Chapter 11. Motor Control and Plasticity

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By Lena H. Sun Federal health officials took the unusual step on Tuesday of warning the public about an increase in a mysterious and rare condition that mostly affects children and can cause paralysis. So far this year, 127 confirmed or suspected cases of acute flaccid myelitis, or AFM, have been reported to the Centers for Disease Control and Prevention — a significant increase over 2017 and a worrying perpetuation of a disease for which there is little understanding. Of the cases announced Tuesday, 62 have been confirmed in 22 states, according to Nancy Messonnier, a top official at the CDC. More than 90 percent of the confirmed cases have been in children 18 and younger, with the average age being 4 years old. The surge has baffled health officials, who on Tuesday announced a change in the way the agency is counting cases. They also wanted to raise awareness about the condition so parents can seek medical care if their child develops symptoms, and so physicians can quickly relay reports of the potential illness to the CDC. “We understand that people, particularly parents, are concerned about AFM,” said Messonnier, director of the National Center for Immunization and Respiratory Diseases. Despite extensive laboratory and other testing, CDC has not been able to find the cause for the majority of the cases. “There is a lot we don’t know about AFM, and I am frustrated that despite all of our efforts, we haven’t been able to identify the cause of this mystery illness." © 1996-2018 The Washington Post

Keyword: Movement Disorders; Development of the Brain
Link ID: 25586 - Posted: 10.17.2018

By Christine Hauser Health authorities in the United States said this week that they were investigating an unusual spike in cases of a rare condition that causes limb paralysis and severe muscle weakness in children. Since mid-September, six cases of the condition, acute flaccid myelitis, in children under 10 years old have been reported to the Minnesota Department of Health, the agency said. Another two possible cases are pending confirmation, officials said. The number of cases of the illness, also known as A.F.M., is the highest in the state since 2014, when there were three reported cases, the health authorities said. Minnesota typically records one case of A.F.M. each year, and some years it does not have any at all, the department said. Officials have not found a specific cause for the illness. On Tuesday, the health authorities said three children suspected to have A.F.M. were being treated at UPMC Children’s Hospital of Pittsburgh. Officials in Colorado said this week that they were investigating a viral infection outbreak among children that included 14 cases of A.F.M. this year. The Centers for Disease Control and Prevention says it has seen an increasing number of people across the United States with the serious condition in the past four years. A.F.M. affects the nervous system and causes, mostly in children, paralysis similar to polio. The signs include sudden muscle weakness in the arms or legs; neck weakness or stiffness; a drooping face or eyelids; difficulty swallowing; and slurred speech, health officials say. Parents usually notice the child’s loss of the use of an arm or a leg. That was the case with Orville Young, a 4-year-old boy in Minnesota who lost mobility in his right arm and had difficulty sitting up and moving his legs. © 2018 The New York Times Company

Keyword: Movement Disorders; Development of the Brain
Link ID: 25562 - Posted: 10.11.2018

Anna Azvolinsky When you move only your right arm, there’s neural activity in both the left and right sides of the brain, researchers report today (October 8) in The Journal of Neuroscience. Recent animal and human studies have hinted that moving muscle on only one side of the body resulted in neural activity from the same side—or ipsilateral—part of the brain. But the data haven’t been convincing enough to completely erase the idea that only the left side of the brain is responsible for movement on the right side of the body or vice versa. The new study shows the ipsilateral brain activity encodes detailed arm movement information including position, speed, and velocity. The results could one day be used to help improve recovery therapies for patients with brain injuries. “This is an important contribution to our understanding of how the brain controls arm movement because it reveals a greater role of ipsilateral brain activity than previously recognized,” writes Nathan Crone, a professor of neurology who runs a cognitive neurophysiology lab at Johns Hopkins University in Maryland and was not involved in the research, in an email to The Scientist. In the study, Eric Leuthardt, professor of neurosurgery, engineering, and neuroscience at Washington University in St. Louis, and his colleagues enlisted four patients with epilepsy who were to undergo surgery and who had electrodes implanted for a week under the skull. The electrodes were placed directly onto the cortex of the patients’ brain cortex regions, including the primary motor cortex—responsible for coordinating voluntary muscle movements. The patients volunteered to perform three-dimensional, individual arm motions while the researchers recorded neural activity from the implanted electrodes. The team then used machine learning to derive speed, velocity, and position information on each movement—gathering data on fine motor movements that cannot be easily captured using noninvasive techniques such as functional magnetic resonance imaging (fMRI). © 1986 - 2018 The Scientist.

Keyword: Movement Disorders
Link ID: 25561 - Posted: 10.11.2018

By Alex Therrien Health reporter, BBC News Doctors have been given permission to give a British man with CJD a pioneering treatment, in a world first. There is currently no treatment for the rare but lethal brain disease, known as the human version of "mad cow disease". Doctors in London were given permission for the trial use on a human for the first time by the Court of Protection. Scientists say lab testing of the man-made antibody has been encouraging, but they admit they do not know how their patient will respond. The patient in this case, who has not been named, has sporadic CJD, the most common form of the disease in humans. This is different from variant CJD, the version linked to eating beef infected by bovine spongiform encephalopathy, or BSE. Sporadic CJD happens when healthy proteins in the human body - prions - become spontaneously misshapen and build up in the brain. The man-made antibody treatment, called PRN100, aims to prevent abnormal prions from being able to attach themselves to healthy proteins, meaning that they cannot grow and cause devastation throughout the brain. University College London Hospitals NHS Foundation Trust (UCLH) is set to use it in a patient for the first time after a judge from the Court of Protection confirmed on Monday that it was lawful and in the patient's best interests to receive it. © 2018 BBC

Keyword: Prions
Link ID: 25554 - Posted: 10.10.2018

Rory Cellan-Jones Technology correspondent Chinese tech giant Tencent and London medical firm Medopad have teamed up to use artificial intelligence in the diagnosis of Parkinson's Disease. A camera captures the way patients move their hands to determine the severity of their symptoms. The research team has trained the system with existing videos of patients who have been assessed by doctors, working with King's College Hospital in London. "We use the AI to measure the deterioration of Parkinson's disease patients without the patient wearing any sensors or devices," explains Dr Wei Fan, head of the Tencent Medical AI lab. The aim is to speed up a motor function assessment process, which usually takes more than half an hour. Using smartphone technology developed by Medopad, the hope is that patients could be assessed within three minutes - and might not even have to attend a hospital. Medopad is a London-based firm that has been developing apps and wearable devices to monitor patients with various medical conditions. It has been growing fast - but is a minnow compared with Tencent, which is spearheading China's huge investment in AI. Medopad's chief executive Dan Vahdat sais that there was no British company that could match what Tencent offered as a partner. "Our ambition is to impact a billion patients around the world - and to be able to get to that kind of scale we need to work with partners that have international reach," he told me. © 2018 BBC

Keyword: Parkinsons
Link ID: 25539 - Posted: 10.08.2018

By Gretchen Reynolds Are we born to be physically lazy? A sophisticated if disconcerting new neurological study suggests that we probably are. It finds that even when people know that exercise is desirable and plan to work out, certain electrical signals within their brains may be nudging them toward being sedentary. The study’s authors hope, though, that learning how our minds may undermine our exercise intentions could give us renewed motivation to move. Exercise physiologists, psychologists and practitioners have long been flummoxed by the difference between people’s plans and desires to be physically active and their actual behavior, which usually involves doing the opposite. Few of us exercise regularly, even though we know that it is important for health and well being. Typically, we blame lack of time, facilities or ability. But recently an international group of researchers began to wonder whether part of the cause might lie deeper, in how we think. For an earlier review, these scientists had examined past research about exercise attitudes and behavior and found that much of it showed that people sincerely wished to be active. In computer-based studies, for example, they would direct their attention to images of physical activity and away from images related to sitting and similar languor. But, as the scientists knew, few people followed through on their aims to be active. So maybe, the scientists thought, something was going on inside their skulls that dampened their enthusiasm for exercise. To find out, they recruited 29 healthy young men and women. All of the volunteers told the scientists that they wanted to be physically active, although only a few of them regularly were. © 2018 The New York Times Company

Keyword: Obesity
Link ID: 25526 - Posted: 10.04.2018

By Michael Price Alien limb syndrome isn’t as extraterrestrial as it sounds—but it’s still pretty freaky. Patients complain that one of their hands has gone “rogue,” reaching for things without their knowledge. “They sit on their hand trying to get it not to move,” says Ryan Darby, a neurologist and neuroscientist at Vanderbilt University in Nashville. “They’re not crazy. They know there’s not something controlling their arm, that it’s not possessed. But they really feel like they don’t have control.” Now, a study analyzing the locations of brain lesions in these patients—and those who have akinetic mutism, in which people can scratch an itch and chew food placed into their mouths without being aware they’ve initiated these movements—are shedding light on how our brains know what’s going on with our bodies. The work shows how neuroscience is beginning to approach elements of the biological nature of free will. “I think it's really nice work, carefully done and thoughtfully presented,” says Kevin Mitchell, a neurogeneticist at Trinity College in Dublin who studies perception and who wasn’t involved in the study. Philosophers have wrestled with questions of free will—that is, whether we are active drivers or passive observers of our decisions—for millennia. Neuroscientists tap-dance around it, asking instead why most of us feel like we have free will. They do this by looking at rare cases in which people seem to have lost it. © 2018 American Association for the Advancement of Science

Keyword: Consciousness
Link ID: 25520 - Posted: 10.02.2018

Sarah Boseley and agencies One in two women will develop dementia or Parkinson’s disease, or have a stroke, in their lifetime, new research suggests. About a third of men aged 45 and half of women of the same age are likely to go on to be diagnosed with one of the conditions, according to a study of more than 12,000 people. The researchers, from the University Medical Center Rotterdam in the Netherlands, said preventive measures could “substantially” reduce the burden of the illnesses. The findings have been published in the Journal of Neurology, Neurosurgery, and Psychiatry. The health of 12,102 people was monitored between 1990 and 2016, with all participants initially under the age of 45. During this period 1,489 were diagnosed with dementia and 263 with parkinsonism – the generic term for a range of symptoms that can be seen in someone with Parkinson’s disease – while 1,285 had a stroke. The overall risk of a 45-year-old later developing one of the three conditions was 48% for women and 36% for men, the researchers said. Dementia was of greatest concern for women, who at 45 years old had a 25.9% risk of going on to develop the condition, compared with 13.7% for men. © 2018 Guardian News and Media Limited

Keyword: Alzheimers; Parkinsons
Link ID: 25517 - Posted: 10.02.2018

Laura Sanders With the help of a spine stimulator and intensive training, a formerly paralyzed man can command his legs to step again. This achievement, described online September 24 in Nature Medicine, inches researchers closer to restoring movement to paraplegic people. The therapy allows 29-year-old Jered Chinnock to control his leg movements with his thoughts. “This is highly significant,” study coauthor Kendall Lee, a neurosurgeon at the Mayo Clinic in Rochester, Minn., said in a news briefing on September 20. A snowmobile wreck left Chinnock paralyzed, unable to move or feel sensations below the chest. His initial rehabilitation focused on acclimating to life in a wheelchair. But three years after the accident, he enrolled in an aggressive study designed to get him moving. Surgeons implanted a stimulator that zaps nerve cells on the spinal cord below the site of Chinnock’s injury. With the stimulator on, therapists led Chinnock through exercises to reactivate muscles and nerves. Over two weeks of training with the stimulator, he could stand and, while lying on his side, make voluntary steplike movements. Those results were published last year in Mayo Clinic Proceedings. Now, after 43 weeks of intense rehabilitation, Chinnock has made even greater strides. He can step on a treadmill on his own, and, with assistance and a walker, can step across the ground. Over the course of one training session, he was able to travel 102 meters, about the length of an American football field, the researchers report. Because he required assistance, researchers describe Chinnock’s motion as “independent stepping” rather than walking. That’s because, in clinical terms, walking describes “a highly coordinated activity in terms of balance, strength and adaptation to the environment,” said Lee’s coauthor Kristin Zhao, also of the Mayo Clinic. |© Society for Science & the Public 2000 - 2018.

Keyword: Movement Disorders; Robotics
Link ID: 25491 - Posted: 09.25.2018

Anthea Lacchia Just 10 minutes of light physical activity is enough to boost brain connectivity and help the brain to distinguish between similar memories, a new study suggests. Scientists at the University of California studying brain activity found connectivity between parts of the brain responsible for memory formation and storage increased after a brief interval of light exercise – such as 10 minutes of slow walking, yoga or tai chi. The findings could provide a simple and effective means of slowing down or staving off memory loss and cognitive decline in people who are elderly or have low levels of physical ability. The scientists asked 36 healthy volunteers in their early 20s to do 10 minutes of light exercise – at 30% of their peak oxygen intake – before assessing their memory ability. The memory test was then repeated on the same volunteers without exercising. The same experiment was repeated on 16 of the volunteers who had either undertaken the same kind of exercise or rested, with researchers scanning their brain to monitor activity. In the brains of those who had exercised they discovered enhanced communication between the hippocampus – a region important in memory storage – and the cortical brain regions, which are involved in vivid recollection of memories. “The memory task really was quite challenging,” said Michael Yassa, a neuroscientist at the University of California, Irvine, and project co-leader. The participants were first shown pictures of objects from everyday life – ranging from broccoli to picnic baskets – and later tested on how well they remembered the images. “We used very tricky similar items to to see if they would remember whether it was this exact picnic basket versus that picnic basket,” he said. © 2018 Guardian News and Media Limited

Keyword: Learning & Memory
Link ID: 25488 - Posted: 09.25.2018

by Marvin M. Lipman, ‘I thought I had Parkinson’s disease!” the 65-year-old stock analyst exclaimed. Over the past six months, her handwriting had deteriorated to the point that she was having difficulty signing checks. Because a good friend of hers had recently received a diagnosis of Parkinson’s disease, she feared the worst. I began to suspect that her concern was groundless when I noticed that both of her hands shook and that she had a barely noticeable to-and-fro motion of her head — two signs that are uncommon in Parkinson’s disease. And as she walked toward the examining room, her gait was normal and her arms swung freely — hardly the stiff, hesitant shuffle so often seen with Parkinson’s. The exam turned up none of the other cardinal manifestations of Parkinson’s: the typical masklike facial expression; the slowed, monotonous speech pattern; and the ratchet-like sensation the examiner feels when alternately flexing and extending the patient’s arm. Moreover, her hand tremors seemed to improve at rest and worsen when asked to do the “finger to nose” test. The diagnosis was unmistakable: She had essential tremor, a nervous-system problem that causes unintentional shaking, most often starting in the hands. © 1996-2018 The Washington Post

Keyword: Movement Disorders
Link ID: 25486 - Posted: 09.25.2018

Jenny Rood In 1999, a paper in Nature Medicine reported that mouse models of the fatal neurodegenerative disorder amyotrophic lateral sclerosis fared better with a simple treatment: a diet supplemented with creatine, a compound that helps regulate energy levels in the brain and muscles (5:347–50). That promising, albeit preliminary, result soon launched not one but three clinical trials, with a total of 386 patients in the US and Europe. Disappointingly, the trials revealed that creatine had no effect in people. It was a familiar outcome: more than 50 other clinical trials of potential amyotrophic lateral sclerosis (ALS) drugs, ranging from lithium to celecoxib (Celebrex), have failed. Also known as Lou Gehrig’s disease, ALS results from the degeneration and death of motor neurons, and affects approximately two to five of every 100,000 people worldwide. ALS’s devastating symptoms—including progressively worsening muscle weakness and spasming, and difficulties with speech, swallowing, and breathing, leading ultimately to paralysis and death—have led to an intense hunt for treatments to halt its progression. Unfortunately, the desire to give patients hope has often outstripped good scientific sense. “Many drugs that have gone into ALS clinical trials shouldn’t have, because the preclinical data package didn’t support it,” says Steve Perrin, CEO and CSO of the nonprofit ALS Therapy Development Institute (TDI) based in Cambridge, Massachusetts. Only five of the 420 ALS therapy candidates that his center has retested in mouse and cellular models have shown a therapeutic effect. © 1986 - 2018 The Scientist

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25469 - Posted: 09.20.2018

By: Albert La Spada, M.D., Ph.D. Altering the DNA sequence of a single gene can be enough to cause a fatal illness, and a medical specialty is devoted to the diagnosis and care of patients who have what doctors have labeled “genetic diseases.” While most of these conditions are very rare (except in certain small human populations that exist in reproductive isolation1), there are thousands of genetic diseases, and at least half of pediatric patients admitted to major children’s medical centers at any given time are afflicted with one of them.2 Single gene mutations can also cause breast, ovarian, and colon cancer in adult patients. Over the last century, our understanding of genetic disease has greatly advanced through the tireless work of clinicians and researchers, as the concept of one gene giving rise to one particular disorder evolved, and the modes of inheritance for different genetic diseases were defined. In the course of this work, certain such diseases (e.g. sickle cell anemia, cystic fibrosis, Duchenne muscular dystrophy, neurofibromatosis) became well known, almost always because they were the most common and the most tragic. Included in this group is a disorder that has been the focus of intense research efforts to define its cause and now to develop an effective treatment: Huntington’s disease (HD). In this primarily neuropsychiatric disorder, most affected individuals first suffer from an inability to control their movements, and develop signs of disease in their 30s or 40s. Because these uncontrolled movements can appear rhythmic, the disease was also named Huntington’s chorea, from the Greek word for dance. The initial phase typically advances for a number of years before HD patients develop cognitive decline, which progresses until they can no longer perform the activities of daily living. At this point, patients are typically admitted to a skilled nursing facility, where they linger in decline for more years before passing away. © 2018 The Dana Foundation

Keyword: Huntingtons
Link ID: 25445 - Posted: 09.13.2018

By Kelly Servick Stay active; age gracefully. Behind this truism, there’s a pile of unanswered scientific questions. Researchers are still sorting out what it is about physical activity that seems to lower the risk of dementia later in life. Even more uncertain is whether the effects of exercise can alter the course of diseases that cause dementia—chief among them, Alzheimer’s disease—once they’ve already taken root. A study published today in Science offers some new clues. In mice that mimic a severe, genetic form of Alzheimer’s disease, a combination of treatments that prompt the growth of new brain cells and protect them from damage can mimic the beneficial effects of exercise in preventing memory decline. So could we someday bottle the effects of exercise to treat Alzheimer’s? And if so, what exactly would we need to bottle? Here’s a rundown of what we know, and what’s still controversial. What’s the link between exercise and brain aging? Many large studies suggest staying active and fit throughout life lowers the risk of memory problems later on. For example, a recent project tracked more than 1000 Swedish women over 4 decades and found that for those judged to have “high” cardiovascular fitness on entering the study—as measured by the maximum workload they could handle on a stationary cycle machine before exhaustion—the onset of dementia was delayed, on average, by 9.5 years compared to those with “medium” fitness. But such studies can’t rule out all other confounding factors that might influence dementia risk—from genes to other aspects of a healthy lifestyle common in regular exercisers. And they don’t explain what exercise actually does to the brain. Does exercise fight the effects of Alzheimer’s disease once someone has it? © 2018 American Association for the Advancement of Scienc

Keyword: Alzheimers; Neurogenesis
Link ID: 25423 - Posted: 09.07.2018

Marcy Cuttler · CBC News Janaya Chekowski-McKenzie was born with the odds against her. On the day she arrived in 2009, she was non-responsive, and she spent a month in hospital with a lung infection. At three months, she had a seizure. Janaya needed hormone replacements to grow and doctors determined she had underdeveloped optic nerves. In spite of these early difficulties, the Beaumont, Alta., youngster has grown up to be a sassy, funny, bright girl with a lion's mane of curly-brown hair. When Janaya started complaining of worsening headaches last January, her mother, Amanda Chekowski, thought it was yet another medical hurdle to overcome. Instead, doctors told her Janaya had a rare, incurable form of brain cancer called diffuse intrinsic pontine glioma, or DIPG. Hearing the news, Chekowski and her family were stunned. They had to figure out how to explain this to an eight-year-old in terms she would understand. Initially, they made a bit of a joke of it. Janaya was told that "we found a booger in your brain that's not supposed to be there and we're going to try to shrink it," said Chekowski. The truth is very different. DIPG is a cancer that targets kids, and thus far, none have survived. But doctors around the world are trying to change that. ©2018 CBC/Radio-Canada.

Keyword: Movement Disorders
Link ID: 25416 - Posted: 09.05.2018

By Jane E. Brody “Use it or lose it.” I’m sure you’re familiar with this advice. And I hope you’ve been following it. I certainly thought I was. I usually do two physical activities a day, alternating among walking, cycling and swimming. I do floor exercises for my back daily, walk up and down many stairs and tackle myriad physical tasks in and around my home. My young friends at the Y say I’m in great shape, and I suppose I am compared to most 77-year-old women in America today. But I’ve noticed in recent years that I’m not as strong as I used to be. Loads I once carried rather easily are now difficult, and some are impossible. Thanks to an admonition from a savvy physical therapist, Marilyn Moffat, a professor at New York University, I now know why. I, like many people past 50, have a condition called sarcopenia — a decline in skeletal muscle with age. It begins as early as age 40 and, without intervention, gets increasingly worse, with as much as half of muscle mass lost by age 70. (If you’re wondering, it’s replaced by fat and fibrous tissue, making muscles resemble a well-marbled steak.) “Sarcopenia can be considered for muscle what osteoporosis is to bone,” Dr. John E. Morley, geriatrician at Saint Louis University School of Medicine, wrote in the journal Family Practice. He pointed out that up to 13 percent of people in their 60s and as many as half of those in their 80s have sarcopenia. As Dr. Jeremy D. Walston, geriatrician at Johns Hopkins University School of Medicine, put it, “Sarcopenia is one of the most important causes of functional decline and loss of independence in older adults.” Yet few practicing physicians alert their older patients to this condition and tell them how to slow or reverse what is otherwise an inevitable decline that can seriously impair their physical and emotional well-being and ability to carry out the tasks of daily life. Sarcopenia is also associated with a number of chronic diseases, increasingly worse insulin resistance, fatigue, falls and, alas, death. © 2018 The New York Times Company

Keyword: Muscles; Development of the Brain
Link ID: 25415 - Posted: 09.05.2018

By Emily Willingham In 1995 the late actor Christopher Reeve, who most famously played Superman, became paralyzed from the neck down after a horseback-riding accident. The impact from the fall left him with a complete spinal cord injury at the neck, preventing his brain from communicating with anything below it. Cases like Reeve’s are generally considered intractable injuries, absent any way to bridge the gap to restore disrupted communication lines. When Reeve died in 2004 a means of reconnection had yet to be built. Now, 14 years later, researchers have coaxed nerve cells to span the divide of a complete spinal cord injury. Their findings, described August 29 in Nature, are specific to only one kind of nerve cell and much work remains before a means of reconnection reaches patients, but the results make an impression. “From the scientific perspective, this is pretty significant,” says Yu-Shang Lee, an assistant professor of medicine at Cleveland Clinic’s Lerner Research Institute, who was not involved in the study. “As far as scientific impact, it is a good leap.” That leap across a completely compromised spinal cord relied on studies in rats and mice. The research team knew a certain type of nerve cell sometimes helps restore signaling from the spinal cord in partial spinal cord injury. Even when all direct connections to the brain are ruined, these cells can help sustain limited walking function, says Michael Sofroniew, professor of neurobiology at the University of California, Los Angeles, one of the senior authors on the study. He and his colleagues banked on the idea these cells, propriospinal neurons, might do the same if they could grow into an area of complete injury in their experimental animals. So they tried to get these cells to extend their electrical conduction fibers, the axons, into the spinal breach. © 2018 Scientific American

Keyword: Regeneration; Movement Disorders
Link ID: 25404 - Posted: 08.31.2018

Laurel Hamers Gene editing can reverse muscular dystrophy in dogs. Using CRISPR/Cas9 in beagle puppies, scientists have fixed a genetic mutation that causes muscle weakness and degeneration, researchers report online August 30 in Science. Corrections to the gene responsible for muscular dystrophy have been made before in mice and human muscle cells in dishes, but never in a larger mammal. The results, though preliminary, bring scientists one step closer to making such treatments a reality for humans, says study coauthor Eric Olson, a molecular biologist at the University of Texas Southwestern Medical Center in Dallas. Duchenne muscular dystrophy is a rare but severe, progressive disease that affects mostly boys and men. People with the disease, which is just one of many types of muscular dystrophy, rarely live past their 20s, usually dying of heart failure. An estimated 300,000 people worldwide suffer from the condition. The disease can be caused by any number of mutations to the gene that makes the protein dystrophin, which is essential for muscle structure and function. The mutations, which are often clustered in one particular region of the gene, usually stop production of the protein. Gene editing targeting that region could correct for these mutations’ effects, restoring protein production. Researchers injected two 1-month-old beagle puppies with a mutation in this hot spot with different doses of a virus carrying the gene-editing machinery. The team then measured dystrophin levels in different muscles after eight weeks. |© Society for Science & the Public 2000 - 201

Keyword: Movement Disorders; Muscles
Link ID: 25403 - Posted: 08.31.2018

By Nicholas Bakalar Symptoms of poor cardiovascular health may be linked to an increased risk for Parkinson’s disease, a new study has found. Researchers used data on 17,163,560 South Koreans over 40 years old and found 44,205 cases of Parkinson’s over the course of a five-year follow-up. They looked for five cardiovascular risk factors that define the metabolic syndrome: abdominal obesity, high triglycerides, high cholesterol, high blood pressure and high glucose readings. The study is in PLOS Medicine. After controlling for age, sex, smoking, alcohol consumption, physical activity, income, body mass index and history of stroke, they found that each component of the metabolic syndrome significantly increased the risk for Parkinson’s disease. The more risk factors a person had, the greater the risk. Compared with having none of the risk factors, having all five was associated with a 66 percent increased risk for Parkinson’s disease. The association was particularly strong for people over 65. There are about 60,000 new diagnoses of Parkinson’s each year in the United States, and about a million Americans are living with the disease. “The metabolic syndrome and its components are independent risk factors for Parkinson’s,” the authors wrote. “Future studies are warranted to examine whether control of metabolic syndrome and its components can decrease the risk of Parkinson’s disease development.” © 2018 The New York Times Company

Keyword: Parkinsons
Link ID: 25376 - Posted: 08.25.2018

David Cyranoski Doctors in Japan are poised to implant neural cells made from ‘reprogrammed’ stem cells into the brains of people with Parkinson’s disease. It is only the third clinical application of induced pluripotent stem (iPS) cells, which are developed by reprogramming the cells of body tissues such as skin to revert to an embryonic-like state, from which they can morph into other cell types. Researchers have used the technique to generate precursors to the neurons that make the neurotransmitter dopamine, which degenerate and die in people with Parkinson’s disease. Physicians at Kyoto University Hospital will inject 5 million of these precursor cells into the brains of seven people with the condition. Because dopamine-producing neurons are involved in motor skills, people with the condition typically experience tremors and stiff muscles. Participants will be observed for two years after the transplantation. One of the trial’s leaders, stem-cell scientist Jun Takahashi at the Center for iPS Cell Research and Application in Kyoto, demonstrated in 2017 that the precursor cells differentiated into dopamine-producing neurons in monkeys that had a version of the disease. They also had improved symptoms1. In 2014, ophthalmologist Masayo Takahashi — Takahashi’s wife — at the RIKEN Center for Developmental Biology in Kobe developed an iPS-cell-based therapy to treat retinal disease. And in May, a team at Osaka University received approval to use cells created from iPS cells to treat heart disease. © 2018 Springer Nature Limited

Keyword: Parkinsons; Stem Cells
Link ID: 25363 - Posted: 08.22.2018