Chapter 11. Motor Control and Plasticity

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Links 1 - 20 of 1940

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

Keyword: Evolution
Link ID: 29194 - Posted: 03.16.2024

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

Keyword: Vision
Link ID: 29153 - Posted: 02.20.2024

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

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

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

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

By Ben Guarino Billionaire technologist Elon Musk announced this week that his company Neuralink has implanted its brain-computer interface into a human for the first time. The recipient was “recovering well,” Musk wrote on his social media platform X (formerly Twitter) on Monday evening, adding that initial results showed “promising neuron spike detection”—a reference to brain cells’ electrical activity. Each wireless Neuralink device contains a chip and electrode arrays of more than 1,000 superthin, flexible conductors that a surgical robot threads into the cerebral cortex. There the electrodes are designed to register thoughts related to motion. In Musk’s vision, an app will eventually translate these signals to move a cursor or produce text—in short, it will enable computer control by thinking. “Imagine if Stephen Hawking could communicate faster than a speed typist or auctioneer. That is the goal,” Musk wrote of the first Neuralink product, which he said is named Telepathy. The U.S. Food and Drug Administration had approved human clinical trials for Neuralink in May 2023. And last September the company announced it was opening enrollment in its first study to people with quadriplegia. Monday’s announcement did not take neuroscientists by surprise. Musk, the world’s richest man, “said he was going to do it,” says John Donoghue, an expert in brain-computer interfaces at Brown University. “He had done the preliminary work, built on the shoulders of others, including what we did starting in the early 2000s.” Neuralink’s original ambitions, which Musk outlined when he founded the company in 2016, included meshing human brains with artificial intelligence. Its more immediate aims seem in line with the neural keyboards and other devices that people with paralysis already use to operate computers. The methods and speed with which Neuralink pursued those goals, however, have resulted in federal investigations into dead study animals and the transportation of hazardous material. © 2024 SCIENTIFIC AMERICAN

Keyword: Robotics
Link ID: 29124 - Posted: 01.31.2024

By Ben Guarino Billionaire technologist Elon Musk announced this week that his company Neuralink has implanted its brain-computer interface into a human for the first time. The recipient was “recovering well,” Musk wrote on his social media platform X (formerly Twitter) on Monday evening, adding that initial results showed “promising neuron spike detection”—a reference to brain cells’ electrical activity. Each wireless Neuralink device contains a chip and electrode arrays of more than 1,000 superthin, flexible conductors that a surgical robot threads into the cerebral cortex. There the electrodes are designed to register thoughts related to motion. In Musk’s vision, an app will eventually translate these signals to move a cursor or produce text—in short, it will enable computer control by thinking. “Imagine if Stephen Hawking could communicate faster than a speed typist or auctioneer. That is the goal,” Musk wrote of the first Neuralink product, which he said is named Telepathy. The U.S. Food and Drug Administration had approved human clinical trials for Neuralink in May 2023. And last September the company announced it was opening enrollment in its first study to people with quadriplegia. Monday’s announcement did not take neuroscientists by surprise. Musk, the world’s richest man, “said he was going to do it,” says John Donoghue, an expert in brain-computer interfaces at Brown University. “He had done the preliminary work, built on the shoulders of others, including what we did starting in the early 2000s.” Neuralink’s original ambitions, which Musk outlined when he founded the company in 2016, included meshing human brains with artificial intelligence. Its more immediate aims seem in line with the neural keyboards and other devices that people with paralysis already use to operate computers. The methods and speed with which Neuralink pursued those goals, however, have resulted in federal investigations into dead study animals and the transportation of hazardous material. © 2024 SCIENTIFIC AMERICAN

Keyword: Robotics
Link ID: 29123 - Posted: 01.31.2024

James O’Brien for Quanta Magazine In recent decades, neuroscience has seen some stunning advances, and yet a critical part of the brain remains a mystery. I am referring to the cerebellum, so named for the Latin for “little brain,” which is situated like a bun at the back of the brain. This is no small oversight: The cerebellum contains three-quarters of all the brain’s neurons, which are organized in an almost crystalline arrangement, in contrast to the tangled thicket of neurons found elsewhere. Encyclopedia articles and textbooks underscore the fact that the cerebellum’s function is to control body movement. There is no question that the cerebellum has this function. But scientists now suspect that this long-standing view is myopic. Or so I learned in November in Washington, D.C., while attending the Society for Neuroscience annual meeting, the largest meeting of neuroscientists in the world. There, a pair of neuroscientists organized a symposium on newly discovered functions of the cerebellum unrelated to motor control. New experimental techniques are showing that in addition to controlling movement, the cerebellum regulates complex behaviors, social interactions, aggression, working memory, learning, emotion and more. The connection between the cerebellum and movement has been known since the 19th century. Patients suffering trauma to the brain region had obvious difficulties with balance and movement, leaving no doubt that it was critical for coordinating motion. Over the decades, neuroscientists developed a detailed understanding of how the cerebellum’s unique neural circuitry controls motor function. The explanation of how the cerebellum worked seemed watertight. Then, in 1998, in the journal Brain, neurologists reported on wide-ranging emotional and cognitive disabilities in patients with damage to the cerebellum. For example, in 1991, a 22-year-old female college student had fallen while ice skating; a CT scan revealed a tumor in her cerebellum. After it was removed surgically, she was a completely different person. The bright college student had lost her ability to write with proficiency, do mental arithmetic, name common objects or copy a simple diagram. Her mood flattened. She hid under covers and behaved inappropriately, undressing in the corridors and speaking in baby talk. Her social interactions, including recognizing familiar faces, were also impaired.

Keyword: Emotions; Movement Disorders
Link ID: 29118 - Posted: 01.27.2024

By David Levin It can start small: a peculiar numbness; a subtle facial tic; an inexplicably stiff muscle. But then time goes by — and eventually, the tremors set in. Roughly a million people in the United States (and roughly 10 million people worldwide) live with Parkinson’s disease, a potent neurological disorder that progressively kills neurons in the brain. As it does so, it can trigger a host of crippling symptoms, from violent tremors to excruciating muscle cramps, terrifying nightmares and constant brain fog. While medical treatments can alleviate some of these effects, researchers still don’t know exactly what causes the disease to occur in the first place. A growing number of studies, however, are suggesting that it may be tied to an unlikely culprit: bacteria living inside our guts. Every one of us has hundreds or thousands of microbial species in our stomach, small intestine and colon. These bacteria, collectively called our gut microbiome, are usually considerate guests: Although they survive largely on food that passes through our insides, they also give back, cranking out essential nutrients like niacin (which helps our body convert food into energy) and breaking down otherwise indigestible plant fiber into substances our bodies can use. As Parkinson’s advances in the brain, researchers have reported that the species of bacteria present in the gut also shift dramatically, hinting at a possible cause for the disease. A 2022 paper published in the journal Nature Communications recorded those differences in detail. After sequencing the mixed-together genomes of fecal bacteria from 724 people — a group with Parkinson’s and another without — the authors saw a number of distinct changes in the guts of people who suffered from the disease. The Parkinson’s group had dramatically lower amounts of certain species of Prevotella, a type of bacterium that helps the body break down plant-based fiber (changes like this in gut flora could explain why people with Parkinson’s disease often experience constipation). At the same time, the study found, two harmful species of Enterobacteriaceae, a family of microbes that includes Salmonella, E. coli and other bugs, proliferated. Those bacteria may be involved in a chain of biochemical events that eventually kill brain cells in Parkinson’s patients, says Tim Sampson, a biologist at Emory University School of Medicine and coauthor of the study.

Keyword: Parkinsons
Link ID: 29098 - Posted: 01.13.2024

By Mark MacNamara The notion of boxing as the “sweet science” is often thought to have been coined in 1956 by the great New Yorker writer A.J. Liebling. He used the term as the title of his definitive book on the sport, but he took it—with much appreciation—from a British sportswriter, Pierce Egan. In 1813, Egan wrote about the “sweet science of bruising” in his master work, Boxiana. The book is a collection of magazine pieces set in a bloody, bare-knuckled world opposite Jane Austen’s. As for the “sweet science,” no one ever really defines it. A carefully thrown knockout punch to a sweet spot on the chin is one possible derivation. There’s also the play on a science with so little apparent sweetness. But that’s not it. The sweet science Liebling and Egan describe had more to do with British principles of “stoic virtues,” “generosity,” and “true courage”—altogether, life in a contradictory place. It’s a square ring, after all, where sometimes hope transcends the specter of an awful inevitability. Or so I’ve come to think, on a journey I’ve begun in the past year, exploring how the sweet science can be used as a treatment for Parkinson’s disease—that increasingly common degenerative disorder of the nervous system, tied to a loss of the brain chemical dopamine, which is involved in movement, memory, motivation, and cognition. Someone told her she moved like a wavy wind sock outside a used car lot. “Exactly how I feel,” she said. In October 2022, a longtime tennis partner noticed something “strange” in my stride, along with a noisy shuffle. “Fatigue,” I replied with pique. The truth is I’m 75 and had known something might not be right for years, particularly the ominous hand tremors, as well as the night-of-the-living-dead gait and a facial expression to match. Add severe anxiety in public places and bizarre nightmares, some quite disturbing. © 2023 NautilusNext Inc.,

Keyword: Parkinsons
Link ID: 29055 - Posted: 12.19.2023

By Esther Landhuis Dropping an ice crystal into a bottle of near-frozen water produces a dramatic effect: very quickly, the liquid crystallizes into a block of ice. At the molecular level, an ice crystal has a distinct shape—a lattice structure. As incoming water molecules reshape to join the lattice, the crystal grows. Some researchers think an analogous process underlies Alzheimer’s disease, Parkinson’s disease and other neurodegenerative illnesses. According to this theory, these diseases begin when a particular protein misfolds, or fails to assume the proper shape for its intended role. That misshapen molecule ensnares normal versions of the protein, causing them to similarly misfold, and over time, these rogue proteins clump into toxic clusters that spread through the brain. In mad cow disease—a brain disorder in cattle that can spread to people who eat meat from ill animals —the toxic proteins, called prions, ravage the mind quickly, leading to dementia and death within months. Prion diseases are rare. About 350 cases of the most common type, Creutzfeldt-Jakob disease, are reported each year in the U.S. By comparison, each year, nearly 500,000 people in the U.S. are diagnosed with Alzheimer’s, which develops more gradually. Plaques made up of abnormal beta-amyloid proteins can accumulate in the brain for years or even decades before a person notices signs of mental decline. While the time lines for toxicity differ, “the mechanism of misfolding is the same,” says Mathias Jucker, a neuroscientist at the Hertie Institute for Clinical Brain Research at the University of Tübingen in Germany. Just as all of the water in a bottle freezes after a “‘misfolded’ water molecule” slips into the vessel, if “you have one misfolded protein, all the other ones will take the same shape.” The idea that many diseases could arise from a common prionlike process raises an intriguing and troubling question: Under certain circumstances, could neurodegenerative disorders be transmitted from person to person? © 2023 SCIENTIFIC AMERICAN,

Keyword: Alzheimers; Prions
Link ID: 29032 - Posted: 12.06.2023

By Sandra G. Boodman The first sign of trouble was difficulty reading. In late 2014 Cathy A. Haft, a New York real estate broker who divides her time between Brooklyn and Long Island, thought she needed new glasses. But an eye exam found that her prescription was largely unchanged. Bladder problems came next, followed by impaired balance, intermittent dizziness and unexplained falls. By 2018 Haft, unable to show properties because she was too unsteady on her feet, was forced to retire. For the next four years specialists evaluated her for neuromuscular and balance-related ear problems in an attempt to explain her worsening condition, which came to include cognitive changes her husband feared was Alzheimer’s disease. In August 2022 Haft, by then dependent on a walker, consulted a Manhattan neurosurgeon. After observing her gait and reviewing images from a recent brain scan, he sent her to a colleague. Less than eight weeks later Haft underwent brain surgery for a condition that is frequently unrecognized or misdiagnosed. The operation succeeded in restoring skills that had gradually slipped away, stunting Haft’s life. “It’s pretty astonishing that this disorder is not that uncommon and no one put the pieces together,” she said. In her case a confluence of confounding symptoms, a complex medical history and the possible failure to take a holistic approach may have led doctors to overlook a condition that can sometimes be reversed — with dramatic results.

Keyword: Movement Disorders; Alzheimers
Link ID: 29020 - Posted: 11.26.2023

By Tina Hesman Saey WASHINGTON — Scientists have uncovered a clue about why it takes so long for Huntington’s disease to develop. And they may have a lead on how to stop the fatal brain disease. Huntington’s is caused by a mistakenly repeated bit of a gene called HTT. Until recently, researchers thought the number of repeats a person is born with doesn’t change, though repeats may expand when passed to future generations. But in some brain cells, the repeats can grow over time to hundreds of copies, geneticist Bob Handsaker reported November 2 at the annual meeting of the American Society of Human Genetics. Once the number of repeats passes a certain point, the activity of thousands of other genes in the brain cells changes drastically, leading the cells to die. These findings suggest that adding repeats to the HTT gene in vulnerable brain cells is what is driving Huntington’s disease, says Handsaker, of the Broad Institute of MIT and Harvard in Cambridge, Mass. The research also suggests that preventing the repeats from growing may stop the development of the disease. The new work gives “serious insight into the disease mechanism,” says Russell Snell, a geneticist at the University of Auckland in New Zealand who was not involved in the work. About 41,000 people in the United States have symptomatic Huntington’s disease, and another 200,000 are at risk of developing it. Inheriting just one copy of a repeat-riddled HTT gene produces symptoms. Even though individuals are born with the disease-causing gene, symptoms don’t usually appear until people are in their 30s to 50s. Those symptoms include depression, mood swings, forgetfulness, balance problems, involuntary movements and slurred speech. Eventually, a person with the disease may be paralyzed and can die from complications such as pneumonia or heart failure. © Society for Science & the Public 2000–2023.

Keyword: Huntingtons
Link ID: 29008 - Posted: 11.15.2023

Liam Drew In a laboratory in San Francisco, California, a woman named Ann sits in front of a huge screen. On it is an avatar created to look like her. Thanks to a brain–computer interface (BCI), when Ann thinks of talking, the avatar speaks for her — and in her own voice, too. In 2005, a brainstem stroke left Ann almost completely paralysed and unable to speak. Last year, neurosurgeon Edward Chang, at the University of California, San Francisco, placed a grid of more than 250 electrodes on the surface of Ann’s brain, on top of the regions that once controlled her body, face and larynx. As Ann imagined speaking certain words, researchers recorded her neural activity. Then, using machine learning, they established the activity patterns corresponding to each word and to the facial movements Ann would, if she could, use to vocalize them. The system can convert speech to text at 78 words per minute: a huge improvement on previous BCI efforts and now approaching the 150 words per minute considered average for regular speech1. Compared with two years ago, Chang says, “it’s like night and day”. In an added feat, the team programmed the avatar to speak aloud in Ann’s voice, basing the output on a recording of a speech she made at her wedding. “It was extremely emotional for Ann because it was the first time that she really felt that she was speaking for almost 20 years,” says Chang. This work was one of several studies in 2023 that boosted excitement about implantable BCIs. Another study2 also translated neural activity into text at unprecedented speed. And in May, scientists reported that they had created a digital bridge between the brain and spinal cord of a man paralysed in a cycling accident3. A BCI decoded his intentions to move and directed a spinal implant to stimulate the nerves of his legs, allowing him to walk. © 2023 Springer Nature Limited

Keyword: Brain imaging; Language
Link ID: 28997 - Posted: 11.11.2023