Chapter 11. Motor Control and Plasticity

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By Bob Grant Prosthetic limbs are rejected by amputees’ bodies at a rate of about 20 percent. Researchers at MIT are seeking to reduce that number, using an amputation procedure that encourages increased feedback between muscles, tendons, and the nervous system so that an artificial limb might stimulate them in a more natural way—giving patients a better sense of proprioception, or where their limb is in space. The key to the surgical technique, demonstrated in rats so far, is to emulate the normal agonist-antagonist pairing of muscles (think biceps and triceps) at the amputation site so that the muscles and nerves surrounding a prosthetic can sense and transmit proprioceptive information about the artificial limb and how much force is being applied to it. The researchers published their work today (May 31) in Science Robotics. “We’re talking about a dramatic improvement in patient care,” Hugh Herr, an MIT professor of media arts and sciences and a coauthor of the study, said in a statement. “Right now there’s no robust neural method for a person with limb amputation to feel proprioceptive positions and forces applied to the prosthesis. Imagine how that would completely hinder one’s ability to move, to successfully balance, or to manipulate objects.” Herr, himself a double-amputee, and his team operated on seven rats, cutting through muscles and nerves in their hind legs. The researchers then grafted on paired muscles, wiring them up to severed nerves. After healing for four months, the rats’ new muscles were contracting and relaxing in tandem, as in naturally paired muscles, and sending electrical signals that reflected the amplitude of the artificial stimulation Herr and his colleagues applied. © 1986-2017 The Scientist

Keyword: Movement Disorders
Link ID: 23693 - Posted: 06.02.2017

By JANE E. BRODY A neighbor of mine was recently told he has a devastating neurological disorder that is usually fatal within a few years of diagnosis. Though a new drug was recently approved for the illness, treatments may only slow progression of the disease for a time or extend life for maybe two or three months. He is a man of about 60 I’ve long considered the quintessential Mr. Fix-it, able to repair everything from bicycles to bathtubs. Now he is facing amyotrophic lateral sclerosis, or Lou Gehrig’s disease — a disease that no one yet knows how to fix. I can only imagine what he is going through because he does not want to talk about it. However, many others similarly afflicted have openly addressed the challenges they faced, though it is usually up to friends and family to express them and advocate for more and better research and public understanding. A.L.S. attacks the nerve cells in the brain and spinal cord that control voluntary muscle movements, like chewing, walking, breathing, swallowing and talking. It is invariably progressive. Lacking nervous system stimulation, the muscles soon begin to weaken, twitch and waste away until individuals can no longer speak, eat, move or even breathe on their own. Last year, the Centers for Disease Control and Prevention estimated that between 14,000 and 15,000 Americans have A.L.S., which makes it sound like a rare disease, but only because life expectancy is so short. A.L.S. occurs throughout the world, and it is probably far more common than generally thought. Over the course of a lifetime, one person in about 400 is likely to develop it, a risk not unlike that of multiple sclerosis. But with the rare exception of an outlier like the brilliant physicist Stephen Hawking, who has had A.L.S. for more than 50 years, it usually kills so quickly that many people do not know anyone living with this disease. Only one person in 10 with A.L.S. is likely to live for a decade or longer. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23675 - Posted: 05.29.2017

Susan Milius A question flamingo researchers get asked all the time — why the birds stand on one leg — may need rethinking. The bigger puzzle may be why flamingos bother standing on two. Balance aids built into the birds’ basic anatomy allow for a one-legged stance that demands little muscular effort, tests find. This stance is so exquisitely stable that a bird sways less to keep itself upright when it appears to be dozing than when it’s alert with eyes open, two Atlanta neuromechanists report May 24 in Biology Letters. “Most of us aren’t aware that we’re moving around all the time,” says Lena Ting of Emory University, who measures what’s called postural sway in standing people as well as in animals. Just keeping the human body vertical demands constant sensing and muscular correction for wavering. Even standing robots “are expending quite a bit of energy,” she says. That could have been the case for flamingos, she points out, since effort isn’t always visible. Translate that improbably long flamingo leg into human terms, and the visible part of the leg would be just the shin down. A flamingo’s hip and knee lie inside the bird’s body. Ting and Young-Hui Chang of the Georgia Institute of Technology tested balance in fluffy young Chilean flamingos coaxed onto a platform attached to an instrument that measures how much they sway. Keepers at Zoo Atlanta hand-rearing the test subjects let researchers visit after feeding time in hopes of catching youngsters inclined toward a nap — on one leg on a machine. “Patience,” Ting says, was the key to any success in this experiment. |© Society for Science & the Public 2000 - 2017

Keyword: Sleep
Link ID: 23656 - Posted: 05.24.2017

By LISA SANDERS, M.D. The woman woke to the sound of her 57-year-old husband sobbing. They’d been married for 30 years, and she had never heard him cry before. “I hurt so much,” he wailed. “I have to go back to the hospital.” The symptoms started two weeks earlier. One afternoon, coming home from his job as a carpenter, he felt hot and tired. He shook with shivers even though the day was warm. He drank a cup of tea and went to bed. The next day he felt fine, until the end of the day, when he felt overwhelmed by the heat and chills again. The day after that was the same. When he woke one morning and saw that his body was covered with pale pink dots — his arms, his face, his chest and thighs — he started to worry. His wife took him to the Griffin Hospital emergency room in Derby, Conn. The first doctor who saw him thought he probably had Lyme disease. Summer had just started, and he’d already seen a lot of cases. He sent the patient home with an antibiotic and steroid pills for the rash. The man took the medications but didn’t get any better. Soon everything started to hurt. His muscles, his joints and his back felt as if he’d been beaten. He dragged himself back to the E.R. He was given pain pills. A few days later, he went to the E.R. a third time and was given more pain meds. After waking up crying, he went yet again, and this time, the doctors admitted him. By then the patient had had several blood tests, which showed no sign of Lyme or other tick-borne diseases. A CT scan was equally uninformative. The next day, the man was walking to the bathroom when his legs gave out and he fell down. The doctor in charge of his care came and examined him once again. The man looked fit and healthy, despite the now-bright-red rash, but his legs were extremely weak. If the doctor applied even light pressure to the raised leg, it sagged back down to the bed. And his feet felt numb. He had a sensation of tingling in his hands, as if they had gone to sleep. That was how the weakness and numbness in his legs started, he told the doctor. And the next day, his hands were so weak he had to use both just to drink a cup of water. © 2017 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 23644 - Posted: 05.22.2017

By: Ted Dinan, M.D., Ph.D, and John F. Cryan, Ph.D. O ver the past few years, the gut microbiota has been implicated in developmental disorders such as schizophrenia and autism, neurodegenerative disorders such as Alzheimer’s disease and Parkinson’s disease, mood disorders such as depression, and even addiction disorders. It now seems strange that for so many decades we viewed the gut microbiota as bacteria that did us no harm but were of little benefit. This erroneous view has been radically transformed into the belief that the gut microbiota is, in effect, a virtual organ of immense importance. What we’ve learned is that what is commonly referred to as “the brain-gut-microbiota axis” is a bidirectional system that enables gut microbes to communicate with the brain and the brain to communicate back to the gut. It may be hard to believe that the microbes in the gut collectively weigh around three pounds—the approximate weight of the adult human brain—and contain ten times the number of cells in our bodies and over 100 times as many genes as our genome. 1 If the essential microbial genes were to be incorporated into our genomes, it is likely that our cells would not be large enough for the extra DNA. Many of those genes in our microbiota are important for brain development and function; they enable gut bacteria to synthesize numerous neurotransmitters and neuromodulators such as γ-aminobutyric acid (GABA), serotonin, dopamine, and short-chain fatty acids. While some of these compounds act locally in the gut, many products of the microbiota are transported widely and are necessary for the proper functioning of diverse organs. This is a two-way interaction: gut microbes are dependent on us for their nourishment. Any pathological process that reduces or increases food intake has implications for our microbes. © 2017 The Dana Foundation. All Rights Reserved.

Keyword: Parkinsons
Link ID: 23636 - Posted: 05.19.2017

By DENISE GRADY A new drug for amyotrophic lateral sclerosis, or Lou Gehrig’s disease, was approved on Friday by the Food and Drug Administration. The drug, called Radicava or edaravone, slowed the progression of the degenerative disease in a six-month study in Japan. It must be given by intravenous infusion and will cost $145,524 a year, according to its manufacturer, MT Pharma America, a subsidiary of the Japanese company Mitsubishi Tanabe Pharma Corporation. Radicava is only the second drug ever approved to treat A.L.S. The first, riluzole, was approved by the F.D.A. more than 20 years ago. Riluzole can increase survival by two or three months. There is no information yet about whether Radicava has any effect on survival. In the study in Japan, 137 patients were picked at random to receive either Radicava or a placebo. At the end of six months, the condition of those taking the drug declined less than those receiving placebos. Dr. Neil A. Shneider, director of the Eleanor and Lou Gehrig ALS Center at Columbia University Medical Center, said, “The effect is modest but significant.” He added, “I’m very happy, frankly, that there is a second drug approved for A.L.S.” The disease kills nerve cells that control voluntary muscles, so patients gradually weaken and become paralyzed. Most die within three to five years, usually from respiratory failure. About 12,000 to 15,000 people in the United States have A.L.S., according to the Centers for Disease Control and Prevention. Dr. Shneider predicted that patients would be eager to try the new drug. He said several of his patients were already receiving it because they had obtained it themselves from Japan. If more want it, he will prescribe it, he said. “It’s very safe,” he said. But he was uncertain about whether he would actually recommend it, because the method of administration is difficult. Patients have to have an intravenous line inserted and left in place indefinitely, which poses an infection risk. The first round of treatment requires a one-hour infusion every day for 14 days, followed by 14 days off. After that, the infusions are given daily for 10 out of 14 days, with 14 days off. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease ; Trophic Factors
Link ID: 23585 - Posted: 05.06.2017

By Andy Coghlan Using a virus to reprogram cells in the brain could be a radical way to treat Parkinson’s disease. People with Parkinson’s have difficulty controlling their movements due to the death of neurons that make dopamine, a brain signalling chemical. Transplants of fetal cells have shown promise for replacing these dead neurons in people with the disease, and a trial is currently under way. But the transplant tissue comes from aborted pregnancies, meaning it is in short supply, and some people may find this ethically difficult. Recipients of these cells have to take immunosuppressant drugs too. Ernest Arenas, at the Karolinska Institute in Stockholm, Sweden, and his team have found a new way to replace lost dopamine-making neurons. They injected a virus into the brains of mice whose dopamine neurons had been destroyed. This virus had been engineered to carry four genes for reprogramming astrocytes – the brain’s support cells – into dopamine neurons. Five weeks later, the team saw improvements in how the mice moved. “They walked better and their gait showed less asymmetry than controls,” says Arenas. This is the first study to show that reprogramming cells in the living brain can lead to such improvements, he says. © Copyright Reed Business Information Ltd.

Keyword: Parkinsons
Link ID: 23488 - Posted: 04.14.2017

In two studies of mice, researchers showed that a drug, engineered to combat the gene that causes spinocerebellar ataxia type 2 (SCA2), might also be used to treat amyotrophic lateral sclerosis (ALS). Both studies were published in the journal Nature with funding from National Institute of Neurological Disorders and Stroke (NINDS), part of the National Institutes of Health. “Our results provide hope that we may one day be able to treat these devastating disorders,” said Stefan M. Pulst, M.D., Dr. Med., University of Utah, professor and chair of neurology and a senior author of one the studies. In 1996, Dr. Pulst and other researchers discovered that mutations in the ataxin 2 gene cause spinocerebellar ataxia type 2, a fatal inherited disorder that primarily damages a part of the brain called the cerebellum, causing patients to have problems with balance, coordination, walking and eye movements. For this study his team found that they could reduce problems associated with SCA2 by injecting mouse brains with a drug programmed to silence the ataxin 2 gene. In the accompanying study, researchers showed that injections of the same type of drug into the brains of mice prevented early death and neurological problems associated with ALS, a paralyzing and often fatal disorder. “Surprisingly, the ataxin 2 gene may act as a master key to unlocking treatments for ALS and other neurological disorders,” said Aaron Gitler, Ph.D., Stanford University, associate professor and senior author of the second study. In 2010, Dr. Gitler and colleagues discovered a link between ataxin 2 mutations and ALS.

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 23486 - Posted: 04.13.2017

By Knvul Sheikh For the past five decades pharmaceutical drugs like levodopa have been the gold standard for treating Parkinson’s disease. These medications alleviate motor symptoms of the disease, but none of them can cure it. Patients with Parkinson’s continue to lose dopamine neurons critical to the motor control centers of the brain. Eventually the drugs become ineffective and patients’ tremors get worse. They experience a loss of balance and a debilitating stiffness takes over their legs. To replace the lost dopamine neurons, scientists have begun investigating stem cell therapy as a potential treatment or even a cure. But embryonic cells and adult stem cells have proved difficult to harness and transplant into the brain. Now a study from the Karolinska Institute in Stockholm shows it is possible to coax the brain’s own astrocytes—cells that typically support and nurture neurons—into producing a new generation of dopamine neurons. The reprogrammed cells display several of the properties and functions of native dopamine neurons and could alter the course of Parkinson’s, according to the researchers. “You can directly reprogram a cell that is already inside the brain and change the function in such a way that you can improve neurological symptoms,” says senior author Ernest Arenas, a professor of medical biochemistry at Karolinska. Previously, scientists had to nudge specialized cells like neurons into becoming pluripotent cells before they could develop a different kind of specialized cell, he says. It was like having to erase all the written instructions for how a cell should develop and what job it should do and then rewriting them all over again. But Arenas and his team found a way to convert the instructions into a different set of commands without erasing them. © 2017 Scientific American

Keyword: Parkinsons; Glia
Link ID: 23475 - Posted: 04.11.2017

By Paul Taylor One of the bummers of getting older, as most baby boomers can attest, is that the list of stuff you don’t do as well as you once did keeps getting longer. Bennett Beach, 67, can measure his decline with a stopwatch. Three hours, 27 minutes, 56 seconds: That’s the difference between his best time in the Boston Marathon (2:27:26) and his worst (5:55:22). On April 17, he’ll be running the famous race once again. If he completes the course in less than six hours, he will have officially finished his 50th consecutive Boston Marathon. No one has ever done that. Nor, as far as he knows, will any of his 32,000 fellow racers be coping, as he is, with the rare and debilitating neurological movement disorder known as task-specific dystonia. Whenever he strides, Beach’s left leg gets hijacked by erratic signals from his brain. His walk is nearly normal, but for the past 15 years he has been running with a severe limp. His pursuit of the milestone has been fueled in roughly equal measure by antithetical parts — an Ahab-grade obsession mixed with an older-but-wiser acceptance of his body’s limits. “If someone had told me 30 years ago I’d be struggling to finish this race in six hours, I’d have said, ‘Spare me.’ Now I’m grateful.” Beach is a marathoner by demeanor: quiet, unassuming, self-effacing, iron-willed. And by body type: 5-foot-7, 125 pounds. He played all sports as a kid, distinguishing himself at none: “I just didn’t have the size or strength.” As a senior in prep school, he happened upon a radio broadcast of the Boston Marathon. “It was 30 degrees, it was sleeting, and these guys were out there running 26 miles,” he remembers. “Just the sort of bizarre, crazy thing I was drawn to. I already knew I’d be in Boston the next year, so I decided I’d give it a shot.” © 1996-2017 The Washington Post

Keyword: Movement Disorders
Link ID: 23471 - Posted: 04.10.2017

By Erik Stokstad A year after a deadly and highly contagious wildlife disease surfaced in Norway, the country is taking action. Chronic wasting disease (CWD), caused by misfolded proteins called prions, has already ravaged deer and elk in North America, costing rural economies millions in lost revenue from hunting. Its presence in Norway’s reindeer and moose—the first cases in Europe—is “a very serious situation for the environment and for our culture and traditions,” says Bjørnar Ytrehus, a veterinary researcher at the Norwegian Institute for Nature Research in Trondheim. Last week, Norway’s minister of agriculture and food gave the green light for hunters to kill off the entire herd in which three infected individuals were found, about 2000 reindeer, or nearly 6% of the country’s wild population. “We have to take action now,” says Karen Johanne Baalsrud, director of plant and animal health at the Norwegian Food Safety Authority in Oslo. The deer’s habitat will be quarantined for at least 5 years to prevent reinfection. The odds of a successful eradication, experts say, will depend largely on how long CWD has been present in Norway. CWD, discovered in 1967, has been found in 24 U.S. states and two Canadian provinces, and it has been spread in part by shipments of infected animals. Many species of cervids are susceptible, including elk, moose, and several kinds of deer. Infected animals typically begin showing symptoms such as weight loss, lethargy, and drooling 2 to 3 years after infection and then die within months. In Wyoming, where CWD has been endemic for decades, up to 40% of some herds are infected, and white-tailed deer populations are declining by 10% a year. © 2017 American Association for the Advancement of Science

Keyword: Prions
Link ID: 23443 - Posted: 04.04.2017

By NICHOLAS BAKALAR Hepatitis infection may increase the risk for Parkinson’s disease, though the reasons for the link remain unknown. British investigators used records of 100,390 patients hospitalized with various forms of hepatitis or H.I.V. from 1999 to 2011. They compared Parkinson’s incidence in these patients with incidence in more than six million people admitted for medical or surgical conditions like cataracts, knee replacement or varicose veins. The study, in Neurology, found that people with hepatitis B had a 76 percent higher risk of having Parkinson’s, and people with hepatitis C a 51 percent higher risk, than the control group. Those with other forms of hepatitis or H.I.V. had no increased risk. The study was restricted to hospitalized patients, and the authors did not have detailed information about the severity and treatment of the diseases. “We can’t be sure what is underlying this association,” said the lead author, Dr. Julia Pakpoor, a researcher at the University of Oxford. “It could be the treatment for the hepatitis, or it could be that Parkinson’s and hepatitis have common risk factors we haven’t identified.” A different kind of study would be needed, she said, to determine possible mechanisms that might be involved. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 23430 - Posted: 03.31.2017

Workplace exposure to electromagentic fields is linked to a higher risk of developing the most common form of motor neurone disease. Amyotrophic lateral sclerosis (ALS) is a disease that ravages the body’s nerve cells, leaving people unable to control their bodies. People can die as soon as two years after first experiencing symptoms. “Several previous studies have found that electrical workers are at increased risk of ALS,” says Neil Pearce, at the London School of Hygiene and Tropical Medicine. “We don’t know why the risk is higher, but the two most likely explanations involve either electrical shocks, or ongoing exposure to extremely low frequency magnetic fields.” Now an analysis of data from more than 58,000 men and 6,500 women suggests it is the latter. Roel Vermeulen, at Utrecht University in the Netherlands, and his team found that people whose jobs exposed them to high levels of very low frequency magnetic fields were twice as likely to develop ALS as people who have never had this kind of occupational exposure. Jobs with relatively highe extremely low frequency electromagnetic fields levels include electric line installers, welders, sewing-machine operators, and aircraft pilots, says Vermuelen. “These are essentially jobs where workers are placed in close proximity to appliances that use a lot of electricity.” © Copyright Reed Business Information Ltd.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23424 - Posted: 03.30.2017

Sarah Boseley Health editor A man who was paralysed from below the neck after crashing his bike into a truck can once again drink a cup of coffee and eat mashed potato with a fork, after a world-first procedure to allow him to control his hand with the power of thought. Bill Kochevar, 53, has had electrical implants in the motor cortex of his brain and sensors inserted in his forearm, which allow the muscles of his arm and hand to be stimulated in response to signals from his brain, decoded by computer. After eight years, he is able to drink and feed himself without assistance. “I think about what I want to do and the system does it for me,” Kochevar told the Guardian. “It’s not a lot of thinking about it. When I want to do something, my brain does what it does.” The experimental technology, pioneered by the Case Western Reserve University in Cleveland, Ohio, is the first in the world to restore brain-controlled reaching and grasping in a person with complete paralysis. For now, the process is relatively slow, but the scientists behind the breakthrough say this is proof of concept and that they hope to streamline the technology until it becomes a routine treatment for people with paralysis. In the future, they say, it will also be wireless and the electrical arrays and sensors will all be implanted under the skin and invisible.

Keyword: Robotics
Link ID: 23423 - Posted: 03.29.2017

By DENISE GRADY Dr. Lewis P. Rowland, a neurologist who made fundamental discoveries in nerve and muscle diseases and clashed with government investigators during the McCarthy era, died on March 16 in Manhattan. He was 91. The cause was a stroke, his son Steven said. Dr. Rowland, the chairman of Columbia University’s neurology department for 25 years, died at NewYork-Presbyterian/Columbia University Medical Center. Dr. Rowland was a prolific researcher and writer, with nearly 500 published scientific articles that focused on devastating neuromuscular diseases, including muscular dystrophy, myasthenia gravis and many rare syndromes. He took a special interest in amyotrophic lateral sclerosis, or A.L.S., also called Lou Gehrig’s disease, which causes degeneration of nerves in the brain and spinal cord, leading to weakness, paralysis and death. Dr. Rowland led research teams that delineated a number of uncommon diseases that had been poorly understood. They also found that in a subgroup of A.L.S. patients, the disease was linked to lymphoma, a cancer of the immune system. Other studies led to the discovery that a gene defect causes an unusual form of dementia in some patients with A.L.S. In myasthenia gravis, Dr. Rowland and his colleagues documented its high death rate and helped identify treatments that prolonged survival. In the 1970s, long before the tools existed to study DNA’s role in neurological diseases like A.L.S., Alzheimer’s and Parkinson’s, Dr. Rowland predicted correctly that genetics would be the key to understanding them. One of his accomplishments at Columbia was the expansion in 1982 of an intensive care unit that added beds for patients who were severely ill with neurological disorders. Before then, it was often difficult to find I.C.U. space for them. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease ; Muscles
Link ID: 23399 - Posted: 03.24.2017

A study in Neurology suggests that analyzing levels of the protein p75ECD in urine samples from people with amyotrophic lateral sclerosis (ALS) may help monitor disease progression as well as determine the effectiveness of therapies. The study was supported by National Institute of Neurological Disorders and Stroke (NINDS) and National Center for Advancing Translational Sciences (NCATS), both part of the National Institutes of Health. Mary-Louise Rogers, Ph.D., senior research fellow at Flinders University in Adelaide, Australia, and Michael Benatar, M.D., Ph.D, professor of neurology at the University of Miami, and their teams, discovered that levels of urinary p75 ECD increased gradually in patients with ALS as their disease progressed over a 2-year study period. “It was encouraging to see changes in p75ECD over the course of the study, because it suggests an objective new method for tracking the progression of this aggressive disease,” said Amelie Gubitz, Ph.D., program director at NINDS. “In addition, it indicates the possibility of assessing whether levels of that protein decrease while patients try future treatments, to tell us whether the therapies are having any beneficial effects.” Further analysis of the samples from 54 patients revealed that those who began the study with lower levels of urinary p75ECD survived longer than did patients who had higher levels of the protein initially, suggesting that it could be a prognostic marker of the disease and may inform patients about their illness. Dr. Benatar and his team noted that this may be useful in selecting participants for clinical trials and in improving study design.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23396 - Posted: 03.23.2017

By Timothy Revell A smartphone app that uses deep learning lets people with Parkinson’s disease test their symptoms at home in just 4 minutes. The app could help people monitor the disease’s progression more closely, and uncover how lifestyle factors may affect their symptoms. “There’s very little understanding as to how Parkinson’s arises, and patients say that every day the condition is different,” says George Roussos at Birkbeck, University of London. People report symptom changes related to everything from exercise to socialising to diet, but it’s not yet possible to build a solid picture of how these factors interact. “To understand these differences, we need to monitor the condition regularly, in a quick and easy way, over a long period of time,” says Roussos. People with Parkinson’s usually only see a specialist once or twice a year. This makes it hard to track the disease progression in an individual in detail, and means that side effects of medication such as deterioration of mood can go unnoticed. With their Android app, called CloudUPDRS, Roussos and his colleagues want to make it easier to track symptoms and flag potential problems earlier. Similar to how a clinician would conduct a Parkinson’s severity test, the app includes both self-assessment questions and physical tests using a smartphone’s sensors. © Copyright Reed Business Information Ltd.

Keyword: Parkinsons
Link ID: 23313 - Posted: 03.04.2017

By Matt Reynolds If you’re happy and you know it, clap someone else’s hands. A muscle stimulation system aims to evoke empathy by triggering involuntary hand gestures in one person in response to mood changes in another. “If you’re moving in the same way as another person you might understand that person better,” says Max Pfeiffer at the University of Hannover in Germany. Pfeiffer and his team wired up four people to an EEG machine that measured changes in the electrical activity in their brain as they watched film clips intended to provoke three emotional responses: amusement, anger and sadness. These people were the “emotion senders”. Each sender was paired with an “emotion recipient” who wore electrodes on their arms that stimulated their muscles and caused their arms and hands to move when the mood of their partner changed. The gestures they made were based on American Sign Language for amusement, anger and sadness. To express amusement, volunteers had their muscles stimulated to raise one arm, to express anger they raised an arm and made a claw gesture, and to express sadness they slowly slid an arm down their chest. These resemble natural movements associated with the feelings, so the team hypothesised that they would evoke the relevant emotion. Asked to rate how well the gestures corresponded to the emotions, the volunteers largely matched the gestures to the correct mood. © Copyright Reed Business Information Ltd.

Keyword: Brain imaging
Link ID: 23302 - Posted: 03.02.2017

By KATHRYN SHATTUCK After his short film screened at the Sundance Film Festival in 2008, a euphoric Simon Fitzmaurice was walking the snowy streets of Park City, Utah, when his foot began to hurt. Back home in Ireland that summer, by then dealing with a pronounced limp, he received a shattering diagnosis: motor neuron disease, or M.N.D. (more commonly known in the United States as A.L.S., or Lou Gehrig’s Disease), a neurological disorder that causes increasing muscle weakness and eventual paralysis and is, in most cases, fatal. The doctor gave Mr. Fitzmaurice, then 33, three or four years to live. That might have been the end of any normal existence. But Mr. Fitzmaurice, by his own measure a “bit of a stubborn bastard,” was determined to leave his wife, Ruth, and their two young sons — with a third on the way — a legacy other than self-pity. The result is Mr. Fitzmaurice’s first feature film, and perhaps his salvation — “My Name Is Emily.” The movie, which opened in limited release in the United States on Feb. 17, stars Evanna Lynch, the airy Luna Lovegood of “Harry Potter” fame, as a teenage outlier in both her Dublin foster home and high school who goes on the lam with her only friend (George Webster) to free her father (Michael Smiley) from a mental hospital. The film — with gorgeous scenes of Ms. Lynch plunged, nymphlike, into a cerulean sea or riding shotgun through the emerald countryside in a canary-yellow vintage Renault — won for best cinematography when it debuted at the Galway Film Fleadh in 2015. “I am not trying to prove anything,” Mr. Fitzmaurice wrote in an email, before quickly reconsidering. “Actually, I am trying to prove something. I remember thinking, ‘I must do this to show my children to never give up.’” Mr. Fitzmaurice was writing with his hands when he began the script for “My Name Is Emily.” By the time he was finished, he was writing with his eyes. © 2017 The New York Times Company

Keyword: ALS-Lou Gehrig's Disease
Link ID: 23275 - Posted: 02.24.2017

Laurel Hamers Clusters of a toxic bacterial protein have a surprising structure, differing from similar clumps associated with Alzheimer’s and Parkinson’s in humans, scientists report in the Feb. 24 Science. These clusters, called amyloids, are defined in part by their structure: straight regions of protein chains called beta strands, folded accordion-style into flat beta sheets, which then stack up to form a fiber. That definition might now need to be broadened. “All the amyloids that have been structurally looked at so far have certain characteristics,” says Matthew Chapman, a biologist at the University of Michigan in Ann Arbor who wasn’t part of the work. “This is the odd amyloid out right now.” In the human brain, misfolded proteins can form amyloids that trigger neurodegenerative diseases. But amyloids aren’t always a sign of something gone wrong — some bacteria make amyloids to help defend their turf. In Staphylococcus aureus, for example, the PSMα3 protein assembles into amyloids that help the bacteria kill other cells. Previous research suggested that PSMα3 clusters were like any other amyloid. But researchers using X-ray crystallography found that instead of straight beta strands, the PSMα3 fiber was made up of curly structures called alpha helices that resemble an old-fashioned phone cord. The helices still formed a familiar fiber shape just like the beta strands did, but the sheets making up that fiber were rippled instead of flat. |© Society for Science & the Public 2000 - 2017.

Keyword: Alzheimers
Link ID: 23274 - Posted: 02.24.2017