21st centuries. And in some cases, they suggest, it can be more efficient than stealthy stalking. The findings bolster the idea that humans evolved to be hunting harriers, says Daniel Lieberman, an evolutionary biologist at Harvard University. “Nobody else has come up with any other explanation for why humans evolved to run long distances,” says Lieberman, who adds that he’s impressed with the paper’s “depth of scholarship.” For decades, some anthropologists have argued that endurance running was among the first hunting techniques employed by early hominins in Africa. Advocates suggest subsequent millennia spent chasing down prey shaped many unique human features, including our springy arched feet, slow-twitch muscle fibers optimized for efficiency, heat-shedding bare skin, and prodigious ability to sweat. The “born to run” idea has become something of an origin story among many endurance athletes. But a pack of skeptics has dogged the theory. Critics cited the higher energetic costs of running over walking and noted that accounts of persistence hunting among modern foragers are rare. Yet hints of such pursuits kept popping up as Eugène Morin, an archaeologist at Trent University and co-author of the new paper, scoured the literature for a book he was writing on hunting among traditional societies. As he pored over early accounts by missionaries, travelers, and explorers, he repeatedly found descriptions of long-distance running and tracking. © 2024 American Association for the Advancement of Science.

Keyword: Evolution
Link ID: 29309 - Posted: 05.16.2024

By J. David Creswell Let’s start thinking differently about exercise. Decades of exercise science research show that when people or animals are given a new exercise routine, they get healthier. But when thinking about the benefits of exercise, most people hold a strong body bias; they focus on how regular exercise builds more lean body mass, helps increase their strength and balance, or improves heart health. Exercise matters even more for our brains, it turns out, in ways that are often overlooked. Here’s how we know. Animal exercise studies typically run rats for weeks on running wheels. The animals gleefully run every night, sprinting several miles over the course of an evening. There are wonderful health benefits in these studies of voluntary running—improved muscle tone and cardiovascular health, and many brain benefits too. But in some studies, there’s an additional experimental condition where some rats exercise with one crucial difference: it’s no longer voluntary exercise. Instead of a freestanding running wheel, rats run on a mechanized wheel that spins, forcing the animals to cover the same distance as the voluntary runners. What happens? When the rats are forced to exercise on a daily basis for several weeks, their bodies become more physically fit, but their brains suffer. Animals regularly forced to exercise have the equivalent of an anxiety disorder, behaving on new tasks in highly anxious and avoidant ways. These animals are more anxious not only compared to the voluntary runners, but also to animals that are not given an opportunity to exercise at all. Yes, forced exercise might be worse than no exercise at all. This work suggests something important about the health benefits of exercise: it is not just about making our muscles work, but what exercise does to our brains. When exercise gives us a sense of control, mastery and joy, our brains become less anxious. If we take that away, by forcing exercise, we can shift it from helpful to harmful. © 2024 SCIENTIFIC AMERICAN,

Keyword: Stress; Depression
Link ID: 29284 - Posted: 05.02.2024

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

By David Adam A diabetes drug related to the latest generation of obesity drugs can slow the development of the symptoms of Parkinson’s disease, a clinical trial suggests1. Participants who took the drug, called lixisenatide, for 12 months showed no worsening of their symptoms — a gain in a condition marked by progressive loss of motor control. Further work is needed to control side effects and determine the best dose, but researchers say that the trial marks another promising step in the decades-long effort to tackle the common and debilitating disorder. “This is the first large-scale, multicentre clinical trial to provide the signs of efficacy that have been sought for so many years,” says Olivier Rascol, a Parkinson’s researcher at Toulouse University Hospital in France, who led the study. The diabetes connection Lixisenatide is a glucagon-like peptide-1 (GLP-1) receptor agonist, making it part of a large family of similar compounds used to treat diabetes and, more recently, obesity. (The weight-loss drug semaglutide, sold under the brand name Wegovy, is a GLP-1 compound.) Many studies have shown a link between diabetes and Parkinson’s2. People with diabetes are around 40% more likely to develop Parkinson’s. And people who have both Parkinson’s and diabetes often see more rapid progression of symptoms than do those who have only Parkinson’s. Animal studies3 have suggested that some GLP-1 drugs, which influence levels of insulin and glucose, can slow the symptoms of Parkinson’s. Smaller trials, published in 20134 and 20175, suggested that the GLP-1 molecule exenatide, another diabetes drug, could do the same in people.

Keyword: Parkinsons
Link ID: 29240 - Posted: 04.04.2024

By Javier C. Hernández The pianist Alice Sara Ott, barefoot and wearing a silver bracelet, was smiling and singing to herself the other day as she practiced a jazzy passage of Ravel at Steinway Hall in Midtown Manhattan. A Nintendo Switch, which she uses to warm up her hands, was by her side (another favored tool is a Rubik’s Cube). A shot of espresso sat untouched on the floor. “I feel I have finally found my voice,” Ott said during a break. “I feel I can finally be myself.” Ott, 35, who makes her New York Philharmonic debut this week, has built a global career, recording more than a dozen albums and appearing with top ensembles. She has become a force for change in classical music, embracing new approaches (playing Chopin on beat-up pianos in Iceland) and railing against stuffy concert culture (she performs without shoes, finding it more comfortable). And Ott, who lives in Munich and has roots in Germany and Japan, has done so while grappling with illness. In 2019, when she was 30, she was diagnosed with multiple sclerosis. She says she has not shown any symptoms since starting treatment, but the disorder has made her reflect on the music industry’s grueling work culture. “I learned to accept that there is a limit and to not go beyond that,” she said. “Everybody knows how to ignore their body and just go on. But there’s always a payback.” Ott has used her platform to help dispel myths about multiple sclerosis, a disorder of the central nervous system that can cause a wide range of symptoms, including muscle spasms, numbness and vision problems. She has taken to social media to detail her struggles and to challenge those who have suggested that the illness has affected her playing. She said she felt she had no choice but to be transparent, saying it was important to show that people with multiple sclerosis could lead full lives. “I don’t consider it as a weakness,” she said. “It’s a fact. I live with it. And I don’t want to make a big drama out of it.” © 2024 The New York Times Company

Keyword: Multiple Sclerosis
Link ID: 29237 - 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

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 Marta Zaraska The renowned Polish piano duo Marek and Wacek didn’t use sheet music when playing live concerts. And yet onstage the pair appeared perfectly in sync. On adjacent pianos, they playfully picked up various musical themes, blended classical music with jazz and improvised in real time. “We went with the flow,” said Marek Tomaszewski, who performed with Wacek Kisielewski until Wacek’s death in 1986. “It was pure fun.” The pianists seemed to read each other’s minds by exchanging looks. It was, Marek said, as if they were on the same wavelength. A growing body of research suggests that might have been literally true. Dozens of recent experiments studying the brain activity of people performing and working together — duetting pianists, card players, teachers and students, jigsaw puzzlers and others — show that their brain waves can align in a phenomenon known as interpersonal neural synchronization, also known as interbrain synchrony. “There’s now a lot of research that shows that people interacting together display coordinated neural activities,” said Giacomo Novembre, a cognitive neuroscientist at the Italian Institute of Technology in Rome, who published a key paper on interpersonal neural synchronization last summer. The studies have come out at an increasing clip over the past few years — one as recently as last week — as new tools and improved techniques have honed the science and theory. They’re finding that synchrony between brains has benefits. It’s linked to better problem-solving, learning and cooperation, and even with behaviors that help others at a personal cost. What’s more, recent studies in which brains were stimulated with an electric current hint that synchrony itself might cause the improved performance observed by scientists. © 2024 the Simons Foundation.

Keyword: Attention
Link ID: 29229 - Posted: 03.30.2024

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

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

Keyword: Evolution
Link ID: 29194 - Posted: 03.16.2024