Chapter 11. Motor Control and Plasticity

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Links 1 - 20 of 1949

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

By Pam Belluck One of the few treatments the Food and Drug Administration has approved for amyotrophic lateral sclerosis has failed a large clinical trial, and its manufacturer said Friday that it was considering whether to withdraw it from the market. The medication, called Relyvrio, was approved less than two years ago, despite questions about its effectiveness in treating the severe neurological disorder. At the time, the F.D.A.’s reviewers had concluded there was not yet sufficient evidence that the medication could help patients live longer or slow the rate at which they lose functions like muscle control, speaking or breathing without assistance. But the agency decided to greenlight the medication instead of waiting two years for results of a large clinical trial, citing data showing the treatment to be safe and the desperation of patients with a disease that often causes death within two to five years. Since then, about 4,000 patients in the United States have received the treatment, a powder that is mixed with water and either drunk or ingested through a feeding tube and carries a list price of $158,000 a year. Now, results of the 48-week trial of 664 patients are in, and they showed that the treatment did not work better than a placebo. “We are surprised and deeply disappointed,” Justin Klee and Joshua Cohen, the co-chief executive officers of Amylyx Pharmaceuticals, the treatment’s manufacturer, said in a statement. They said they would announce their plans for the medication within eight weeks, “which may include voluntarily withdrawing” it from the market. “We will be led in our decisions by two key principles: doing what is right for people living with A.LS., informed by regulatory authorities and the A.L.S. community, and by what the science tells us,” Mr. Klee and Mr. Cohen said. There are only two other approved A.L.S. medications in the United States: riluzole, approved in 1995, which can extend survival by several months, and edaravone, approved in 2017, which can slow progression by about 33 percent. © 2024 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 29186 - Posted: 03.09.2024

By Lisa Sanders, M.D. Surrounded by the detritus of a Thanksgiving dinner, the woman was loading the dishwasher when a loud thump thundered through the house. She hurried out of the kitchen to find her husband of 37 years sitting on the second-floor landing. Her son and son-in-law, an emergency-room doctor, crouched at his side. Her husband protested that he was fine, then began to scooch himself on his bottom into the bedroom. The two young men helped him to his feet. The man’s body shook with a wild tremor that nearly knocked him down again. “I was getting into bed and fell,” he explained — though the bed was too far away to make this at all likely. “Get some sleep,” the woman said gently once her husband was settled in the bed. “We’ll go to the hospital in the morning.” Her daughter and son-in-law had arrived that morning and already mentioned the change they noticed in the 70-year-old senior. The normally gregarious man was oddly quiet. And the tremor he had for as long as they could remember was much more prominent. His hands shook so much he had trouble using his fork and ended up eating much of his Thanksgiving dinner with his fingers. And now this fall, this confusion — they were worried. His wife was also worried. Just after Halloween, she traveled for business, and when she came back, her husband was much quieter than usual. Even more concerning: When he spoke, he didn’t always make sense. “Have you had a stroke?” she asked her first day home. He was fine, he insisted. But a few days later she came home from work to find his face covered with cuts. He was shaving, he said, but his hand shook so much that he kept cutting himself. “There is something wrong with me,” he acknowledged. It was Thanksgiving week, but she was able to get him an appointment at his doctor’s office the next day. They were seen by the physician assistant (P.A.). She was kind, careful and thorough. After hearing of his confusion, she asked the man what day it was. “Friday?” he offered uncertainly. It was Wednesday. Could he touch his finger to his nose and then to her finger, held an arm’s length away? He could not. His index finger carved jagged teeth in the air as he sought his own nose then stretched to touch her finger. And when she asked him to stand, his entire body wobbled dangerously. “It’s all happened so quickly,” the man’s wife said. The P.A. reviewed his lab tests. They were all normal. She then ordered an M.R.I. of the brain. That, she explained, should give them a better idea of what direction to take. But, she added, if he falls or seems © 2024 The New York Times Company

Keyword: Neurotoxins; Movement Disorders
Link ID: 29182 - Posted: 03.07.2024

By Clay Risen Mary Bartlett Bunge, who with her husband, Richard, studied how the body responds to spinal cord injuries and continued their work after his death in 1996, ultimately discovering a promising treatment to restore movement to millions of paralyzed patients, died on Feb. 17, at her home in Coral Gables, Fla. She was 92. The Miami Project to Cure Paralysis, a nonprofit research organization with which Dr. Bunge (pronounced BUN-ghee) was affiliated, announced the death. “She definitely was the top woman in neuroscience, not just in the United States but in the world,” Dr. Barth Green, a co-founder and dean at the Miami Project, said in a phone interview. Dr. Bunge’s focus for much of her career was on myelin, a mix of proteins and fatty acids that coats nerve fibers, protecting them and boosting the speed at which they conduct signals. Early in her career, she and her husband, whom she met as a graduate student at the University of Wisconsin in the 1950s, used new electron microscopes to describe the way that myelin developed around nerve fibers, and how, after because of injury or illness, it receded, in a process called demyelination. Treating spinal-cord injuries is one of the most frustrating corners of medical research. Thousands of people are left partially or fully paralyzed after automobile accidents, falls, sports injuries and gun violence each year. Unlike other parts of the body, the spinal cord is stubbornly difficult to rehabilitate. Through their research, the Bunges concluded that demyelination was one reason spinal-cord injuries have been so difficult for the body to repair — an insight that in turn opened doors to the possibility of reversing it through treatments. © 2024 The New York Times Company

Keyword: Glia; Regeneration
Link ID: 29175 - Posted: 03.05.2024

By Liam Drew The first person to receive a brain-monitoring device from neurotechnology company Neuralink can control a computer cursor with their mind, Elon Musk, the firm’s founder, revealed this week. But researchers say that this is not a major feat — and they are concerned about the secrecy around the device’s safety and performance. The company is “only sharing the bits that they want us to know about”, says Sameer Sheth, a neurosurgeon specializing in implanted neurotechnology at Baylor College of Medicine in Houston, Texas. “There’s a lot of concern in the community about that.” Threads for thoughts Musk announced on 29 January that Neuralink had implanted a brain–computer interface (BCI) into a human for the first time. Neuralink, which is headquartered in Fremont, California, is the third company to start long-term trials in humans. Some implanted BCIs sit on the brain’s surface and record the average firing of populations of neurons, but Neuralink’s device, and at least two others, penetrates the brain to record the activity of individual neurons. Neuralink’s BCI contains 1,024 electrodes — many more than previous systems — arranged on innovative pliable threads. The company has also produced a surgical robot for inserting its device. But it has not confirmed whether that system was used for the first human implant. Details about the first recipient are also scarce, although Neuralink’s volunteer recruitment brochure says that people with quadriplegia stemming from certain conditions “may qualify”.

Keyword: Robotics; Brain imaging
Link ID: 29163 - Posted: 02.25.2024

By Annie Melchor When the first known flying dinosaurs took to the skies some 150 million years ago, the evolutionary leap relied on adaptations to their nervous system. The changes remained a mystery, though, because of the paucity of fossilized neural tissue. Now fresh clues have emerged from a study that started with the long-gone dinosaurs’ living kin: the common pigeon, Columba livia. Flight taps neural pathways involving the pigeon’s cerebellum, the new works shows, which prompted study investigator Amy Balanoff and her team to look specifically at that structure in digital brain “endocasts,” created by CT scanning fossilized dinosaur skulls. “The birds can help us look for certain things within these extinct animals,” says Balanoff, assistant professor of evolutionary biology at Johns Hopkins University. “Then these extinct animals can tell us about the evolutionary history leading up to living birds.” An analysis of the endocasts — from 10 dinosaur specimens dating to between 90 and 150 million years ago — revealed that the volume of the cerebellum expanded in birds’ closest relatives, but not in more distant ones. And at some point, the cerebellum began folding — instead of growing — to accommodate more neurons within a fixed cranial space, Balanoff says. The results suggest that the cerebellum was “flight-ready before flying,” says Crístian Gutiérrez-Ibáñez, an evolutionary biology research associate at the University of Alberta who was not involved in the study. “So the question is, why did dinosaurs get such a big cerebellum?” © 2024 Simons Foundation

Keyword: Evolution; Movement Disorders
Link ID: 29162 - Posted: 02.25.2024

Fen-Biao Gao Around 55 million people worldwide suffer from dementia such as Alzheimer’s disease. On Feb. 22, 2024, it was revealed that former talk show host Wendy Williams had been diagnosed with frontotemporal dementia, or FTD, a rare type of dementia that typically affects people ages 45 to 64. Bruce Willis is another celebrity who was diagnosed with the syndrome, according to his family. In contrast to Alzheimer’s, in which the major initial symptom is memory loss, FTD typically involves changes in behavior. The initial symptoms of FTD may include changes in personality, behavior and language production. For instance, some FTD patients exhibit inappropriate social behavior, impulsivity and loss of empathy. Others struggle to find words and to express themselves. This insidious disease can be especially hard for families and loved ones to deal with. There is no cure for FTD, and there are no effective treatments. Up to 40% of FTD cases have some family history, which means a genetic cause may run in the family. Since researchers identified the first genetic mutations that cause FTD in 1998, more than a dozen genes have been linked to the disease. These discoveries provide an entry point to determine the mechanisms that underlie the dysfunction of neurons and neural circuits in the brain and to use that knowledge to explore potential approaches to treatment. I am a researcher who studies the development of FTD and related disorders, including the motor neuron disease amyotrophic lateral sclerosis, or ALS. ALS, also known as Lou Gehrig’s disease, results in progressive muscle weakness and death. Uncovering the similarities in pathology and genetics between FTD and ALS could lead to new ways to treat both diseases. Genes contain the instructions cells use to make the proteins that carry out functions essential to life. Mutated genes can result in mutated proteins that lose their normal function or become toxic. © 2010–2024, The Conversation US, Inc.

Keyword: Alzheimers; ALS-Lou Gehrig's Disease
Link ID: 29161 - Posted: 02.25.2024

By Miryam Naddaf Moving a prosthetic arm. Controlling a speaking avatar. Typing at speed. These are all things that people with paralysis have learnt to do using brain–computer interfaces (BCIs) — implanted devices that are powered by thought alone. These devices capture neural activity using dozens to hundreds of electrodes embedded in the brain. A decoder system analyses the signals and translates them into commands. Although the main impetus behind the work is to help restore functions to people with paralysis, the technology also gives researchers a unique way to explore how the human brain is organized, and with greater resolution than most other methods. Scientists have used these opportunities to learn some basic lessons about the brain. Results are overturning assumptions about brain anatomy, for example, revealing that regions often have much fuzzier boundaries and job descriptions than was thought. Such studies are also helping researchers to work out how BCIs themselves affect the brain and, crucially, how to improve the devices. “BCIs in humans have given us a chance to record single-neuron activity for a lot of brain areas that nobody’s ever really been able to do in this way,” says Frank Willett, a neuroscientist at Stanford University in California who is working on a BCI for speech. The devices also allow measurements over much longer time spans than classical tools do, says Edward Chang, a neurosurgeon at the University of California, San Francisco. “BCIs are really pushing the limits, being able to record over not just days, weeks, but months, years at a time,” he says. “So you can study things like learning, you can study things like plasticity, you can learn tasks that require much, much more time to understand.” © 2024 Springer Nature Limited

Keyword: Brain imaging; Robotics
Link ID: 29159 - Posted: 02.22.2024

By Angie Voyles Askham The primary visual cortex carries, well, visual information — or so scientists thought until early 2010. That’s when a team at the University of California, San Francisco first described vagabond activity in the brain area, called V1, in mice. When the animals started to run on a treadmill, some neurons more than doubled their firing rate. The finding “was kind of mysterious,” because V1 was thought to represent only visual signals transmitted from the retina, says Anne Churchland, professor of neurobiology at the University of California, Los Angeles, who was not involved in that work. “The idea that running modulated neural activity suggested that maybe those visual signals were corrupted in a way that, at the time, felt like it would be really problematic.” The mystery grew over the next decade, as a flurry of mouse studies from Churchland and others built on the 2010 results. Both arousal and locomotion could shape the firing of primary visual neurons, those newer findings showed, and even subtle movements such as nose scratches contribute to variance in population activity, all without compromising the sensory information. A consensus started to form around the idea that sensory cortical regions encode broader information about an animal’s physiological state than previously thought. At least until last year, when two studies threw a wrench into that storyline: Neither marmosets nor macaque monkeys show any movement-related increase in V1 signaling. Instead, running seems to slightly suppress V1 activity in marmosets, and spontaneous movements have no effect on the same cells in macaques. The apparent differences across species raise new questions about whether mice are a suitable model to study the primate visual system, says Michael Stryker, professor of physiology at the University of California, San Francisco, who led the 2010 work. “Maybe the primate’s V1 is not working the same as in the mouse,” he says. “As I see it, it’s still a big unanswered question.” © 2024 Simons Foundation

Keyword: Vision
Link ID: 29153 - Posted: 02.20.2024

Nancy S. Jecker & Andrew Ko Putting a computer inside someone’s brain used to feel like the edge of science fiction. Today, it’s a reality. Academic and commercial groups are testing “brain-computer interface” devices to enable people with disabilities to function more independently. Yet Elon Musk’s company, Neuralink, has put this technology front and center in debates about safety, ethics and neuroscience. In January 2024, Musk announced that Neuralink implanted its first chip in a human subject’s brain. The Conversation reached out to two scholars at the University of Washington School of Medicine – Nancy Jecker, a bioethicst, and Andrew Ko, a neurosurgeon who implants brain chip devices – for their thoughts on the ethics of this new horizon in neuroscience. How does a brain chip work? Neuralink’s coin-size device, called N1, is designed to enable patients to carry out actions just by concentrating on them, without moving their bodies. Subjects in the company’s PRIME study – short for Precise Robotically Implanted Brain-Computer Interface – undergo surgery to place the device in a part of the brain that controls movement. The chip records and processes the brain’s electrical activity, then transmits this data to an external device, such as a phone or computer. The external device “decodes” the patient’s brain activity, learning to associate certain patterns with the patient’s goal: moving a computer cursor up a screen, for example. Over time, the software can recognize a pattern of neural firing that consistently occurs while the participant is imagining that task, and then execute the task for the person. © 2010–2024, The Conversation US, Inc.

Keyword: Robotics; Learning & Memory
Link ID: 29151 - Posted: 02.20.2024

By Claudia López Lloreda By squirting cells from a 3D printer, researchers have created tissue that looks—and acts—like a chunk of brain. In recent years, scientists have learned how to load up 3D printers with cells and other scaffolding ingredients to create living tissues, but making realistic brainlike constructs has been a challenge. Now, one team has shown that, by modifying its printing techniques, it can print and combine multiple subtypes of cells that better mimic signaling in the human brain. “It’s remarkable that [the researchers] can replicate” how brain cells work, says Riccardo Levato, a regenerative medicine researcher at Utrecht University who was not involved with the study. “It’s the first demonstration that, with some simple organization [of cells], you can start getting some interesting functional [responses].” The new technology, described last week in Cell Stem Cell, could offer advantages over existing techniques that neuroscientists use to create 3D brain tissues in the lab. One common approach involves using stem cells to grow miniature brainlike blobs called organoids. But researchers can’t control the types of cells or their precise location in these constructs. Each organoid “is unique,” making it difficult to reproduce research results, says neuroscientist Su-Chun Zhang of the University of Wisconsin–Madison, an author of the new study. With the right kind of 3D printing, however, “you can control where different cell types are placed,” says developmental biologist Francis Szele of the University of Oxford. Past studies have used 3D printers to construct brain tissues that allowed researchers to study how the cells matured and made connections, and even integrate printed tissue into mouse brains. But those constructs had limited functionality. And efforts that produced more functional printed tissue used rat cells, not human cells. © 2024 American Association for the Advancement of Science.

Keyword: Development of the Brain; Robotics
Link ID: 29145 - Posted: 02.10.2024