Chapter 5. The Sensorimotor System

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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

By Jack Tamisiea An elephant’s trunk has 40,000 muscles and weighs more than a Burmese python. The appendage is strong enough to uproot a tree, yet sensitive enough to suction up fragile tortilla chips. But how does an elephant’s brain help accomplish these feats of dexterity? That has been difficult to study, according to Michael Brecht, a neuroscientist at the Humboldt University of Berlin. Weighing in excess of 10 pounds, the elephant’s brain degrades quickly after death and is a hassle to store. “I tend to think that the big animals are a bit neglected because we don’t do enough work on big brains,” Dr. Brecht said. Dr. Brecht and his colleagues were fortunate enough to gain access to a trove of elephant brains from animals that had died of natural causes or were euthanized for health reasons and ended up either frozen or in a fixative substance at the Leibniz Institute for Zoo and Wildlife Research in Berlin. In a study published Wednesday in the journal Science Advances, Dr. Brecht and his colleagues reported that elephants had more facial neurons than any other land mammal, which might contribute to trunk dexterity and other anatomical abilities. The study also helped to pinpoint major differences between the neural wirings of African savanna elephants and Asian elephants. Using the brains of four Asian elephants and four African savanna elephants, the researchers homed in on the facial nucleus, a bundle of neurons concentrated in the brainstem and hooked up to facial nerves. In mammals, these neurons serve as the control center for facial muscles. They’re in command whenever you wrinkle your nose, purse your lips or raise your eyebrows. They also help elephants employ their trunks. The researchers divided the facial nucleus into regions of neurons that controlled the elephant’s ears, lips and trunk. African elephants sported 63,000 facial neurons, while their Asian cousins had 54,000. The only mammals with more are dolphins, which pack nearly 90,000 facial neurons into their sensitive snouts. While his team expected both African savanna and Asian elephants to possess massive stores of facial neurons, Dr. Brecht said the discrepancy between the two species was noteworthy. © 2022 The New York Times Company

Keyword: Evolution; Pain & Touch
Link ID: 28533 - Posted: 10.28.2022

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

by Carey Gillam and Aliya Uteuova For decades, Swiss chemical giant Syngenta has manufactured and marketed a widely used weed-killing chemical called paraquat, and for much of that time the company has been dealing with external concerns that long-term exposure to the chemical may be a cause of the incurable brain ailment known as Parkinson’s disease. Syngenta has repeatedly told customers and regulators that scientific research does not prove a connection between its weedkiller and the disease, insisting that the chemical does not readily cross the blood-brain barrier, and does not affect brain cells in ways that cause Parkinson’s. But a cache of internal corporate documents dating back to the 1950s reviewed by the Guardian suggests that the public narrative put forward by Syngenta and the corporate entities that preceded it has at times contradicted the company’s own research and knowledge. And though the documents reviewed do not show that Syngenta’s scientists and executives accepted and believed that paraquat can cause Parkinson’s, they do show a corporate focus on strategies to protect product sales, refute external scientific research and influence regulators. In one defensive tactic, the documents indicate that the company worked behind the scenes to try to keep a highly regarded scientist from sitting on an advisory panel for the US Environmental Protection Agency (EPA). The agency is the chief US regulator for paraquat and other pesticides. Company officials wanted to make sure the efforts could not be traced back to Syngenta, the documents show. And the documents show that insiders feared they could face legal liability for long-term, chronic effects of paraquat as long ago as 1975. One company scientist called the situation “a quite terrible problem” for which “some plan could be made … ”

Keyword: Parkinsons; Neurotoxins
Link ID: 28522 - Posted: 10.22.2022

By Diana Kwon A Scottish woman named Joy Milne made headlines in 2015 for an unusual talent: her ability to sniff out people afflicted with Parkinson’s disease, a progressive neurodegenerative illness that is estimated to affect nearly a million people in the U.S. alone. Since then a group of scientists in the U.K. has been working with Milne to pinpoint the molecules that give Parkinson’s its distinct olfactory signature. The team has now zeroed in on a set of molecules specific to the disease—and has created a simple skin-swab-based test to detect them. Milne, a 72-year-old retired nurse from Perth, Scotland, has hereditary hyperosmia, a condition that endows people with a hypersensitivity to smell. She discovered that she could sense Parkinson’s with her nose after noticing her late husband, Les, was emitting a musky odor that she had not detected before. Eventually, she linked this change in scent to Parkinson’s when he was diagnosed with the disease many years later. Les passed away in 2015. In 2012 Milne met Tilo Kunath, a neuroscientist at the University of Edinburgh in Scotland, at an event organized by the research and support charity Parkinson’s UK. Although skeptical at first, Kunath and his colleagues decided to put Milne’s claims to the test. They gave her 12 T-shirts, six from people with Parkinson’s and six from healthy individuals. She correctly identified the disease in all six cases—and the one T-shirt from a healthy person she categorized as having Parkinson’s belonged to someone who went on to be diagnosed with the disease less than a year later. Advertisement Subsequently, Kunath, along with chemist Perdita Barran of the University of Manchester in England and her colleagues, has been searching for the molecules responsible for the change in smell that Milne can detect. The researchers used mass spectrometry to identify types and quantities of molecules in a sample of sebum, an oily substance found on the skin’s surface. They discovered changes to fatty molecules known as lipids in people with Parkinson’s. © 2022 Scientific American

Keyword: Chemical Senses (Smell & Taste); Parkinsons
Link ID: 28510 - Posted: 10.13.2022

Ian Sample Science editor It was while watching University Challenge that the doctor first suspected something wrong with Jeremy Paxman. Normally highly animated, the TV presenter was less effusive and exuberant than usual. He had acquired what specialists in the field call the “Parkinson’s mask”. Paxman was formally diagnosed with Parkinson’s disease in hospital after he collapsed while walking his dog and found himself in hospital. There, Paxman recalled in an ITV documentary, the doctor walked in and said: “I think you’ve got Parkinson’s”. For Paxman, at least, the news came out of the blue. Parkinson’s was first described in medical texts more than 200 years ago, yet there is still no cure. It’s a common condition, particularly in the over-50s. About 1 in 37 people in the UK will be diagnosed at some point in their life. Existing drugs aim to manage patients’ symptoms, rather than slow down or stop the condition’s progression. But scientists have made progress in understanding the neurodegenerative disorder. The hope now is that gamechanging therapies are finally on the horizon. Advertisement “Parkinson’s is a hugely complex condition and there’s probably no single cure,” says Katherine Fletcher, a research communications manager at Parkinson’s UK. “It’s the progressive loss of dopamine-producing cells in the brain. If you want to slow or stop the condition, you somehow need to protect those cells or maybe even regrow those cells in the brain. That is the ultimate goal.” Why brain cells die off in Parkinson’s is still unknown. The condition strikes a brain region called the substantia nigra, where neurons make a chemical called dopamine. The loss of these brain cells causes dopamine to plunge, and this drives most of the problems patient’s experience. It is not a fast decline: typically, patients only become aware of symptoms when about 80% of nerve cells in the substantia nigra have failed. © 2022 Guardian News & Media Limited or its affiliated companies.

Keyword: Parkinsons
Link ID: 28507 - Posted: 10.08.2022

By Pam Belluck A new medication for A.L.S., the devastating neurological disorder that causes paralysis and death, will have a list price of $158,000 a year, its manufacturer disclosed Friday. The treatment, to be marketed as Relyvrio, is a combination of two existing drugs and will be available to patients in the United States in about four to six weeks, according to officials of the company, Amylyx Pharmaceuticals. Relyvrio was approved by the Food and Drug Administration on Thursday, even though the agency’s analysis 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. The F.D.A. decided to greenlight the drug instead of waiting until 2024 for results of a large clinical trial partly because the treatment is considered to be safe. The agency said that although the evidence of effectiveness was uncertain, “given the serious and life-threatening nature of A.L.S. and the substantial unmet need, this level of uncertainty is acceptable in this instance.” A.L.S., or amyotrophic lateral sclerosis — also called Lou Gehrig’s disease — often strikes patients in the prime of life and frequently causes death within two to five years. It is diagnosed in about 6,000 people worldwide each year, and Amylyx estimates that there are about 29,000 people living with the disease in the United States. Amylyx officials predicted that most patients would pay little or nothing for the treatment because the company expects insurers, both private and public, to cover it. Amylyx plans to provide it free to uninsured patients experiencing financial hardship. Still, the list price is much higher than that recommended by the Institute for Clinical and Economic Review, a nonprofit organization that evaluates the value of medicines. In a statement, the group’s chief medical officer, Dr. David Rind, said that while “there are clear benefits to patients with a rapidly fatal disease to have early access to a safe therapy,” his organization had concluded that “an annual price of $9,100 to $30,700 would be reasonable if the therapy actually works.” © 2022 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28495 - Posted: 10.01.2022

By Jim Robbins Tens of thousands of bar-tailed godwits are taking advantage of favorable winds this month and next for their annual migration from the mud flats and muskeg of southern Alaska, south across the vast expanse of the Pacific Ocean, to the beaches of New Zealand and eastern Australia. They are making their journey of more than 7,000 miles by flapping night and day, without stopping to eat, drink or rest. “The more I learn, the more amazing I find them,” said Theunis Piersma, a professor of global flyway ecology at the University of Groningen in the Netherlands and an expert in the endurance physiology of migratory birds. “They are a total evolutionary success.” The godwit’s epic flight — the longest nonstop migration of a land bird in the world — lasts from eight to 10 days and nights through pounding rain, high winds and other perils. It is so extreme, and so far beyond what researchers knew about long-distance bird migration, that it has required new investigations. In a recent paper, a group of researchers said the arduous journeys challenge “underlying assumptions of bird physiology, orientation, and behavior,” and listed 11 questions posed by such migrations. Dr. Piersma called the pursuit of answers to these questions “the new ornithology.” The extraordinary nature of what bar-tailed and other migrating birds accomplish has been revealed in the last 15 years or so with improvements to tracking technology, which has given researchers the ability to follow individual birds in real time and in a detailed way along the full length of their journey. “You know where a bird is almost to the meter, you know how high it is, you know what it’s doing, you know its wing-beat frequency,” Dr. Piersma said. “It’s opened a whole new world.” The known distance record for a godwit migration is 13,000 kilometers, or nearly 8,080 miles. © 2022 The New York Times Company

Keyword: Animal Migration; Sleep
Link ID: 28484 - Posted: 09.21.2022

By Jonathan Moens An artificial intelligence can decode words and sentences from brain activity with surprising — but still limited — accuracy. Using only a few seconds of brain activity data, the AI guesses what a person has heard. It lists the correct answer in its top 10 possibilities up to 73 percent of the time, researchers found in a preliminary study. The AI’s “performance was above what many people thought was possible at this stage,” says Giovanni Di Liberto, a computer scientist at Trinity College Dublin who was not involved in the research. Developed at the parent company of Facebook, Meta, the AI could eventually be used to help thousands of people around the world unable to communicate through speech, typing or gestures, researchers report August 25 at arXiv.org. That includes many patients in minimally conscious, locked-in or “vegetative states” — what’s now generally known as unresponsive wakefulness syndrome (SN: 2/8/19). Most existing technologies to help such patients communicate require risky brain surgeries to implant electrodes. This new approach “could provide a viable path to help patients with communication deficits … without the use of invasive methods,” says neuroscientist Jean-Rémi King, a Meta AI researcher currently at the École Normale Supérieure in Paris. King and his colleagues trained a computational tool to detect words and sentences on 56,000 hours of speech recordings from 53 languages. The tool, also known as a language model, learned how to recognize specific features of language both at a fine-grained level — think letters or syllables — and at a broader level, such as a word or sentence. © Society for Science & the Public 2000–2022.

Keyword: Language; Robotics
Link ID: 28470 - Posted: 09.10.2022

By Laurie McGinley Independent advisers to the Food and Drug Administration on Wednesday voted 7 to 2 to recommend approval of an experimental ALS drug with strong support from patients and advocates, making it likely the hotly debated treatment will be cleared by the agency within weeks. The vote was a stunning turnaround from late March when the panel voted 6 to 4 to recommend against FDA approval. At that meeting, the FDA’s Peripheral and Central Nervous System Drugs Advisory Committee concluded the evidence from a single clinical trial — with just 137 patients and some follow-up data — was not sufficient to show the drug, called AMX0035, slowed a degenerative disease that usually kills people within three to five years. But on Wednesday, after hours of discussion, several advisers said that additional analyses submitted by the drug’s manufacturer, Cambridge-based Amylyx, bolstered the case for approval, even though uncertainties remain. Advisers were also affected by the disease’s severity and the lack of effective treatments. A vow by a top Amylyx official to pull the drug from the market if a larger study, with 600 patients, fails to show effectiveness was also a factor in the vote. The FDA, which usually follows the recommendation of its outside advisers but is not required to, is expected to decide whether to approve the drug by Sept. 29. The improved fortunes of the medicine came despite criticism from FDA staff as recently as last week about the treatment’s effectiveness, the conduct of its clinical trial and the researchers’ interpretation of the data. But the medicine is considered safe, and the agency has been under intense pressure from ALS patients and physicians who say the treatment holds promise for a fatal disease that typically causes rapid deterioration and death.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28467 - Posted: 09.10.2022

Researchers have published two papers describing how they identified a potential new pathway for treating a sporadic form of amyotrophic lateral sclerosis (ALS). The studies were published as part of a cooperative research agreement between the National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health, and the Switzerland-based biotechnology company GeNeuro Inc. One unusual side effect of hundreds of thousands of years of evolution is that the human genome now contains DNA sequences from ancient retroviruses—referred to as human endogenous retroviruses (HERVs). Though most remain dormant, reactivation of HERVs have been implicated in several neurodegenerative diseases, including ALS. The first of these papers shows that a specific HERV produces a protein that can be found in the cerebrospinal fluid (CSF) of people with ALS. This protein, called HERV-K ENV, is toxic when added to neurons grown in laboratory dishes. In addition, a special kind of mouse genetically designed to create HERV-K ENV develops symptoms very similar to ALS. Adding the CSF from people with ALS to lab-grown neurons resulted in damage to the cells. When a synthetic antibody designed specifically to recognize HERV-K ENV was added as well to those neurons, the toxic effects were reduced. These findings together suggest that the improper activation of the HERV-K ENV gene could be the cause of the symptoms seen in certain cases of sporadic ALS. The discovery that a synthetic antibody to HERV-K ENV could be protective led the researchers to look at whether the immune system of people with ALS produced any antibodies, as well. In the second paper, the authors show that indeed higher levels of antibodies against HERV-K ENV were seen in the blood of a group of people with ALS as compared to healthy donors. The pattern of antibodies against this viral protein was also more complex in persons with ALS. In addition, there was also a correlation between higher antibody levels against HERV-K ENV and longer overall survival.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 28455 - Posted: 08.31.2022

By Anil Oza Sitting alone in the cockpit of a small biplane, Martin Wikelski listens for the pings of a machine by his side. The sonic beacons help the ecologist stalk death’s-head hawkmoths (Acherontia atropos) fluttering across the dark skies above Konstanz, Germany — about 80 kilometers north of the Swiss Alps. The moths, nicknamed for the skull-and-crossbones pattern on their backs, migrate thousands of kilometers between northern Africa and the Alps during the spring and fall. Many migratory insects go where the wind takes them, says Ring Carde, an entomologist at the University of California, Riverside who is not a member of Wikelski’s team. Death’s-head hawkmoths appear to be anything but typical. “When I follow them with a plane, I use very little gas,” says Wikelski, of the Max Planck Institute of Animal Behavior in Munich. “That shows me that they are supposedly choosing directions or areas that are probably supported by a little bit of updraft.” A new analysis of data collected from 14 death’s-head hawkmoths suggest that these insects indeed pilot themselves, possibly relying in part on an internal compass attuned to Earth’s magnetic field. The moths not only fly along a straight path, they also stay the course even when winds change, Wikelski and colleagues report August 11 in Science. The findings could help predict how the moths’ flight paths might shift as the globe continues warming, Wikelski says. Like many animals, death’s-head hawkmoths will probably move north in search of cooler temperatures, he suspects. To keep tabs on the moths, Wikelski’s team glued radio transmitters to their backs, which is easier to do than one might expect. “Death’s-head hawkmoths are totally cool,” Wikelski says. They’re also huge. Weighing as much as three jellybeans, the moths are the largest in Europe. That makes attaching the tiny tags a cinch, though the moths don’t like it very much. “They talk to you, they shout at you a little bit,” he says. © Society for Science & the Public 2000–2022.

Keyword: Animal Migration
Link ID: 28451 - Posted: 08.27.2022

By Betsy Mason 08.05.2022 What is special about humans that sets us apart from other animals? Less than some of us would like to believe. As scientists peer more deeply into the lives of other animals, they’re finding that our fellow creatures are far more emotionally, socially, and cognitively complex than we typically give them credit for. A deluge of innovative research is revealing that behavior we would call intelligent if humans did it can be found in virtually every corner of the animal kingdom. Already this year scientists have shown that Goffin’s cockatoos can use multiple tools at once to solve a problem, Australian Magpies will cooperate to remove tracking devices harnessed to them by scientists, and a small brown songbird can sometimes keep time better than the average professional musician — and that’s just among birds. This pileup of fascinating findings may be at least partly responsible for an increase in people’s interest in the lives of other animals — a trend that’s reflected in an apparent uptick in books and television shows on the topic, as well as in legislation concerning other species. Public sentiment in part pushed the National Institutes of Health to stop supporting biomedical research on chimpanzees in 2015. In Canada, an outcry led to a ban in 2019 on keeping cetaceans like dolphins and orcas in captivity. And earlier this year, the United Kingdom passed an animal welfare bill that officially recognizes that many animals are sentient beings capable of suffering, including invertebrates like octopuses and lobsters. Many of these efforts are motivated by human empathy for animals we’ve come to see as intelligent, feeling beings like us, such as chimpanzees and dolphins. But how can we extend that concern to the millions of other species that share the planet with us?

Keyword: Vision; Hearing
Link ID: 28447 - Posted: 08.27.2022