Chapter 11. Motor Control and Plasticity

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By Denise Grady A lifelong swimmer leapt into deep water near his lakeside home, and was horrified to find himself completely unable to swim. Had his wife not rescued him, he might have drowned. He had recently received an electronic brain implant to control tremors and other symptoms of Parkinson’s disease, and somehow the signals from the device had knocked out his ability to coordinate his arms and legs for swimming. He was one of nine patients, all good swimmers despite having Parkinson’s, who had the same strange, dangerous side effect from deep brain stimulators. Three of them tried turning off the stimulators, and immediately could swim again, according to an article in the journal Neurology by a medical team from the University of Zurich. At first, doctors thought the case of the man in the lake was an isolated event, Dr. Christian R. Baumann, an author of the paper, said in an interview. But when the same thing happened to another patient, one who had been a competitive swimmer, Dr. Baumann and his colleagues began to ask other patients about swimming. They found seven more cases among about 250 patients. About 150,000 people worldwide have brain implants made by Medtronic, the leading manufacturer, the company said. Most had the implants for relief of Parkinson’s symptoms. The swimming problem is not that common Dr. Baumann said, adding: “I think it’s a minority of patients. We find many who are still wonderfully able to swim and we don’t know why. We have no clue. They are treated in the same region of the brain. But this is life-threatening, and we need to pay more attention in the future.” Now, Dr. Baumann warns all patients with stimulators never to go into deep water alone. © 2019 The New York Times Company

Keyword: Parkinsons
Link ID: 26860 - Posted: 11.29.2019

Catherine Offord A clinical trial of a gene therapy for Duchenne muscular dystrophy has been halted after a patient suffered serious side effects following treatment, Reuters reports today (November 12). After receiving Solid Biosciences’s experimental therapy, SGT-001, the patient experienced kidney injury and drops in red blood cell count, leading the US Food and Drug Administration (FDA) to place the study on hold. “We are encouraged that this patient is recovering,” Ilan Ganot, Solid Biosciences’s CEO, president, and cofounder, says in a statement. “In the coming weeks, we anticipate that we will have a better understanding of the biological activity and potential benefit of SGT-001. We look forward to sharing this additional data and working with the FDA to resolve the clinical hold and determining next steps for the program.” SGT-001 has been administered to six people so far, and involves the transfer of an engineered version of the dystrophin gene DMD, which is dysfunctional in people with Duchenne muscular dystrophy, using an adeno-associated virus (AAV) as a vector. Sarepta Therapeutics, Pfizer, and other biopharmaceutical companies are investigating similar approaches to treat the condition, although the choice of AAV varies. See “Positive Trial Results for Experimental DMD Gene Therapy” This isn’t the first time Solid Biosciences’s trial of SGT-001 has been put on hold. Early last year, the FDA halted the same study after a patient receiving a low dose of the therapy experienced a drop in red blood cell count and had to be hospitalized. The company was allowed to resume the trial last June after making changes to the study design. © 1986–2019 The Scientist

Keyword: Movement Disorders; Muscles
Link ID: 26816 - Posted: 11.14.2019

Nicole Ireland · Recent video from Thailand showing paralyzed Humboldt Broncos hockey player Ryan Straschnitzki moving his legs after an electrical stimulation device was surgically implanted in his spine has sparked excitement — as well as questions — about therapies available to Canadians with spinal injuries. The procedure Straschnitzki, 20, had is called epidural stimulation, and although promising, it's still highly experimental, experts in both Canada and the U.S. say. It's in early stages of clinical trials in the U.S. and Europe to evaluate the safety and effectiveness of restoring physical abilities — from bowel and bladder function to moving arms and legs — to people who desperately want to get some normalcy back after spinal injury. Barry Munro understands all too well why people's immediate reaction is to ask why they can't try the procedure here in Canada. He's been hoping for — and working toward — finding a cure for spinal cord injury ever since he dove into a lake in his 20s and was left quadriplegic. Now 55, Munro is chief development officer for the Canadian Spinal Research Organization and works with the North American Spinal Injury Consortium. For more than 30 years, he's seen the headlines come and go, inciting hope that a cure is on the horizon. "I've been down this road before," Munro told CBC News. "I really, really believe in finding a cure and believe it will happen and I have that hope. But — there's a big but — we have to be careful." Milos Popovich, director of the KITE Research Institute at the University Health Network's Toronto Rehabilitation Institute, echoes that need to proceed with caution. He said that epidural stimulation must proceed through many more stages of scientifically sound clinical trials to prove it works before it could be made available as a therapy in Canada. ©2019 CBC/Radio-Canada.

Keyword: Regeneration; Movement Disorders
Link ID: 26810 - Posted: 11.11.2019

By Tina Hesman Saey A newly discovered type of mitochondrial self-destruction may make some brain cells vulnerable to ALS, also known as Lou Gehrig’s disease. In mice genetically engineered to develop some forms of a degenerative nerve disease similar to amyotrophic lateral sclerosis, energy-generating organelles called mitochondria appear to dismantle themselves without help from usual cell demolition crews. This type of power plant self-destruction was spotted in upper motor neurons, brain nerve cells that help initiate and control movements, but not in neighboring cells, researchers report November 7 in Frontiers in Cellular Neuroscience. Death of those upper motor neurons is a hallmark of ALS, and the self-destructing mitochondria may be an early step that sets those cells up to die later. Pembe Hande Özdinler, a cellular neuroscientist at Northwestern University Feinberg School of Medicine in Chicago, and her colleagues have dubbed the mitochondrial dissolution “mitoautophagy.” It is a distinct process from mitophagy, the usual way that cellular structures called autophagosomes and lysosomes remove damaged mitochondria from the cell, Özdinler says. Usually, clearing out old or damaged mitochondria is important for cells to stay healthy. When mitochondria sustain too much damage, they may trigger the programmed death of the entire cell, known as apoptosis (SN: 8/9/18). Özdinler’s team spotted what she describes as “awkward” mitochondria in electron microscope images of upper motor neurons from 15-day-old mice. These unweaned mice are equivalent to human teenagers, Özdinler says. ALS typically doesn’t strike until people are 40 to 70 years old. But by the time symptoms appear, motor neurons are already damaged, so Özdinler’s group looked at the young mice to capture the earliest signs of the disease. © Society for Science & the Public 2000–2019

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26804 - Posted: 11.08.2019

Maheen Mausoof Adamson, Ph.D. The 1982 science fiction film classic Blade Runner is a gritty detective story set in the dystopian future that raises questions about what it means to be human. In the film, Harrison Ford plays Rick Deckard, a police officer turned bounty hunter searching the streets of Los Angeles for a replicant (human-like androids) rebellion leader Roy Batty. Batty is presented as a technologically perfected being fitted with a human-template brain completely rewired to create an enemy to be deathly feared. Fear of the perfect altered brain is prominent in science fiction—and may be particularly prevalent today, amid growing concerns about genetic editing and artificial intelligence. The prospect of a fully artificial human brain remains very distant. However, we are in the midst of a neuromodulation revolution that will increase our ability to treat disease and optimize human performance. We must, however, carefully consider the benefits and risks of these techniques in fully evaluating their potential for society as well as the individual. A large number of patients suffering from neurological or psychiatric disorders—depression, pain, and post-traumatic stress disorder among them—are resistant to or can develop resistance to standard medication and psychotherapy, suggesting the need for new approaches. Neuromodulation may possibly be such an approach. The term (aka neurostimulation) refers to direct stimulation and modification of the nervous system through the use of electrical, chemical, or mechanical signals. Neuromodulation therapy is already used to treat many brain disorders, most commonly movement disorders, chronic pain, and depression. © 2019 The Dana Foundation.

Keyword: Parkinsons; Depression
Link ID: 26797 - Posted: 11.07.2019

By Gretchen Reynolds Being physically fit may sharpen the memory and lower our risk of dementia, even if we do not start exercising until we are middle-aged or older, according to two stirring new studies of the interplay between exercise, aging, aerobic fitness and forgetting. But both studies, while underscoring the importance of activity for brain health, also suggest that some types of exercise may be better than others at safeguarding and even enhancing our memory. The scientific evidence linking exercise, fitness and brain health is already hefty and growing. Multiple studies have found that people with relatively high levels of endurance, whatever their age, tend to perform better on tests of thinking and memory than people who are out of shape. Other studies associate better fitness with less risk for developing Alzheimer’s disease. But many of these studies have been one-time snapshots of people’s lives and did not delve into whether and how changing fitness over time might alter people’s memory skills or dementia risk. They did not, in other words, tell us whether, by midlife or retirement age, it might be too late to improve our brain health with exercise. So, for the first of the new studies, which was published this month in The Lancet Public Health, researchers at the Norwegian University of Science and Technology in Trondheim, Norway, helpfully decided to look into that very issue, taking advantage of the reams of health data available on average Norwegians. They began by turning to records from a large-scale health study that had enrolled almost every adult resident in the region around Trondheim beginning in the 1980s. The participants completed health and medical testing twice, about 10 years apart, that included estimates of their aerobic fitness. © 2019 The New York Times Company

Keyword: Alzheimers
Link ID: 26794 - Posted: 11.06.2019

By Gretchen Reynolds Taking more steps during the day may be related to better sleep at night, according to an encouraging new study of lifestyle and sleep patterns. The study, which delved into the links between walking and snoozing, suggests that being active can influence how well we sleep, whether we actually exercise or not. Sleep and exercise scientists have long been intrigued and befuddled by the ties between physical activity and somnolence. To most of us, it might seem as if that relationship should be uncomplicated, advantageous and one-way. You work out, grow tired and sleep better that night. But a variety of past studies indicate that the effects of exercise on sleep are more scrambled than that. In some studies, when people work out strenuously, they sleep relatively poorly, suggesting that intense exercise might disrupt slumber. Other experiments have found that the impacts of exertion and sleep work both ways; after a night of ragged sleep, people often report finding their normal workout extra wearing. Past research also has produced conflicting results about whether and how the timing of exercise matters, and if afternoon workouts aid or impair that night’s sleep. Most of these past studies have focused on planned exercise, though, not more incidental, everyday physical activity, and much of the research has involved people with clinical sleep problems, such as insomnia. Little has been known about whether simply moving around more during the day, absent formal exercise, might influence sleep, particularly in people who already tend to sleep fairly well. © 2019 The New York Times Company

Keyword: Sleep
Link ID: 26771 - Posted: 10.30.2019

By Robert Martone We humans have evolved a rich repertoire of communication, from gesture to sophisticated languages. All of these forms of communication link otherwise separate individuals in such a way that they can share and express their singular experiences and work together collaboratively. In a new study, technology replaces language as a means of communicating by directly linking the activity of human brains. Electrical activity from the brains of a pair of human subjects was transmitted to the brain of a third individual in the form of magnetic signals, which conveyed an instruction to perform a task in a particular manner. This study opens the door to extraordinary new means of human collaboration while, at the same time, blurring fundamental notions about individual identity and autonomy in disconcerting ways. Direct brain-to-brain communication has been a subject of intense interest for many years, driven by motives as diverse as futurist enthusiasm and military exigency. In his book Beyond Boundaries one of the leaders in the field, Miguel Nicolelis, described the merging of human brain activity as the future of humanity, the next stage in our species’ evolution. (Nicolelis serves on Scientific American’s board of advisers.) He has already conducted a study in which he linked together the brains of several rats using complex implanted electrodes known as brain-to-brain interfaces. Nicolelis and his co-authors described this achievement as the first “organic computer” with living brains tethered together as if they were so many microprocessors. The animals in this network learned to synchronize the electrical activity of their nerve cells to the same extent as those in a single brain. The networked brains were tested for things such as their ability to discriminate between two different patterns of electrical stimuli, and they routinely outperformed individual animals. © 2019 Scientific American

Keyword: Robotics; Language
Link ID: 26770 - Posted: 10.30.2019

By Maya Vijayaraghavan On Jan. 1, my husband asked me whether he would die that year. I said no. It happened to be my birthday, and I wanted to feel jubilant despite the tragic turn of events in our life. I thought Rahul might have another year, that he might beat the odds of dying this year. In other words, his hazard ratio was favorable compared with someone else in his situation. He liked talking about something related, hazard scores — a composite score of one’s genetic risk for a particular outcome such as diagnosis of a disease. It was his thing as a neuroscientist-physician. He developed one for Alzheimer’s disease, and was on his way to developing one for amyotrophic lateral sclerosis (ALS), the disease he had been studying even before he got sick with it. In reality, he had declined significantly since his diagnosis of ALS two years prior. First, he lost his speech, then his mobility, and very quickly breathing became a struggle. But any talk of decline came with an acceptance that his life was imminently finite, and neither of us were willing to accept that outcome. But Rahul did die, six months after that conversation. I remember some of our last conversations, when things were very difficult. His forewarning that this existence with him teetering at the brink of life and death was much easier than the life I would lead as a widow, raising two young children. I think neither of us really understood that the emptiness I’d feel would be soul-crushing. That I would cry all the time. That I would miss him so much. That I would become a ghost of my former self. That this thing they call complicated grief, in which healing doesn’t occur as it’s supposed to, and which supposedly happens only after a year, is something that I feel now. That I would think constantly about the time when my husband was first diagnosed and he got into a fight with our then-3-year-old (now 5) about how he could not carry him because he did not have the strength to and not because he did not want to.

Keyword: ALS-Lou Gehrig's Disease
Link ID: 26761 - Posted: 10.28.2019

By Owain Clarke BBC Wales health correspondent World-leading research is helping scientists find new ways of trying to help younger people who have had a stroke get back to work. The study led by Manchester Metropolitan University found the speed a patient can walk is a major factor in determining how likely they are able to return to the workplace. Researchers have been working with physiotherapists and patients in Wales. It includes moving rehabilitation outdoors, including the Brecon Beacons. It is hoped it could lead to new rehabilitation methods being developed to target younger stroke patients. The average age to have a stroke in the UK is 72 for men and 78 for women. But there has been a 40% worldwide rise in people under 65 who have strokes in the last decade, according to the researchers. Image copyright Manchester Metropolitan University Image caption Researchers are studying the skeletons of stroke patients to see how joints perform when they walk What does the science say? It looked at 46 patients across Wales who had a stroke when younger than 65 years old and only 23% were able to return to work It found walking speed was a key predictor of whether a younger adult who has had a stroke could return to work They calculated a walking speed threshold of 0.93m/s (3ft a second) was a good benchmark for the likelihood of returning to work - and as a result this could be a goal set during rehabilitation As well as looking at the best environment for younger patients to recover in, it is now looking at using CGI technology to study joints to find out how stroke patients walk Nikki Tomkinson had a stroke at 53. "The world started shifting" while she was out driving in Cardiff. © 2019 BBC

Keyword: Stroke
Link ID: 26759 - Posted: 10.28.2019

By Kelly Servick CHICAGO, ILLINOIS—By harnessing the power of imagination, researchers have nearly doubled the speed at which completely paralyzed patients may be able to communicate with the outside world. People who are “locked in”—fully paralyzed by stroke or neurological disease—have trouble trying to communicate even a single sentence. Electrodes implanted in a part of the brain involved in motion have allowed some paralyzed patients to move a cursor and select onscreen letters with their thoughts. Users have typed up to 39 characters per minute, but that’s still about three times slower than natural handwriting. In the new experiments, a volunteer paralyzed from the neck down instead imagined moving his arm to write each letter of the alphabet. That brain activity helped train a computer model known as a neural network to interpret the commands, tracing the intended trajectory of his imagined pen tip to create letters (above). Eventually, the computer could read out the volunteer’s imagined sentences with roughly 95% accuracy at a speed of about 66 characters per minute, the team reported here this week at the annual meeting of the Society for Neuroscience. The researchers expect the speed to increase with more practice. As they refine the technology, they will also use their neural recordings to better understand how the brain plans and orchestrates fine motor movements. © 2019 American Association for the Advancement of Science.

Keyword: Robotics; Brain imaging
Link ID: 26745 - Posted: 10.24.2019

Anna Azvolinsky Nearly 30 years ago, Kamran Khodakhah, now a neuroscientist at Albert Einstein College of Medicine, signed up for a TV repair course that met several times a week at night at a local community college in London. While many of the other students were attending with the obvious goal of repairing TVs and other appliances, Khodakhah had a different aim. He reasoned that if he could understand how a television worked, he could design new tools to study the rat brain slices he had collected. Khodakhah was working as a PhD student in the lab of neuroscientist David Ogden at the National Institute for Medical Research, trying to determine whether a particular signaling pathway—the inositol trisphosphate (InsP3)/calcium signaling pathway—could be activated in nerve cells called Purkinje neurons. They are found in the cerebellum and have a high density of InsP3 receptors. By taking the TV repair class, Khodakhah wanted to learn to build an electronic circuit to enhance his camera images in order to better visualize the Purkinje cells within slices of the cerebellum and to study the InsP3/calcium ion signaling pathway. He used the new imaging setup, combined with existing lab tools such as flash photolysis, to introduce inert precursor molecules of InsP3—called caged InsP3—into Purkinje neurons in cerebellar slices prepared from rat brains. When stimulated with light, a caged InsP3 molecule is rapidly converted into an active form that binds to InsP3 receptors. Khodakhah then used a fluorescent calcium indicator and recorded the calcium channel activity to see if the binding of InsP3 receptors caused release of calcium from internal stores. At the time, researchers knew that in liver and other non-neuronal cells, InsP3 molecules act as messengers, stimulating the release of calcium ions, which then activates internal cellular pathways. Whether something similar happened in Purkinje neurons wasn’t clear, but if it did, the process might reveal something about how the cerebellum coordinates movement, Khodakhah thought. © 1986–2019 The Scientist.

Keyword: Movement Disorders
Link ID: 26736 - Posted: 10.23.2019

By Pam Belluck About 10 days after what seemed like a garden-variety cold, Luca Waugh, a healthy 4-year-old, developed troubling symptoms. Suddenly, his neck became so weak that he fell backward. Then his right arm couldn’t move. Within days, recalled his mother, Dr. Riley Bove, he developed “head-to-toe paralysis, where he could kind of move his eyes a little bit and one side of his face.” Doctors diagnosed Luca with acute flaccid myelitis or A.F.M., a mysterious neurological condition that can cause limb weakness and polio-like paralysis, mostly in young children. A.F.M. is rare, but in 2014, when Luca became afflicted, health authorities identified a burst of 120 cases. Since then, A.F.M. has made headlines as cases have spiked every two years, and nearly 600 have been confirmed across the country since 2014. What exactly causes A.F.M. has eluded experts, frustrating attempts to prevent or treat it. Now, a study by a team that includes Luca’s mother, Dr. Bove, who happens to be a neurologist, provides strong evidence of a likely cause. It involved dozens of children with A.F.M., including Luca, whose paralysis improved after weeks of hospitalization but who remains disabled five years later. The research, published Monday in the journal Nature Medicine, points to a long-suspected culprit: enteroviruses, a group of common viruses that usually produce mild effects, but can sometimes cause neurological symptoms. Using sophisticated laboratory techniques, researchers found antibodies to enteroviruses in the cerebrospinal fluid of nearly 70 percent of the children with A.F.M., a sign their bodies had mobilized to defend against enterovirus infection. © 2019 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 26734 - Posted: 10.22.2019

Allison Aubrey The condition strikes young children. It can start with run-of-the-mill virus symptoms, like fever or sniffles. But, then the kids lose control of their limbs, may have trouble swallowing or breathing, or even end up paralyzed. This terrifying experience happened to more than 570 families since 2014, whose children were struck with an illness called acute flaccid myelitis, or AFM. "It was really scary," says Susan Coyne, the mother of a son, Evan Mazanec, who developed AFM back in 2014 when he was 7 years old. "When this first started, no one really knew what it was," she says. It came on quickly, starting with a fever and an ear infection. Coyne says the limb weakness and paralysis began several days later — just as Evan was getting over the fever. He lost control of his arms and legs. "He couldn't move them, he couldn't lift them, he couldn't walk," Coyne says. He spent a year and a half in intensive rehab. He had to learn to walk and move his arms again. "It set him back years," Coyne says. Scientists have struggled to understand what causes this rare childhood disease. Now, one theory is gaining ground. A paper published Monday in the journal Pediatrics finds the condition may be triggered by a virus. The disease follows a pattern: Scientists have documented outbreaks every other year, beginning in 2014, and again in 2016 and 2018. Last year, there were 233 cases in the U.S. It strikes young kids, average age of 6. And, it can lead to long-term paralysis. © 2019 npr

Keyword: Movement Disorders; Development of the Brain
Link ID: 26684 - Posted: 10.09.2019

By Jason Gutierrez MANILA — President Rodrigo Duterte of the Philippines has revealed that he has a neuromuscular disease that has led to a slew of medical problems, including making his eye droop. Mr. Duterte, who was in Russia for a state visit, told the Filipino community there on Saturday night that he has myasthenia gravis, a chronic autoimmune disease that leads to skeletal muscle weakness. He said the disease ran in his family. The revelation came amid continued public speculation about his health. There have been periods when the famously bombastic president has been out of the public eye for days, prompting headlines guessing about his whereabouts, and even rumors of his death. But his communications officers have said that Mr. Duterte, 74, like any other older person, needs his own personal time. The president revealed the ailment after he apparently made a joke about not being able to look straight at a woman with whom he had danced a duet during the event in Moscow. “I have a talent,” Mr. Duterte said, according to official transcripts provided by his office afterward. “When I look at you, my other eye droops. Do you see? The other eye is smaller. It goes where it wants.” He added: “Actually, that’s myasthenia gravis. It’s a nerve malfunction.” Mr. Duterte said his grandfather had also had the disease, adding, “So I believe, really, in genetics.” The disease often affects the muscles that control the eyes, facial expression, speaking and swallowing, according to the Philippine Medical Association. Mr. Duterte came to power in 2016 vowing to rid the country of drug dealers and to wipe out other crimes. Since then, the Philippines’ war on drugs has led to thousands of killings allegedly by the police and vigilantes, which rights groups have denounced as an atrocity. © 2019 The New York Times Company

Keyword: Movement Disorders; Neuroimmunology
Link ID: 26676 - Posted: 10.07.2019

By James Gallagher Health and science correspondent A man has been able to move all four of his paralysed limbs with a mind-controlled exoskeleton suit, French researchers report. Thibault, 30, said taking his first steps in the suit felt like being the "first man on the Moon". His movements, particularly walking, are far from perfect and the robo-suit is being used only in the lab. But researchers say the approach could one day improve patients' quality of life. And he can control each of the arms, manoeuvring them in three-dimensional space How easy was it to use? Thibault, who does not want his surname revealed, was an optician before he fell 15m in an incident at a night club four years ago. The injury to his spinal cord left him paralysed and he spent the next two years in hospital. But in 2017, he took part in the exoskeleton trial with Clinatec and the University of Grenoble. Initially he practised using the brain implants to control a virtual character, or avatar, in a computer game, then he moved on to walking in the suit. "It was like [being the] first man on the Moon. I didn't walk for two years. I forgot what it is to stand, I forgot I was taller than a lot of people in the room," he said. It took a lot longer to learn how to control the arms. © 2019 BBC.

Keyword: Robotics
Link ID: 26670 - Posted: 10.04.2019

Ashley Yeager During her time as a postdoc at the University of Basel in Switzerland, Sarah Shahmoradian decided to study the abnormal aggregates of protein that develop inside nerve cells and contribute to Parkinson’s disease. The protein clumps develop over time in the brains of Parkinson’s patients, leading some scientists to think they wreak havoc on nerve cells, causing severe damage and hastening their death. A fresh look at the clumps, called Lewy bodies, with cutting-edge microscopy tools could reveal insights that might lead to new treatments for Parkinson’s, Shahmoradian recalls thinking. “The original goal was to really find out what the building blocks of Lewy bodies are, what they are made of, and what they actually look like.” The clumps were first identified in the early 1900s, appearing as abnormal material in nerve cells viewed under a microscope. Additional studies using antibodies that bound to various proteins revealed that the clumps contained a protein called α-synuclein, and after more work probing Lewy bodies, scientists developed a rough sketch of their structure—essentially, a dense mass surrounded by a halo of twisted filaments of α-synuclein. It’s these filaments, known as fibrils, that Shahmoradian and her colleagues were most interested to analyze in postmortem human brains. Fibrils had been repeatedly produced in cultured cells and in animal models, but no one had ever gotten a clear view of them in human brain tissue. “We were originally looking for fibrils,” Shahmoradian says, “but unexpectedly, we found an abundance of . . . mitochondria, other organelles, and lipid membranes [in the Lewy bodies].” The researchers also found evidence of lysosomes, organelles that facilitate cellular waste removal. They did see α-synuclein in the Lewy bodies, as well, but the cores of the structures weren’t composed of twisted and tangled fibrils as researchers had thought. Instead, the protein was intermingled with other cellular material. © 1986–2019 The Scientist

Keyword: Parkinsons
Link ID: 26669 - Posted: 10.03.2019

By Gretchen Reynolds Physically fit young adults have healthier white matter in their brains and better thinking skills than young people who are out of shape, according to a large-scale new study of the links between aerobic fitness and brain health. The findings suggest that even when people are youthful and presumably at the peak of their mental prowess, fitness — or the lack of it — may influence how well their brains and minds work. We already have plenty of tantalizing evidence that aerobic fitness can beneficently shape our brains and cognition. In animal experiments, mice and rats that run on wheels or treadmills produce far more new neurons in their brains than sedentary animals and perform better on tests of rodent intelligence and memory. Similarly, studies involving people show strong relationships between being physically active or fit and having greater brain volume and stronger thinking abilities than people with low fitness or who rarely exercise. But most of these past studies focused on middle-aged or older adults, whose brains often are starting to sputter and contract with age. For them, fitness and exercise are believed to help slow any decline, keeping brain tissue and function relatively youthful. Much less has been known about whether fitness likewise might be related to the structure and function of healthy, younger people’s brains. So, for the new study, which was published last month in Scientific Reports, scientists at the University of Münster in Germany decided to look inside the skulls of a large group of young adults. They began by turning to a hefty trove of data gathered as part of the Human Connectome Project, an international collaborative effort that aims to help map much of the human brain and tease out how it works. © 2019 The New York Times Company

Keyword: Development of the Brain
Link ID: 26662 - Posted: 10.02.2019

By Dean McLaughlin BBC News NI A Londonderry man who was diagnosed with Parkinson's at the age of 30 says more young people need to be aware of the disease. Ronan Coyle first noticed the symptoms at 24 but only found out what the problem was six years later. "People think I'm drunk when I walk down the street," he told BBC Radio Foyle. Now 37, Ronan plays golf and squash and likes to swim to take his mind off the disease. A spokesperson for Parkinson's UK said playing sport "helps ease the mind". Parkinson's is thought to be linked to a chemical called dopamine, which is lacking in the brains of people with the condition. There are more than 40 symptoms and these can include vomiting as the body struggles to process food in the gut. Parkinson's can also affect people's mood. Often a person will feel they have got to grips with their condition and then a new symptom will emerge. It was while studying for his Irish history and politics degree that Ronan first noticed the symptoms. "I was writing notes for an essay and I couldn't write properly," he said. "Come exam time, I was under a lot of stress. It got really bad. "Then I noticed my walking was funny. I went to a couple of neurologists and they more or less said you have a tremor and that it was nothing to worry about." When Ronan turned 30 he was referred to a neurologist in Belfast. After a number of scans it was confirmed that he had the disease. © 2019 BBC

Keyword: Parkinsons
Link ID: 26658 - Posted: 10.01.2019

Jon Hamilton Too much physical exertion appears to make the brain tired. That's the conclusion of a study of triathletes published Thursday in the journal Current Biology. Researchers found that after several weeks of overtraining, athletes became more likely to choose immediate gratification over long-term rewards. At the same time, brain scans showed the athletes had decreased activity in an area of the brain involved in decision-making. The finding could explain why some elite athletes see their performance decline when they work out too much — a phenomenon known as overtraining syndrome. The distance runner Alberto Salazar, for example, experienced a mysterious decline after winning the New York Marathon three times and the Boston Marathon once in the early 1980s. Salazar's times fell off even though he was still in his mid-20s and training more than ever. "Probably [it was] something linked to his brain and his cognitive capacities," says Bastien Blain, an author of the study and a postdoctoral fellow at University College London. (Salazar didn't respond to an interview request for this story.) Blain was part of a team that studied 37 male triathletes who volunteered to take part in a special training program. "They were strongly motivated to be part of this program, at least at the beginning," Blain says. Half of the triathletes were instructed to continue their usual workouts. The rest were told to increase their weekly training by 40%. The result was a training program so intense that these athletes began to perform worse on tests of maximal output. After three weeks, all the participants were put in a brain scanner and asked a series of questions designed to reveal whether a person is more inclined to choose immediate gratification or a long-term reward. "For example, we ask, 'Do you prefer $10 now or $60 in six months,' " Blain says. © 2019 npr

Keyword: Attention
Link ID: 26656 - Posted: 09.28.2019