By Jennie Erin Smith José Echeverría spends restless days in a metal chair reinforced with boards and padded with a piece of foam that his mother, Nohora Vásquez, adjusts constantly for his comfort. The chair is coming loose and will soon fall apart. Huntington’s disease, which causes José to move his head and limbs uncontrollably, has already left one bed frame destroyed. At 42, he is still strong. José’s sister Nohora Esther Echeverría, 37, lives with her mother and brother. Just two years into her illness, her symptoms are milder than his, but she is afraid to walk around her town’s steep streets, knowing she could fall. A sign on the front door advertises rum for sale that does not exist. The family’s scarce resources now go to food — José and Nohora Esther must eat frequently or they will rapidly lose weight — and medical supplies, like a costly cream for Jose’s skin. Huntington’s is a hereditary neurodegenerative disease caused by excess repetitions of three building blocks of DNA — cytosine, adenine, and guanine — on a gene called huntingtin. The mutation results in a toxic version of a key brain protein, and a person’s age at the onset of symptoms relates, roughly, to the number of repetitions the person carries. Early symptoms can include mood disturbances — Ms. Vásquez remembers how her late husband had chased the children out of their beds, forcing her to sleep with them in the woods — and subtle involuntary movements, like the rotations of Nohora Esther’s delicate wrists. The disease is relatively rare, but in the late 1980s a Colombian neurologist, Jorge Daza, began observing a striking number of cases in the region where Ms. Vásquez lives, a cluster of seaside and mountain towns near Barranquilla. Around the same time, American scientists led by Nancy Wexler were working with an even larger family with Huntington’s in neighboring Venezuela, gathering and studying thousands of tissue samples from them to identify the genetic mutation responsible. © 2023 The New York Times Company

Keyword: Huntingtons; Genes & Behavior
Link ID: 28796 - Posted: 05.23.2023

By Meredith Wadman A groundbreaking epidemiological study has produced the most compelling evidence yet that exposure to the chemical solvent trichloroethylene (TCE)—common in soil and groundwater—increases the risk of developing Parkinson’s disease. The movement disorder afflicts about 1 million Americans, and is likely the fastest growing neurodegenerative disease in the world; its global prevalence has doubled in the past 25 years. The report, published today in JAMA Neurology, involved examining the medical records of tens of thousands of Marine Corps and Navy veterans who trained at Marine Corps Base Camp Lejeune in North Carolina from 1975 to 1985. Those exposed there to water heavily contaminated with TCE had a 70% higher risk of developing Parkinson’s disease decades later compared with similar veterans who trained elsewhere. The Camp Lejeune contingent also had higher rates of symptoms such as erectile dysfunction and loss of smell that are early harbingers of Parkinson’s, which causes tremors; problems with moving, speaking, and balance; and in many cases dementia. Swallowing difficulties often lead to death from pneumonia. About 90% of Parkinson’s cases can’t be explained by genetics, but there have been hints that exposure to TCE may trigger it. The new study, led by researchers at the University of California, San Francisco (UCSF), represents by far the strongest environmental link between TCE and the disease. Until now, the entire epidemiological literature included fewer than 20 people who developed Parkinson’s after TCE exposure. The Camp Lejeune analysis “is exceptionally important,” says Briana De Miranda, a neurotoxicologist at the University of Alabama at Birmingham who studies TCE’s pathological impacts in the brains of rats. “It gives us an extremely large population to assess a risk factor in a very carefully designed epidemiological study.”

Keyword: Parkinsons; Neurotoxins
Link ID: 28785 - Posted: 05.18.2023

Scott Hensley In a split vote, advisers to the Food and Drug Administration recommended that the agency approve the first gene therapy for Duchenne muscular dystrophy, the most common form of the genetic illness. The vote, 8 to 6, came after a day of testimony from speakers for Sarepta Therapeutics, the maker of the gene therapy called SRP-9001, FDA scientists and families whose children have Duchenne muscular dystrophy. The question before the panel was whether the benefits for the treatment outweigh the risks. While the FDA is not bound by the recommendations of its outside advisers, it usually follows them. The agency is expected to decide by the end of May. Gene therapy for muscular dystrophy stirs hopes and controversy Duchenne muscular dystrophy is the most common inherited neuromuscular disorder among children. It affects an estimated 10,000 to 12,000 children in the U.S. The genetic condition mainly afflicts boys and leads to progressive muscle damage, loss of ability to movement and eventually death. Sarepta's treatment involves a single infusion of viruses that has been genetically modified to carry a gene to patients' muscles to produce a miniature version of a protein called dystrophin. Patients with Duchenne muscular dystrophy are missing the muscle-protecting protein or don't make enough of it. While not a cure, Sarepta argues that its "micro-dystrophin" treatment can help slow the progression of the disease. The company's request for approval rested mainly on how much micro-dystrophin the treatment produces in patients' muscles instead of waiting for clear, real-world evidence that it's actually helping patients. © 2023 npr

Keyword: Muscles; Movement Disorders
Link ID: 28780 - Posted: 05.13.2023

By Rebecca Robbins The Food and Drug Administration on Tuesday authorized the first drug for a rare genetic form of the neurological disorder A.L.S., despite uncertainty about the treatment’s effectiveness. The decision reflects the agency’s push toward greater flexibility in approving treatments for patients with devastating illnesses and few, if any, options. Biogen, the pharmaceutical company bringing the drug to market, said it would price the drug “within a range comparable to other recently launched A.L.S. treatments.” An A.L.S. therapy approved last year was priced at $158,000 annually. The drug, which is known scientifically as tofersen and will be sold under the brand name Qalsody, targets a mutation in a gene known as SOD1 that is present in about 2 percent of the roughly 6,000 cases of A.L.S. diagnosed in the United States each year. Fewer than 500 people in the United States at any given time are expected to be eligible. The agency authorized the treatment via a policy that allows a drug to be fast-tracked onto the market under certain circumstances before there is conclusive proof that it works. Biogen will be required to provide confirmatory evidence, from ongoing clinical research, to keep the drug on the market. The decision is the first conditional approval granted for a medication for A.L.S., or amyotrophic lateral sclerosis, which generally causes paralysis and death within a few years. Fewer than half the patients eligible for Qalsody survive more than three years after their diagnosis. The approval is based on evidence that the drug can significantly reduce levels of a protein that has been linked to damage to nerve cells. Biogen has argued that these results are reasonably likely to help patients, even though the drug, in a clinical trial, did not significantly slow the progression of the disease, as measured by patients’ ability to speak, swallow and perform other activities of daily living. © 2023 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28753 - Posted: 04.26.2023

By Nora Bradford The classical view of how the human brain controls voluntary movement might not tell the whole story. That map of the primary motor cortex — the motor homunculus — shows how this brain region is divided into sections assigned to each body part that can be controlled voluntarily (SN: 6/16/15). It puts your toes next to your ankle, and your neck next to your thumb. The space each part takes up on the cortex is also proportional to how much control one has over that part. Each finger, for example, takes up more space than a whole thigh. A new map reveals that in addition to having regions devoted to specific body parts, three newfound areas control integrative, whole-body actions. And representations of where specific body parts fall on this map are organized differently than previously thought, researchers report April 19 in Nature. Research in monkeys had hinted at this. “There is a whole cohort of people who have known for 50 years that the homunculus isn’t quite right,” says Evan Gordon, a neuroscientist at Washington University School of Medicine in St. Louis. But ever since pioneering brain-mapping work by neurosurgeon Wilder Penfield starting in the 1930s, the homunculus has reigned supreme in neuroscience. Gordon and his colleagues study synchronized activity and communication between different brain regions. They noticed some spots in the primary motor cortex were linked to unexpected areas involved in action control and pain perception. Because that didn’t fit with the homunculus map, they wrote it off as a result of imperfect data. “But we kept seeing it, and it kept bugging us,” Gordon says. So the team gathered functional MRI data on volunteers as they performed various tasks. Two participants completed simple movements like moving just their eyebrows or toes, as well as complex tasks like simultaneously rotating their wrist and moving their foot from side to side. The fMRI data revealed which parts of the brain activated at the same time as each task was done, allowing the researchers to trace which regions were functionally connected to one another. Seven more participants were recorded while not doing any particular task in order to look at how brain areas communicate during rest. © Society for Science & the Public 2000–2023.

Keyword: Brain imaging
Link ID: 28748 - Posted: 04.22.2023

Max Kozlov The bizarre-looking ‘homunculus’ is one of neuroscience’s most fundamental diagrams. Found in countless textbooks, it depicts a deformed constellation of body parts mapped onto a narrow strip of the brain, showing the corresponding brain regions that control each part. But a study published in Nature1 on 19 April reveals that this brain strip, called the primary motor cortex, is much more complex than the famous diagram suggests. It might coordinate complex movements involving multiple muscles through connections to brain regions responsible for critical thinking, maintaining the body’s physiology and planning actions. The new results could help scientists better understand and treat brain injuries. “This study is very interesting and very important,” says Michael Graziano, a neuroscientist at Princeton University in New Jersey. It’s becoming clear that the primary motor cortex isn’t “just a simple roster of muscles down the brain that control the toes to the tongue”, he says. Little man in the brain The idea of the homunculus dates to the late nineteenth century, when researchers noticed that electrically stimulating the primary motor cortex corresponded to specific body parts twitching. Later work found that some body parts, such as the hands, feet and mouth, took up a disproportionate amount of space in the primary motor cortex compared with the rest of the body. In 1937, these findings culminated with the first publication of the motor homunculus, which translates to ‘little man’ in Latin. Neurosurgeon Wilder Penfield’s 1948 diagram of the motor homunculus (left) shows the areas of the primary motor cortex that control each body part. A new study redraws the diagram (right), adding regions connected to brain areas responsible for coordinating complex movements.Credit: E. Gordon et al./Nature © 2023 Springer Nature Limited

Keyword: Brain imaging
Link ID: 28747 - Posted: 04.22.2023

Asher Mullard The US Food and Drug Administration (FDA) is set to rule soon on the approval of a new drug for a rare form of amyotrophic lateral sclerosis (ALS). The hotly anticipated decision is expected to signpost the agency’s vision for neurological drugs — and its willingness to be flexible in the regulation of these therapeutics. People with the disease desperately need new treatments, because they face a degenerative condition that causes neuronal death and typically leads to fatal respiratory failure within three years of symptoms appearing1. Tofersen, developed by the biotechnology firms Biogen in Cambridge, Massachusetts, and Ionis Pharmaceuticals in Carlsbad, California, did not slow patients’ decline in a phase III trial2. However, some say the trial was too short, and point out that there were signs of possible benefit, such as a reduction in a biomarker of neuronal damage and death called neurofilament light chain (NFL). Because of this, Biogen has asked the FDA to approve the drug on an ‘accelerated’ basis, to fast-track it to patients with a guarantee that future trial data will determine whether it works. If approved, tofersen will become the latest example of the agency’s evolving approach to neurological drug development, which could boost industry investment in brain diseases. A vote of confidence for the drug would also supercharge interest in using NFL as a tool to measure brain health and to test drugs in future. “This could be the start of a new era,” says Valentina Bonetto, a neuroscientist at the Mario Negri Institute for Pharmacological Research in Milan, Italy. In March, the FDA convened a panel to discuss the tofersen data set. Its nine independent advisers rallied behind accelerated approval for the drug, voting unanimously that the available evidence supports a “reasonably likely” chance that tofersen will help people with SOD1 ALS. This rare disease is caused by genetic mutations that affect the protein SOD1, leading it to form toxic clumps in motor neurons in the brain, brainstem and spinal cord. The agency usually follows the recommendations of its advisory committee. © 2023 Springer Nature Limited

Keyword: ALS-Lou Gehrig's Disease ; Neuroimmunology
Link ID: 28744 - Posted: 04.18.2023

By Oliver Whang What is the relationship between mind and body? Maybe the mind is like a video game controller, moving the body around the world, taking it on joy rides. Or maybe the body manipulates the mind with hunger, sleepiness and anxiety, something like a river steering a canoe. Is the mind like electromagnetic waves, flickering in and out of our light-bulb bodies? Or is the mind a car on the road? A ghost in the machine? Maybe no metaphor will ever quite fit because there is no distinction between mind and body: There is just experience, or some kind of physical process, a gestalt. These questions, agonized over by philosophers for centuries, are gaining new urgency as sophisticated machines with artificial intelligence begin to infiltrate society. Chatbots like OpenAI’s GPT-4 and Google’s Bard have minds, in some sense: Trained on vast troves of human language, they have learned how to generate novel combinations of text, images and even videos. When primed in the right way, they can express desires, beliefs, hopes, intentions, love. They can speak of introspection and doubt, self-confidence and regret. But some A.I. researchers say that the technology won’t reach true intelligence, or true understanding of the world, until it is paired with a body that can perceive, react to and feel around its environment. For them, talk of disembodied intelligent minds is misguided — even dangerous. A.I. that is unable to explore the world and learn its limits, in the ways that children figure out what they can and can’t do, could make life-threatening mistakes and pursue its goals at the risk of human welfare. “The body, in a very simple way, is the foundation for intelligent and cautious action,” said Joshua Bongard, a roboticist at the University of Vermont. “As far as I can see, this is the only path to safe A.I.” At a lab in Pasadena, Calif., a small team of engineers has spent the past few years developing one of the first pairings of a large language model with a body: a turquoise robot named Moxie. About the size of a toddler, Moxie has a teardrop-shaped head, soft hands and alacritous green eyes. Inside its hard plastic body is a computer processor that runs the same kind of software as ChatGPT and GPT-4. Moxie’s makers, part of a start-up called Embodied, describe the device as “the world’s first A.I. robot friend.” © 2023 The New York Times Company

Keyword: Intelligence; Robotics
Link ID: 28735 - Posted: 04.12.2023

By Amber Dance Isabelle Lousada was in her early 30s when she collapsed at her Philadelphia wedding in 1995. A London architect, she had suffered a decade of mysterious symptoms: tingling fingers, swollen ankles, a belly distended by her enlarged liver. The doctors she first consulted suggested she had chronic fatigue syndrome or that she’d been partying and drinking too hard. But her new brother-in-law, a cardiologist, felt that something else must be going on. A fresh series of doctor’s visits led, finally, to the proper diagnosis: Malformed proteins had glommed together inside Lousada’s bloodstream and organs. Those giant protein globs are called amyloid, and the diagnosis was amyloidosis. Amyloid diseases that affect the brain, such as Alzheimer’s and Parkinson’s diseases, receive the lion’s share of attention from medical professionals and the press. In contrast, amyloid diseases that affect other body parts are less familiar and rarely diagnosed conditions, says Gareth Morgan, a biochemist at Boston University Chobanian & Avedisian School of Medicine. Physicians may struggle to recognize and distinguish them, especially in early stages. Treatment options have also been limited — Lousada, now CEO of the nonprofit Amyloidosis Research Consortium in Newton, Massachusetts, was fortunate to survive thanks to a stem cell transplant that is too grueling or unsuitable for many with amyloidosis. Several new medications have come out in the last five years — and these, Lousada says, “have been real game-changers.” But although these therapies can block the formation of new, damaging amyloid, they can’t dissolve the amyloid that’s already built up. The body has natural processes to do so, but these are often too slow to clear years’ worth of built-up amyloid, especially in older individuals. And so patients still deal with amyloid clogging their organs, and people still die of amyloidosis, even if they survive longer than they once did. © 2023 Annual Reviews

Keyword: Alzheimers; Parkinsons
Link ID: 28731 - Posted: 04.09.2023

By Darren Incorvaia Sitting in an exam room, surrounded by doctors and scientists, Heather Rendulic opened her left hand for the first time since suffering a series of strokes nine years earlier when she was in her early 20s. “It was an amazing feeling for me to be able to do that again,” Rendulic says. “It’s not something I ever thought was possible.” But immediately after a surgically implanted device sent electrical pulses into her spinal cord, Rendulic could not only open her hand but also showed other marked improvements in arm mobility, researchers report February 20 in Nature Medicine. “We all started crying,” Marco Capogrosso, a neuroscientist at the University of Pittsburgh, said in a February 15 news conference. “We didn’t really expect this could work as fast as that.” The approach is similar to that recently used for patients paralyzed by spinal cord injuries (SN: 08/03/22). It represents a promising new technique for restoring voluntary movement to those left with upper-body paralysis following strokes, the team says. A stroke occurs when blood supply to parts of the brain is cut off, often causing short-term or long-term issues with movement, speech and vision. Stroke is a leading, and often underappreciated, cause of paralysis; in the United States alone, 5 million people are living with some form of motor deficit due to stroke. While physical therapy can provide some improvements, no treatment exists to help these patients regain full control of their limbs — and their lives. Strokes cause paralysis because the connection between the brain and the spinal cord is damaged; the brain tries to tell the spinal cord to move certain muscles, but the message is muddled. © Society for Science & the Public 2000–2023.

Keyword: Stroke; Robotics
Link ID: 28678 - Posted: 02.22.2023

Max Kozlov A group of brain cells in mice becomes active both when the animals fight and when they watch other mice fight, a study1 shows. The work hints that such ‘mirror neurons’, which fire when an animal either observes or takes part in a particular activity, could shape complex social behaviours, such as aggression. The mirror neurons described in the study are the first to be found in the hypothalamus, an evolutionarily ancient brain region — suggesting that mirror neurons’ original purpose might have been to enhance defence and, ultimately, reproductive success, the authors speculate. The study was published in Cell on 15 February. “We’ve now shown that mirror neurons functionally participate in the behaviours they’re mirroring,” says Nirao Shah, a neuroscientist at Stanford University in California who co-authored the study. “That changes what we think about mirror neurons.” First identified in monkeys in the 1990s, mirror neurons generally fire when an animal takes a certain action, but they also fire when it sees another animal perform the same action. Previous work has linked mirror neurons’ activity to simple behaviours, such as reaching for an object, but not to complex social behaviours, such as fighting. But exactly how mirror-neuron activity contributes to cognitive functions has been controversial, says Pier Francesco Ferrari, a neuroethologist at the Institute of Cognitive Science Marc Jeannerod in Lyon, France. Some researchers have argued that the fact that mirror neurons fire both when an animal observes a behaviour and when it performs that behaviour itself shows that these neurons are involved in a higher-order awareness of others’ actions — and perhaps even contribute to empathy. But others say that there is little evidence to support this theory. © 2023 Springer Nature Limited

Keyword: Aggression; Attention
Link ID: 28674 - Posted: 02.18.2023

By Diana Kwon Alan Alda was running for his life. The actor, best known for his role on the television series M*A*S*H, wasn’t on a set. This threat was real—or at least it felt that way. So when he saw a bag of potatoes in front of him, he grabbed it and threw it at his attacker. Suddenly, the scene shifted. He was in his bedroom, having lurched out of sleep, and the sack of potatoes was a pillow he’d just chucked at his wife. Acting out dreams marks a disorder that occurs during the rapid eye movement (REM) phase of sleep. Called RBD, for REM sleep behavior disorder, it affects an estimated 0.5 to 1.25 percent of the general population and is more commonly reported in older adults, particularly men. Apart from being hazardous to dreamers and their partners, RBD may foreshadow neurodegenerative disease, primarily synucleinopathies—conditions in which the protein α-synuclein (or alpha-synuclein) forms toxic clumps in the brain. Not all nocturnal behaviors are RBD. Sleepwalking and sleep talking, which occur more often during childhood and adolescence, take place during non-REM sleep. This difference is clearly distinguishable in a sleep laboratory, where clinicians can monitor stages of sleep to see when a person moves. Nor is RBD always associated with a synucleinopathy: it can also be triggered by certain drugs such as antidepressants or caused by other underlying conditions such as narcolepsy or a brain stem tumor. When RBD occurs in the absence of these alternative explanations, the chance of future disease is high. Some epidemiological studies suggest that enacted dreaming predicts a more than 80 percent chance of developing a neurodegenerative disease within the patient’s lifetime. It may also be the first sign of neurodegenerative disease, which on average shows up within 10 to 15 years after onset of the dream disorder. One of the most common RBD-linked ailments is Parkinson’s disease, characterized mainly by progressive loss of motor control. Another is Lewy body dementia, in which small clusters of α-synuclein called Lewy bodies build up in the brain, disrupting movement and cognition. A third type of synucleinopathy, multiple system atrophy, interferes with both movement and involuntary functions such as digestion. RBD is one of the strongest harbingers of future synucleinopathy, more predictive than other early markers such as chronic constipation and a diminished sense of smell.

Keyword: Parkinsons; Sleep
Link ID: 28642 - Posted: 01.25.2023

ByMeredith Wadman A massive data mining study has found numerous associations between common viruses like the flu and devastating neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease, and amyotrophic lateral sclerosis (ALS, also known as Lou Gehrig’s disease). The findings expand on previous research linking individual viruses to neurological diseases. But experts caution that the study, which relied on electronic medical records rather than biological samples, merely describes correlations and doesn’t prove causation. Still, it’s “really exciting,” says Kristen Funk, a neuroimmunologist who studies Alzheimer’s at the University of North Carolina, Charlotte. Rather than homing in on, say, the relationship between herpes simplex infections and Alzheimer’s—a recent focus in her own field—“this research broadens that scope to look at different viruses and more neurodegenerative diseases.” Scientists have found connections between viruses and neurodegenerative diseases before. Previous studies uncovered ties between the influenza virus and Parkinson’s, for example, and between genital warts (caused by human papillomavirus) and dementia. A landmark project published in Science last year cemented another connection: Epidemiologists who analyzed 2 decades of data from the blood tests of 10 million U.S. soldiers reported that it’s nearly impossible to develop multiple sclerosis without first being infected with the Epstein-Barr virus—a ubiquitous pathogen long suspected of causing MS. Inspired by that paper, National Institutes of Health (NIH) researchers wondered whether they could mine other large databases to tease out more associations. They focused on viral links to six neurodegenerative diseases: Alzheimer’s, Parkinson’s, dementia, ALS, MS, and vascular dementia. (Some scientists dispute that MS and vascular dementia are neurodegenerative diseases.)

Keyword: Alzheimers; Parkinsons
Link ID: 28638 - Posted: 01.25.2023

By Tom Siegfried Survival of the fittest often means survival of the fastest. But fastest doesn’t necessarily mean the fastest moving. It might mean the fastest thinking. When faced with the approach of a powerful predator, for instance, a quick brain can be just as important as quick feet. After all, it is the brain that tells the feet what to do — when to move, in what direction, how fast and for how long. And various additional mental acrobatics are needed to evade an attacker and avoid being eaten. A would-be meal’s brain must decide whether to run or freeze, outrun or outwit, whether to keep going or find a place to hide. It also helps if the brain remembers where the best hiding spots are and recalls past encounters with similar predators. All in all, a complex network of brain circuitry must be engaged, and neural commands executed efficiently, to avert a predatory threat. And scientists have spent a lot of mental effort themselves trying to figure out how the brains of prey enact their successful escape strategies. Studies in animals as diverse as mice and crabs, fruit flies and cockroaches are discovering the complex neural activity — in both the primitive parts of the brain and in more cognitively advanced regions — that underlies the physical behavior guiding escape from danger and the search for safety. Lessons learned from such studies might not only illuminate the neurobiology of escape, but also provide insights into how evolution has shaped other brain-controlled behaviors. This research “highlights an aspect of neuroscience that is really gaining traction these days,” says Gina G. Turrigiano of Brandeis University, past president of the Society for Neuroscience. “And that is the idea of using ethological behaviors — behaviors that really matter for the biology of the animal that’s being studied — to unravel brain function.” © 2022 Annual Reviews

Keyword: Aggression; Attention
Link ID: 28609 - Posted: 12.24.2022

By Christina Jewett and Cade Metz A jumble of cords and two devices the size of soda cans protrude from Austin Beggin’s head when he undergoes testing with a team of researchers studying brain implants that are meant to restore function to those who are paralyzed. Despite the cumbersome equipment, it is also when Mr. Beggin feels the most free. He was paralyzed from the shoulders down after a diving accident eight years ago, and the brain device picks up the electrical surges that his brain generates as he envisions moving his arm. It converts those signals to cuffs on the major nerves in his arm. They allow him to do things he had not done on his own since the accident, like lift a pretzel to his mouth. “This is like the first time I’ve ever gotten the opportunity or I’ve ever been privileged and blessed enough to think, ‘When I want to open my hand, I open it,’” Mr. Beggin, 30, said. Days like that are always “a special day.” The work at the Cleveland Functional Electrical Stimulation Center represents some of the most cutting-age research in the brain-computer interface field, with the team connecting the brain to the arm to restore motion. It’s a field that Elon Musk wants to advance, announcing in a recent presentation that brain implants from his company Neuralink would someday help restore sight to the blind or return people like Mr. Beggin to “full-body functionality.” Mr. Musk also said the Neuralink device could allow anyone to use phones and other machines with new levels of speed and efficiency. Neuroscientists and Mr. Beggin alike see such giant advances as decades away, though. Scientists who have approval to test such devices in humans are inching toward restoring normal function in typing, speaking and limited movements. Researchers caution that the goal is much harder and more dangerous than it may seem. And they warn that Mr. Musk’s goals may never be possible — if it is even worth doing in the first place. © 2022 The New York Times Company

Keyword: Robotics
Link ID: 28591 - Posted: 12.13.2022

By Kevin Hartnett A mouse is running on a treadmill embedded in a virtual reality corridor. In its mind’s eye, it sees itself scurrying down a tunnel with a distinctive pattern of lights ahead. Through training, the mouse has learned that if it stops at the lights and holds that position for 1.5 seconds, it will receive a reward — a small drink of water. Then it can rush to another set of lights to receive another reward. This setup is the basis for research published in July in Cell Reports by the neuroscientists Elie Adam, Taylor Johns and Mriganka Sur of the Massachusetts Institute of Technology. It explores a simple question: How does the brain — in mice, humans and other mammals — work quickly enough to stop us on a dime? The new work reveals that the brain is not wired to transmit a sharp “stop” command in the most direct or intuitive way. Instead, it employs a more complicated signaling system based on principles of calculus. This arrangement may sound overly complicated, but it’s a surprisingly clever way to control behaviors that need to be more precise than the commands from the brain can be. Control over the simple mechanics of walking or running is fairly easy to describe: The mesencephalic locomotor region (MLR) of the brain sends signals to neurons in the spinal cord, which send inhibitory or excitatory impulses to motor neurons governing muscles in the leg: Stop. Go. Stop. Go. Each signal is a spike of electrical activity generated by the sets of neurons firing. The story gets more complex, however, when goals are introduced, such as when a tennis player wants to run to an exact spot on the court or a thirsty mouse eyes a refreshing prize in the distance. Biologists have understood for a long time that goals take shape in the brain’s cerebral cortex. How does the brain translate a goal (stop running there so you get a reward) into a precisely timed signal that tells the MLR to hit the brakes? Simons Foundation, All Rights Reserved © 2022

Keyword: Movement Disorders
Link ID: 28573 - Posted: 11.30.2022

By Sidney Perkowitz In 2019, Edward Chang, a neurosurgeon at the University of California, San Francisco, opened the skull of a 36-year-old man, nicknamed “Pancho,” and placed a thin sheet of electrodes on the surface of his brain.1 The electrodes gather electrical signals from the motor neurons that control the movement of the mouth, larynx, and other body parts to produce speech. A small port, implanted on top of Pancho’s head, relayed the brain signals to a computer. This “brain-computer interface,” or BCI, solved an intractable medical problem. In 2003, Pancho, a field worker in California’s vineyards, was involved in a car crash. Days after undergoing surgery, he suffered a brainstem stroke, reported the New York Times Magazine.2 The stroke robbed Poncho of the power of speech. He could communicate only by laboriously spelling out words one letter at a time with a pointing device. After training with the computer outfitted with deep-learning algorithms that interpreted his brain activity, Pancho could think the words that he wanted to say, and they would appear on the computer screen. Scientists called the results “groundbreaking”; Pancho called them “life-changing.” The clinical success of BCIs (there are other stories to go along with Pancho’s) appear to vindicate the futurists who claim that BCIs may soon enhance the brains of healthy people. Most famously, Ray Kurzweil, author of The Singularity Is Near, has asserted that exponentially rapid developments in neuroscience, bioscience, nanotechnology, and computation will coalesce and allow us to transcend the limitations of our bodies and brains. A major part of this huge shift will be the rise of artificial intelligences that are far more capable than human brains. It is an inevitability of human evolution, Kurzweil thinks, that the two kinds of intelligence will merge to form powerful hybrid brains, which will define the future of humanity. This, he predicted, would happen by 2045. While futuristic scenarios like Kurzweil’s are exciting to ponder, they are brought back down to Earth by the technological capabilities of brain-computer hybrids as they exist today. BCIs are impressive, but the path from helping stroke victims to giving people superpowers is neither direct nor inevitable. © 2022 NautilusThink Inc,

Keyword: Brain imaging; Robotics
Link ID: 28570 - Posted: 11.30.2022

By Elizabeth Preston Ryan Grant was in his 20s and serving in the military when he learned that the numbness and tingling in his hands and feet, as well as his unshakeable fatigue, were symptoms of multiple sclerosis. Like nearly a million other people with MS in the United States, Grant had been feeling his immune system attack his central nervous system. The insulation around his nerves was crumbling, weakening the signals between his brain and body. The disease can have a wide range of symptoms and outcomes. Now 43, Grant has lost the ability to walk, and he has moved into a veterans’ home in Oregon, so that his wife and children don’t have to be his caretakers. He’s all too familiar with the course of the illness and can name risk factors he did and didn’t share with other MS patients, three-quarters of whom are female. But until recently, he hadn’t heard that many scientists now believe the most important factor behind MS is a virus.  For decades, researchers suspected that Epstein-Barr virus, a common childhood infection, is linked to multiple sclerosis. In January, the journal Science pushed that connection into headlines when it published the results of a two-decade study of people who, like Grant, have served in the military. The study’s researchers concluded that EBV infection is “the leading cause” of MS.  Bruce Bebo, executive vice president of research at the nonprofit National Multiple Sclerosis Society, which helped fund the study, said he believes the findings fall just short of proving causation. They do, however, provide “probably the strongest evidence to date of that link between EBV and MS,” he said. Epstein-Barr virus has infected about 95 percent of adults. Yet only a tiny fraction of them will develop multiple sclerosis. Other factors are also known to affect a person’s MS risk, including genetics, low vitamin D, smoking, and childhood obesity. If this virus that infects nearly everyone on Earth causes multiple sclerosis, it does so in concert with other actors in a choreography that scientists don’t yet understand.

Keyword: Multiple Sclerosis; Neuroimmunology
Link ID: 28565 - Posted: 11.23.2022

Dyani Lewis Neuroscientists have identified the nerve cells responsible for helping paralysed people to walk again, opening up the possibility of targeted therapies that could benefit a wider range of people with spinal-cord injuries1. Severe spinal-cord injuries can disrupt the connection between the brain and the networks of nerve cells in the lower spine that control walking. In 2018, neuroscientist Grégoire Courtine at the Swiss Federal Institute of Technology in Lausanne and his colleagues showed that delivering electrical pulses to those lower-spine nerves — a technique known as epidural electrical stimulation (EES) — could, when combined with intensive training, get people with this kind of spinal-cord injury walking again2. All three participants in a trial went from having severe or complete motor paralysis and minimal sensation in their legs to being able to take steps on their own, or with a walker or crutches. Two other teams showed similar results that year3,4. Courtine’s team has now extended the work, showing that the system works in people who have lost all sensation in their legs. The group reports in Nature today that nine participants in the same trial — three of whom had complete paralysis and no sensation in their legs — regained the ability to walk after training paired with EES delivered by devices implanted in their spines. Five months into the trial, all participants could bear their own weight and take steps, using a walker for stability. Four no longer need the EES to be switched on to walk. This sustained recovery suggests that the stimulation triggers remodelling of the spinal neurons to bring the locomotion network back on line. “The amount of hope that it gives to people with spinal-cord injury is incredible,” says Marc Ruitenberg, a neurologist at the University of Queensland in Brisbane, Australia, who studies spinal-cord injury. © 2022 Springer Nature Limited

Keyword: Regeneration
Link ID: 28546 - Posted: 11.13.2022

Nina Lakhani The mystery behind the astronomical rise in neurological disorders like Parkinson’s disease and Alzheimer’s could be caused by exposure to environmental toxins that are omnipresent yet poorly understood, leading doctors warn. At a conference on Sunday, the country’s leading neurologists and neuroscientists will highlight recent research efforts to fill the gaping scientific hole in understanding of the role environmental toxins – air pollution, pesticides, microplastics, forever chemicals and more – play in increasingly common diseases like dementias and childhood developmental disorders. Humans may encounter a staggering 80,000 or more toxic chemicals as they work, play, sleep and learn – so many that it is almost impossible to determine their individual effects on a person, let alone how they may interact or the cumulative impacts on the nervous system over a lifespan. Some contact with environmental toxins is inevitable given the proliferation of plastics and chemical pollutants, as well as America’s hands off regulatory approach, but exposure is unequal. In the US, communities of color, Indigenous people and low income families are far more likely to be exposed to a myriad of pollutants through unsafe housing and water, manufacturing and agricultural jobs, and proximity to roads and polluting industrial plants, among other hazards. It’s likely genetic makeup plays a role in how susceptible people are to the pathological effects of different chemicals, but research has shown higher rates of cancers and respiratory disease in environmentally burdened communities. © 2022 Guardian News & Media Limited

Keyword: Alzheimers; Parkinsons
Link ID: 28526 - Posted: 10.26.2022