By Joanne Silberner A hug, a handshake, a therapeutic massage. A newborn lying on a mother’s bare chest. Physical touch can buoy well-being and lessen pain, depression and anxiety, according to a large new analysis of published research released on Monday in the journal Nature Human Behaviour. Researchers from Germany and the Netherlands systematically reviewed years of research on touch, strokes, hugs and rubs. They also combined data from 137 studies, which included nearly 13,000 adults, children and infants. Each study compared individuals who had been physically touched in some way over the course of an experiment — or had touched an object like a fuzzy stuffed toy — to similar individuals who had not. For example, one study showed that daily 20-minute gentle massages for six weeks in older people with dementia decreased aggressiveness and reduced the levels of a stress marker in the blood. Another found that massages boosted the mood of breast cancer patients. One study even showed that healthy young adults who caressed a robotic baby seal were happier, and felt less pain from a mild heat stimulus, than those who read an article about an astronomer. Positive effects were particularly noticeable in premature babies, who “massively improve” with skin-to-skin contact, said Frédéric Michon, a researcher at the Netherlands Institute for Neuroscience and one of the study’s authors. “There have been a lot of claims that touch is good, touch is healthy, touch is something that we all need,” said Rebecca Boehme, a neuroscientist at Linkoping University in Sweden, who reviewed the study for the journal. “But actually, nobody had looked at it from this broad, bird’s eye perspective.” © 2024 The New York Times Company

Keyword: Pain & Touch; Emotions
Link ID: 29252 - 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

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 Emily Makowski & I spend my days surrounded by thousands of written words, and sometimes I feel as though there’s no escape. That may not seem particularly unusual. Plenty of people have similar feelings. But no, I’m not just talking about my job as a copy editor here at Scientific American, where I edit and fact-check an endless stream of science writing. This constant flow of text is all in my head. My brain automatically translates spoken words into written ones in my mind’s eye. I “see” subtitles that I can’t turn off whenever I talk or hear someone else talking. This same speech-to-text conversion even happens for the inner dialogue of my thoughts. This mental closed-captioning has accompanied me since late toddlerhood, almost as far back as my earliest childhood memories. And for a long time, I thought that everyone could “read” spoken words in their head the way I do. What I experience goes by the name of ticker-tape synesthesia. It is not a medical condition—it’s just a distinctive way of perceiving the surrounding world that relatively few people share. Not much is known about the neurophysiology or psychology of this phenomenon, sometimes called “ticker taping,” even though a reference to it first appeared in the scientific literature in the late 19th century. Ticker taping is considered a form of synesthesia, an experience in which the brain reroutes one kind of incoming sensory information so that it is processed as another. For example, sounds might be perceived as touch, allowing the affected person to “feel” them as tactile sensations. As synesthesia goes, ticker taping is relatively uncommon. “There are varieties of synesthesia which really have just been completely under the radar..., and ticker tape is really one of those,” says Mark Price, a cognitive psychologist at the University of Bergen in Norway. The name “ticker-tape synesthesia” itself evokes the concept’s late 19th-century origins. At that time stock prices transmitted by telegraph were printed on long paper strips, which would be torn into tiny bits and thrown from building windows during parades. © 2024 SCIENTIFIC AMERICAN,

Keyword: Attention; Language
Link ID: 29238 - 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 Saugat Bolakhe For desert ants, Earth’s magnetic field isn’t just a compass: It may also sculpt their brains. Stepping outside their nest for the first time, young ants need to learn how to forage. The ants train partly by walking a loop near their nests for the first three days. During this stroll, they repeatedly pause and then pirouette to gaze back at the nest entrance, learning how to find their way back home. But when the magnetic field around the nest entrance was disturbed, ant apprentices couldn’t figure out where to look, often gazing in random directions, researchers report in the Feb. 20 Proceedings of the National Academy of Sciences. What’s more, the altered magnetic field seemed to affect connections between neurons in the learning and memory centers in the young ants’ brains. The finding “may make it easier to better understand how magnetic fields are sensed [in animals]” as scientists now know one way that magnetic fields can influence brain development, says Robin Grob, a biologist at the Norwegian University of Science and Technology in Trondheim. For years, scientists have known that some species of birds, fishes, turtles, moths and butterflies rely on Earth’s magnetic field to navigate (SN: 4/3/18). In 2018, Grob and other scientists added desert ants to that list. Young ants first appeared to use the magnetic field as a reference while learning how to use landmarks and the sun as guides to orient themselves in the right direction to gaze back toward the nest with its small, hard-to-see entrance. However, knowing where in the brain magnetic cues are processed has proved challenging. © Society for Science & the Public 2000–2024.

Keyword: Animal Migration; Development of the Brain
Link ID: 29227 - 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 Alejandra Manjarrez People wear gloves when making a snowman for a reason: Handling cold stuff can hurt. A new mouse study reveals what may be a key player in this response: a protein already known to enable sensory neurons in worms to detect cold. New evidence published this week in Nature Neuroscience confirms that this protein has the same function in mammals. “The paper is exciting,” says Theanne Griffith, a neuroscientist at the University of California, Davis who was not involved in the research. She notes that the protein, called GluK2, is found in the brain and has “traditionally been thought to play a major role in learning and memory.” The new work shows that elsewhere in the body, it has an unsuspected and “completely divergent role.” We perceive touch, pain, and temperature thanks to a system of nerves that extends throughout our bodies. Researchers have identified skin sensors that detect hot and warm stimuli. Cold sensors, though, have proved more challenging to find. Researchers have proposed various candidates but found limited and contradictory evidence for their function. An ion channel named TRPM8 is the exception. Famous for detecting the “cool” sensation of menthol, it also detects cold temperatures and helped earn its discoverers the Nobel Prize in Physiology or Medicine in 2021. “Nobody questions that TRPM8 is a cold sensor,” says sensory neurobiologist Félix Viana of the Institute for Neuroscience in Alicante, Spain. But it could not be the whole story. It works most efficiently at temperatures above roughly 10°C, and mice lacking the gene for TRPM8 can still detect very cold temperatures. A few years ago, University of Michigan neuroscientists Shawn Xu and Bo Duan and their colleagues found another candidate: a protein on certain sensory neurons in the tiny roundworm Caenorhabditis elegans that causes the animals to avoid temperatures between 17°C and 18°C, which are colder than their preferred temperatures. Preliminary data from that study hinted that the equivalent protein in mammals, GluK2, also allowed mice to sense cold.

Keyword: Pain & Touch
Link ID: 29190 - Posted: 03.16.2024

By Regina G. Barber, Anil Oza, Ailsa Chang, Rachel Carlson Neuroscientist Nathan Sawtell has spent a lot of time studying a funky looking electric fish characterized by its long nose. The Gnathonemus petersii, or elephantnose fish, can send and decipher weak electric signals, which Sawtell hopes will help neuroscientists better understand how the brain pieces together information about the outside world. But as Sawtell studied these electric critters, he noticed a pattern he couldn't explain: the fish tend to organize themselves in a particular orientation. "There would be a group of subordinates in a particular configuration at one end of the tank, and then a dominant fish at the other end. The dominant fish would swim in and break up the group, and they would scatter. A few seconds later, the group would coalesce and it would stay there for hours at a time in this stationary configuration," Sawtell, who runs a lab at Columbia University's Zuckerman Institute says. Initially Sawtell and his team couldn't put together why the fish were always hanging out in this configuration. "What could they really be talking to each other about all of this time?" A new study released this week in Nature by Sawtell and colleagues at Columbia University could have one potential answer: the fish are creating an electrical network that is larger than any field an individual fish can muster alone. In this collective field, the whole school of fish get instantaneous information on changes in the water around them, like approaching predators. Rather than being confused by the flurry of electric signals from other fish, "these fish were clever enough to exploit the pulses of group members to sense their environment," Sawtell says. © 2024 npr

Keyword: Pain & Touch
Link ID: 29187 - Posted: 03.09.2024

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