Chapter 11. Motor Control and Plasticity

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By Esther Landhuis As the sun went down on a recent Friday, the hospital clinic buzzed with activity. “Loads of patients turned up without appointments,” says Sarah Tabrizi, a neurologist at University College London. It wasn’t just the typical post-holiday rush. Many rushed in, Tabrizi suspects, after hearing news last month about a potential new therapy for Huntington’s disease, a brain disorder that cripples the body and blurs speech and thinking, sometimes not too long after a person’s 30th birthday. Like other neurodegenerative disorders such as Lou Gehrig’s, Parkinson’s and Alzheimer’s, Huntington’s has no cure. Over decades biotech companies have poured billions of dollars into developing and testing pharmaceuticals for these devastating conditions, only to unleash storms of disappointment. Yet in December a ray of something approximating hope poked through when a California company released preliminary findings from its small Huntington’s study. Results from this early-stage clinical trial have not yet been published or reported at medical meetings. But some researchers have growing confidence that the drug should work for Huntington’s and perhaps other diseases with clear genetic roots. The initial data showed enough promise to convince Roche to license the drug from California-based Ionis Pharmaceuticals, which sponsored the recent Huntington’s trial. The pharma giant paid Ionis $45 million for the right to conduct further studies and work with regulatory agencies to bring the experimental therapy to market. © 2018 Scientific American

Keyword: Huntingtons
Link ID: 24536 - Posted: 01.17.2018

Just 10 minutes of aerobic exercise can improve executive function by priming parts of the brain used to laser focus on the task at hand, according to a new study. This paper, “Executive-Related Oculomotor Control Is Improved Following a 10-minute Single-Bout of Aerobic Exercise: Evidence from the Antisaccade Task,” was published in the January 2018 issue of Neuropsychologia. This research was conducted by Matthew Heath, who is a kinesiology professor and supervisor in the Graduate Program in Neuroscience at the University of Western Ontario, along with UWO master’s student Ashna Samani. For this study, Samani and Heath asked a cohort of healthy young adults to either sit quietly and read magazines or perform 10 minutes of moderate-to-vigorous physical activity (MVPA) on a stationary bicycle. (MVPA aerobic intensity is hard enough that you might break a sweat but easy enough that you can carry on a conversation.) Immediately after the 10-minute reading task or time spent doing aerobic exercise, the researchers used eye-tracking equipment to gauge antisaccades, which is a way to measure varying degrees of executive control. As the authors explain in the study abstract, “Antisaccades are an executive task requiring a goal-directed eye movement (i.e., a saccade) mirror-symmetrical to a visual stimulus. The hands- and language-free nature of antisaccades coupled with the temporal precision of eye-tracking technology make it an ideal tool for identifying executive performance changes.” © 1991-2018 Sussex Publishers, LLC

Keyword: Attention
Link ID: 24476 - Posted: 01.02.2018

By Keith Doucette, In what her mother calls a "Christmas miracle," a Nova Scotia woman who suffered a catastrophic brain injury in a 1996 car accident communicated one-on-one with her mother for the first time in 21 years. Louise Misner said her 37-year-old daughter Joellan Huntley used eye-motion cameras and software on an iPad to respond to a comment from Misner about her clothes. Huntley has been severely disabled since she was 15, unable to walk or talk and is fed through a tube. She has always responded to family members' presence by making sounds, but was unable to communicate any thoughts. The breakthrough occurred during a Christmas Day visit at the Kings Regional Rehabilitation Centre in Waterville, N.S. "I said, 'Joellan, I like your new Christmas outfit you got on,"' Misner said in a telephone interview on Friday. Misner said her daughter then used the technology to find an icon for a short-sleeved shirt. "And then she said no, and went to a long-sleeve shirt because she was trying to tell me what she had on." Misner said her reaction to the long-hoped-for communication was immediate. "Christmas miracle," she said. "It was God's way of telling me that she's finally achieved what she needed to since the accident." Settlement helped buy technology Huntley was thrown from a car that had swerved to avoid a dog running loose along a road in Centreville, N.S., on April 18, 1996. The accident claimed the life of her boyfriend and a young girl who was the sister of the driver. ©2017 CBC/Radio-Canada.

Keyword: Movement Disorders; Robotics
Link ID: 24469 - Posted: 12.30.2017

By Sharon Begley Technologies to detect brain activity — fine, we’ll come right out and call it mind reading — as well as to change it are moving along so quickly that “a bit of a gold rush is happening, both on the academic side and the corporate side,” Michel Maharbiz of the University of California, Berkeley, told a recent conference at the Massachusetts Institute of Technology. Here are three fast-moving areas of neuroscience we’ll be watching in 2018: Neural dust/neurograins Whatever you call these electronics, they’re really, really tiny. We’re eagerly awaiting results from DARPA’s $65 million neural engineering program, which aims to develop a brain implant that can communicate digitally with the outside world. The first step is detecting neurons’ electrochemical signaling (DARPA, the Pentagon’s Defense Advanced Research Projects Agency, says 1 million neurons at a time would be nice). To do that, scientists at Brown University are developing salt-grain-sized “neurograins” containing an electrode to detect neural firing as well as to zap neurons to fire, all via a radio frequency antenna. Advertisement Maharbiz’s “neural dust” is already able to do the first part. The tiny wireless devices can detect what neurons are doing, he and his colleagues reported in a 2016 rat study. (The study’s lead scientist recently moved to Elon Musk’s startup Neuralink, one of a growing number of brain-tech companies.) Now Maharbiz and team are also working on making neural dust receive outside signals and cause neurons to fire in certain ways. Such “stimdust” would be “the smallest [nerve] stimulator ever built,” Maharbiz said. Eventually, scientists hope, they’ll know the neural code for, say, walking, letting them transmit the precise code needed to let a paralyzed patient walk. They’re also deciphering the neural code for understanding spoken language, which raises the specter of outside signals making people hear voices — raising ethical issues that, experts said, neurotech will generate in abundance. © 2017 Scientific American

Keyword: Brain imaging; Robotics
Link ID: 24468 - Posted: 12.29.2017

By Helen Shen Brain-controlled prosthetic devices have the potential to dramatically improve the lives of people with limited mobility resulting from injury or disease. To drive such brain-computer interfaces, neuroscientists have developed a variety of algorithms to decode movement-related thoughts with increasing accuracy and precision. Now researchers are expanding their tool chest by borrowing from the world of cryptography to decode neural signals into movements. During World War II, codebreakers cracked the German Enigma cipher by exploiting known language patterns in the encrypted messages. These included the typical frequencies and distributions of certain letters and words. Knowing something about what they expected to read helped British computer scientist Alan Turing and his colleagues find the key to translate gibberish into plain language. Many human movements, such as walking or reaching, follow predictable patterns, too. Limb position, speed and several other movement features tend to play out in an orderly way. With this regularity in mind, Eva Dyer, a neuroscientist at the Georgia Institute of Technology, decided to try a cryptography-inspired strategy for neural decoding. She and her colleagues published their results in a recent study in Nature Biomedical Engineering. “I’ve heard of this approach before, but this is one of the first studies that’s come out and been published,” says Nicholas Hatsopoulos, a neuroscientist at the University of Chicago, who was not involved in the work. “It’s pretty novel.” © 2017 Scientific American,

Keyword: Movement Disorders; Robotics
Link ID: 24462 - Posted: 12.28.2017

By Sally Abrahams BBC News For years, Mary Rose struggled to get off to sleep or to stay asleep, because she felt like she was being attacked by insects. "Imagine having a swarm of bees buzzing inside the skin of your legs, biting you," she says, describing the sensation that overwhelmed her. "It's really very, very painful." Now in her 80s, the art historian has a condition called restless legs syndrome (RLS), which tortures her at night. "It makes you want to scratch your legs and get up and walk about - it was just impossible to lie down and sleep because one's legs were twitching in this uncontrollable way," she explained. The symptoms were so severe, she didn't want to go to bed at night. 'No sleep at all' Mary Rose can't remember when the problem began, but the condition went undiagnosed for years. "People would say 'oh you've got cramp; you must take quinine or sleep with corks in your bed'. And I did all these things." Of course, they had no effect. She also tried rubbing ointment into her legs to ease the stinging sensation, but that never lasted long enough to let her sleep through the night. Visits to her GP also failed to bring relief. Eventually, she was referred to the sleep clinic at Guy's and St Thomas's hospitals in London, where she's now being treated by neurologist Dr Guy Leschziner. "Restless legs syndrome is a common neurological disorder that causes an irresistible urge to move, particularly at night, and is often linked with unpleasant sensations in the legs," Dr Leschziner explains. "It affects up to one in 20 adults," he continues, "and can cause severe sleep deprivation." At its worst, Mary Rose was surviving on only a few hours' sleep at night, sometimes even less. "I have had complete nights without any sleep at all," she says. © 2017 BBC

Keyword: Sleep; Movement Disorders
Link ID: 24457 - Posted: 12.26.2017

Michael May Carl Luepker suffers from a nerve disorder which causes involuntary muscle spasms. He lived with the symptoms for 30 years until he discovered he'd passed the genetic disorder on to his son. NOEL KING, HOST: Parents make all kinds of sacrifices for their children, but what do you do when you want to save your child from experiencing the same kind of suffering you have experienced? NPR's Michael May brings us the story of one father who's searching for a way to ease his son's discomfort that's caused by a shared genetic disorder. MICHAEL MAY, BYLINE: Carl Luepker suffers from dystonia, a disorder that causes involuntary muscle spasms. When I met him 30 years ago, Carl's spasms were in his right hand. Then they spread to the muscles of his face until they garbled his speech. Last December, Carl sat down in the office of his neurologist, Dr. Jerrold Vitek, to discuss a surgery called deep brain stimulation. CARL LUEPKER: My fears are - obviously, first is death. MAY: It's not an easy decision to let a doctor drill a hole in your skull and put electrodes deep in your brain. LUEPKER: Those are sort of my three biggest fears, are death, loss of cognition and any behavioral changes I might incur from the procedure. JERROLD VITEK: Well, Carl, what I would say is that the potential risk is about a 1 to 2 percent chance that there'd be a significant bleed. That's the greatest risk. The chance of benefit is marked. The vast majority of people will benefit. MAY: Deep brain stimulation has been called a pacemaker for the brain. It regulates the neurons that are misfiring. It's used for everything from Parkinson's disease to major depression. Scientists still don't understand exactly why DBS works. But for some patients, it dramatically reduces symptoms. At first, scientists literally destroyed the part of the brain that was malfunctioning. Vitek says there's a reason doctors would be willing to try something so brutal. VITEK: One word will answer that - desperation. © 2017 npr

Keyword: Movement Disorders; Genes & Behavior
Link ID: 24456 - Posted: 12.26.2017

By Katarina Zimmer | CRISPR-Cas9 gene editing can extend survival in a mouse model of amyotrophic lateral sclerosis (ALS), a fatal neurodegenerative disease, according to a study published yesterday (December 20) in Science Advances. “The treatment did not make the ALS mice normal and it is not yet a cure,” study coauthor David Schaffer, a professor of chemical and biomolecular engineering at the University of California, Berkeley, says in a press release. “But based upon what I think is a really strong proof of concept, CRISPR-Cas9 could be a therapeutic molecule for ALS.” ALS, or Lou Gehrig’s disease, affects some 20,000 Americans and is characterized by the premature death of motor neurons in the brain stem and spinal cord. The disease causes progressive muscle deterioration and eventually results in paralysis and death. There are no available treatments to delay the muscle wasting and currently approved drugs can extend survival by a few months at most. Schaffer and his colleagues suspected that ALS could be treated through genome editing because some forms of the disease (around 20 percent of inherited forms and 2 percent of all cases) are caused by dominant mutations in a gene that encodes superoxide dismutase 1 (SOD1), an enzyme that helps protect cells against toxic free radicals. © 1986-2017 The Scientist

Keyword: ALS-Lou Gehrig's Disease ; Genes & Behavior
Link ID: 24454 - Posted: 12.22.2017

By Elizabeth Quigley BBC Scotland news Scientists are close to establishing what causes a smell associated with sufferers of Parkinson's disease. They hope it could lead to the first diagnostic test for the disease. The breakthrough came after Joy Milne astonished doctors with her ability to detect the disease through smell under scientific conditions. A team from Manchester has found distinctive molecules that seem to be concentrated on the skin of Parkinson's patients. One in 500 people in the UK has Parkinson's - that is 127,000 across Britain. Musky smell It can leave them struggling to walk, speak and sleep. Currently there is no definitive test for the disease, with clinicians diagnosing patients by observing symptoms. This is how the disease has been diagnosed since 1817, when James Parkinson first established it as a recognised medical condition. However, that could change because of Joy Milne from Perth, whose husband Les was told he had Parkinson's at the age of 45. About a decade before her consultant anaesthetist husband was diagnosed, Joy noticed she could detect an unusual musky smell. Joy said: "We had a very tumultuous period, when he was about 34 or 35, where I kept saying to him, 'you've not showered. You've not brushed your teeth properly'. "It was a new smell - I didn't know what it was. I kept on saying to him, and he became quite upset about it. So I just had to be quiet." The retired nurse only linked the odour to the disease after meeting people with the same distinctive smell at a Parkinson's UK support group. © 2017 BBC.

Keyword: Parkinsons; Chemical Senses (Smell & Taste)
Link ID: 24438 - Posted: 12.19.2017

Hannah Devlin Science correspondent They are diseases that threaten more than physical health: memories, personality, and the ability to move and speak are incrementally stolen. And until this year neurodegenerative diseases, from Alzheimer’s to ALS, had been entirely unstoppable. However, a breakthrough in Huntington’s disease this week suggests this bleak picture could be about to change. The landmark trial was the first to show that the genetic defect that causes Huntington’s could be corrected, raising hopes that the drug will become the first to slow the progress of the disease – or even stop it. The Huntington’s results alone would have been remarkable enough, but they come just a month after the same experimental class of drugs were revealed to help patients with a different degenerative disease, called Spinal Muscular Atrophy (SMA). Babies with the most severe form of SMA normally never develop the strength to sit up or roll over, but after four years on the drug, some of these children are starting to stand and take their first steps with a walker. The two trials have triggered a wave of optimism that drugs built on similar principles could be used to target a wide range of deadly brain disorders, possibly even Alzheimer’s and Parkinson’s. “I don’t want to overstate this too much, but this could be a turning point,” said Prof John Hardy, a neuroscientist at University College London who was awarded the Breakthrough prize for his work on Alzheimer’s. © 2017 Guardian News and Media Limited

Keyword: Huntingtons; Movement Disorders
Link ID: 24429 - Posted: 12.16.2017

By GRETCHEN REYNOLDS Intense treadmill exercise can be safe for people who have recently been given diagnoses of Parkinson’s disease and may substantially slow the progression of their condition, according to an important new study of adults in the early stages of the disease. But the same study’s results also indicate that gentler exercise, while safe for people with Parkinson’s, does not seem to delay the disease’s advance. As most of us know, Parkinson’s disease is a progressive neurological disorder that involves problems with motor control. Symptoms like weakness, stiffness, loss of balance and falls can make exercise difficult and potentially hazardous. Though Parkinson’s is currently incurable, its symptoms can be eased for a time with various drugs. But most of those drugs lose their effectiveness in people over time. So some researchers have begun searching for other treatment options, particularly for use in the beginning stages of the disease. If people with early Parkinson’s could brake the disease’s advance and delay their need to start medications, the researchers have reasoned, they might change the arc of their disease, delaying its most severe effects. That possibility recently led a consortium of researchers from Northwestern University, the University of Colorado’s Anschutz Medical Campus in Aurora and other institutions to look at exercise as a treatment. There were precedents. Animal studies already had shown that exercise reduced symptoms and slowed physical decline in a rodent version of Parkinson’s. But rodents are not people. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 24423 - Posted: 12.14.2017

Hannah Devlin Science correspondent A landmark trial for Huntington’s disease has announced positive results, suggesting that an experimental drug could become the first to slow the progression of the devastating genetic illness. The results have been hailed as “enormously significant” because it is the first time any drug has been shown to suppress the effects of the Huntington’s mutation that causes irreversible damage to the brain. Current treatments only help with symptoms, rather than slowing the disease’s progression. Prof Sarah Tabrizi, director of University College London’s Huntington’s Disease Centre who led the phase 1 trial, said the results were “beyond what I’d ever hoped ... The results of this trial are of ground-breaking importance for Huntington’s disease patients and families,” she said. The results have also caused ripples of excitement across the scientific world because the drug, which is a synthetic strand of DNA, could potentially be adapted to target other incurable brain disorders such as Alzheimer’s and Parkinson’s. The Swiss pharmaceutical giant Roche has paid a $45m licence fee to take the drug forward to clinical use. Huntington’s is an incurable degenerative disease caused by a single gene defect that is passed down through families. The first symptoms, which typically appear in middle age, include mood swings, anger and depression. Later patients develop uncontrolled jerky movements, dementia and ultimately paralysis. Some people die within a decade of diagnosis. © 2017 Guardian News and Media Limited

Keyword: Huntingtons; Genes & Behavior
Link ID: 24419 - Posted: 12.11.2017

Hannah Devlin Huntington’s has blighted Peter Allen’s family for generations. He watched his mother, Stephanie, slowly die from the disease and before that his grandmother, Olive, fell victim to the same illness. At 51 years old, Peter is the first of his generation to show signs of the illness, but his sister, Sandy, and brother, Frank, know they are also carrying the gene. The onset of Huntington’s is insidious. Psychological changes typically come first – tiredness, mood swings, apathy and anger. Four years ago, Peter was formally diagnosed as symptomatic when he began suffering anxiety and panic attacks so severe he would become convinced that he couldn’t swallow. In retrospect, the depression he suffered in his thirties may have been an earlier manifestation of changes happening his brain. In person, Peter is articulate, funny and exudes affection for his wife and siblings, but there are small signs of the changes that are underway. Every now and then he pauses to search for the right word. A loss of dexterity means he can no longer write or sign his name, his balance is unsteady and, when tired, his speech becomes slurred. “You know that you’re gradually lessening,” he says. A lack of awareness about the disease and its symptoms means people sometimes assume he is drunk. “I’ve been asked to leave pubs before I’ve even had a drink,” he says. “I don’t go to those pubs any more.” Peter took redundancy from his marketing job at Network Rail in 2015 and has not returned to full-time work, although he is retraining to become a garden designer. Anti-depressant drugs have helped bring the psychological symptoms under control. In future, he will be offered other drugs to stiffen his muscles, which helps reduce involuntary movements. But no current treatments can slow the relentless progression of the disease, the loss of memory, motor control and eventually the ability to think. © 2017 Guardian News and Media Limited

Keyword: Huntingtons; Genes & Behavior
Link ID: 24418 - Posted: 12.11.2017

Carl Zimmer When you drive toward an intersection, the sight of the light turning red will (or should) make you step on the brake. This action happens thanks to a chain of events inside your head. Your eyes relay signals to the visual centers in the back of your brain. After those signals get processed, they travel along a pathway to another region, the premotor cortex, where the brain plans movements. Now, imagine that you had a device implanted in your brain that could shortcut the pathway and “inject” information straight into your premotor cortex. That may sound like an outtake from “The Matrix.” But now two neuroscientists at the University of Rochester say they have managed to introduce information directly into the premotor cortex of monkeys. The researchers published the results of the experiment on Thursday in the journal Neuron. Although the research is preliminary, carried out in just two monkeys, the researchers speculated that further research might lead to brain implants for people with strokes. “You could potentially bypass the damaged areas and deliver stimulation to the premotor cortex,” said Kevin A. Mazurek, a co-author of the study. “That could be a way to bridge parts of the brain that can no longer communicate.” In order to study the premotor cortex, Dr. Mazurek and his co-author, Dr. Marc H. Schieber, trained two rhesus monkeys to play a game. The monkeys sat in front of a panel equipped with a button, a sphere-shaped knob, a cylindrical knob, and a T-shaped handle. Each object was ringed by LED lights. If the lights around an object switched on, the monkeys had to reach out their hand to it to get a reward — in this case, a refreshing squirt of water. © 2017 The New York Times Company

Keyword: Learning & Memory; Movement Disorders
Link ID: 24408 - Posted: 12.08.2017

By RONI CARYN RABIN A. Bell’s palsy is a temporary partial facial paralysis that occurs when the nerve controlling the facial muscles is inflamed. But identifying the underlying cause of the inflammation “is a question for the ages,” said Dr. Joseph Safdieh, a neurologist at Weill Cornell Medicine and a fellow of the American Academy of Neurology. The current prevailing theory is that Bell’s palsy develops after a viral infection activates the immune system, Dr. Safdieh said, adding that “once the immune system is activated, it goes and attacks a nerve.” The condition usually affects only one side of the face, causing asymmetry or drooping on one side (the reason for that is not known either). Some experts believe Bell’s palsy is related to the herpes simplex or common cold sore virus. But several large randomized controlled trials that compared treatment with antiviral agents and prednisolone, an oral steroid that suppresses the immune system, found the steroid to be most effective. The results reinforce the idea that the condition is caused by an immune system reaction rather than the virus itself, Dr. Safdieh said. The condition has also been associated with recent vaccinations and upper respiratory infections, “but many people are vaccinated and have upper respiratory infections and don’t develop Bell’s palsy,” Dr. Safdieh said. “The ultimate answer is ‘we don’t know,’ but that many things that activate the immune system can trigger it.” One specific cause that should be ruled out is Lyme disease, especially if Bell’s palsy develops in the summer or early fall or in children, in whom it is less common, Dr. Safdieh said. Treatment will differ if the patient has Lyme disease. © 2017 The New York Times Company

Keyword: Movement Disorders
Link ID: 24385 - Posted: 12.04.2017

By Lydia Denworth A macaque monkey sat in front of a computer. A yellow square—the target—appeared in the periphery on the left side of the screen. After a few seconds delay, a second target appeared on the right. The question was: Which target would the monkey look at first? So far so routine as neuroscience experiments go, but the next step was unusual. By non-invasively directing bursts of inaudible acoustic energy at a specific visual area of the brain, a team of scientists steered the animal’s responses. If they focused on the left side of the brain, the monkey looked to the right more often. If they focused on the right side, the monkey looked to the left more often. The results of the experiment, which were presented last week at the annual Society for Neuroscience meeting, marked the first time that focused ultrasound was safely and effectively used in a nonhuman primate to alter brain activity rather than destroy tissue. A second study, in sheep, had similar results. “The finding paves the way to noninvasive stimulation of specific brain regions in humans,” says Jan Kubanek, a neural engineer at Stanford University School of Medicine and lead author of the macaque study. The technology might ultimately be used to diagnose or treat neurological diseases and disorders like Parkinson’s disease, epilepsy, addiction and depression. Other scientists are optimistic. “The idea that, with a very carefully designed dose, you could actually deliver [focused ultrasound] and stimulate the brain in the place you want and modulate a circuit rather than damage it, is a really important proof of principle,” said Helen Mayberg, MD, of Emory University School of Medicine, who was not involved with the study. © 2017 Scientific American

Keyword: Parkinsons; Depression
Link ID: 24384 - Posted: 12.01.2017

By DENISE GRADY Scientists have found prions — abnormal proteins widely believed to cause a rare, brain-destroying disease — in the skin of 23 patients who had died from it, according to a study published on Wednesday. The discovery suggests that skin samples might be used to improve detection of the disorder, Creutzfeldt-Jakob disease, which now is usually diagnosed with much more difficult procedures, like brain biopsies or autopsies. But the presence of prions in the skin also raises unsettling questions about whether medical instruments could become contaminated even during surgery that does not involve the brain and then spread the disease to other patients. The prions stick to stainless steel and are notoriously hard to destroy. Creutzfeldt-Jakob disease affects one person in a million worldwide, with about 300 cases a year in the United States, according to the National Institutes of Health. People are typically about age 60 when it starts. It is cruel and rapidly fatal: Most patients die within a year of becoming ill. They deteriorate mentally, weaken, move uncontrollably, and may become blind and unable to speak. The disease belongs to the same class of brain disorders as mad-cow disease. The findings do not mean that Creutzfeldt-Jakob disease can be transmitted by touch or casual contact, said the senior author of the study, Dr. Wen-Quan Zou, at Case Western University School of Medicine. Patients are not dangerous, he emphasized. The researchers also said that although the disease had been transmitted decades ago by corneal transplants and certain neurosurgical procedures, there was no definitive evidence that other types of surgery had ever spread it. And the levels found in skin are far lower than those in the brain. Despite the new findings, there is no reason to change the medical care given to patients with the disease or to people known to have genetic mutations that may predispose them to Creutzfeldt-Jakob or related illnesses, the researchers said. © 2017 The New York Times Company

Keyword: Prions
Link ID: 24356 - Posted: 11.24.2017

(Reuters) - Cytokinetics Inc will stop developing one of its treatments for ALS, which afflicts Stephen Hawking, after the drug failed in a late-stage trial, the company said on Tuesday, sending its shares tumbling about 35 percent. The drugmaker said two of the three doses it was testing failed to show a statistically significant difference compared to a placebo when measured by their ability to lower the lungs’ ‘slow vital capacity’, a measure of respiratory function. Amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease, is a fatal neuro-degenerative condition that affects nerve cells in the brain and the spinal cord. Deaths and disability in ALS patients are strongly related to respiratory failure, according to Cytokinetics. More than 6,000 people are diagnosed with the disease in the United States every year, according to the ALS Association. ALS garnered international attention in 2014 with the “Ice Bucket Challenge”, which involved people pouring ice-cold water on themselves, posting a video on social media, and donating funds for research on the disease. After the failure of its drug tirasemtiv, Cytokinetics said it will focus on its other ALS treatment, CK-2127107, that it is developing in collaboration with Japan’s Astellas Pharma Inc. Cytokinetics’ chief executive, Robert Blum, said he believes that the limitations of tirasemtiv will be addressed in the development of CK-2127107. © 2017 Business Insider Inc.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 24345 - Posted: 11.22.2017

By NIRAJ CHOKSHI The Rev. Jesse L. Jackson, the longtime civil rights leader and former Democratic presidential candidate, said Friday he has Parkinson’s disease. In a letter posted on Twitter on Friday afternoon, Mr. Jackson, 76, shared the news and his struggle to accept it. “Recognition of the effects of this disease on me has been painful, and I have been slow to grasp the gravity of it,” he wrote. “For me, a Parkinson’s diagnosis is not a stop sign but rather a signal that I must make lifestyle changes and dedicate myself to physical therapy in hopes of slowing the disease’s progression.” Parkinson’s is a movement disorder. Its symptoms include muscle tremors and stiffness and poor balance and coordination. It typically begins after age 50 and can cause difficulty sleeping, chewing, swallowing or speaking. Mr. Jackson has been a civil rights advocate for 50 years and sought the Democratic presidential nominations in 1984 and 1988. He was also a close associate of the Rev. Dr. Martin Luther King Jr. Mr. Jackson wrote that he and his family about three years ago began to notice he was having increasing difficulty performing routine tasks and was initially reluctant to see doctors. He said he saw the diagnosis as “an opportunity” to use his platform to advocate a cure and said that he would not let it disrupt his other advocacy. “I will continue to try to instill hope in the hopeless, expand our democracy to the disenfranchised and free innocent prisoners around the world,” he wrote. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 24338 - Posted: 11.20.2017

By RONI CARYN RABIN A. Parkinsonism refers to a group of movement abnormalities — such as stiffness, slowness, shuffling of the feet and often tremor — that are classic features of Parkinson’s disease but that can also be caused by medications and other disorders with overlapping symptoms, said Dr. Michael S. Okun, a neurologist and the national medical director of the Parkinson’s Foundation. He said that he makes no assumptions about the cause of parkinsonism “until I see the patient and pinpoint the diagnosis.” Determining the cause of parkinsonism involves asking a series of questions, starting with, “Do we think this is regular Parkinson’s disease?” said Dr. Okun, who is also co-director of the Center for Movement Disorders and Neurorestoration at the University of Florida College of Medicine in Gainesville. Though a diagnosis of Parkinson’s disease strikes fear in patients, Dr. Okun said that the illness, a neurodegenerative brain disorder caused by the loss of dopamine-containing neurons and other cells, progresses slowly in many people and generally responds well to drugs that replenish dopamine in the brain. Some patients whose parkinsonism is not caused by Parkinson’s disease also respond to these drugs, but the medications are most effective for people with Parkinson’s disease, Dr. Okun said. It’s important to rule out other potential causes of parkinsonism, he said. The condition can be triggered by antipsychotic medications that affect dopamine levels in the brain, as well as by other drugs, including stimulants like amphetamines and cocaine. Discontinuing the drugs may stop the symptoms over time, though not always. Parkinsonism may also be caused by repeated injuries to the head, exposure to various toxins or brain lesions. Once doctors rule out Parkinson’s disease, they must consider several other serious neurological disorders. The three most common ones are multiple system atrophy, a degenerative disorder also referred to as Shy-Drager syndrome, which may or may not respond well to Parkinson’s medications; progressive supranuclear palsy, or PSP, which also may respond to high doses of drugs that replace dopamine in the brain; and corticobasal degeneration (CBD). Patients with a form of dementia called Lewy body dementia may also exhibit symptoms of parkinsonism, which may or may not respond to dopamine. Various other movement disorders, called ataxias or dystonias, also may display features of parkinsonism. © 2017 The New York Times Company

Keyword: Parkinsons
Link ID: 24335 - Posted: 11.17.2017