Chapter 11. Motor Control and Plasticity

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By Gretchen Reynolds Sitting for hours without moving can slow the flow of blood to our brains, according to a cautionary new study of office workers, a finding that could have implications for long-term brain health. But getting up and strolling for just two minutes every half-hour seems to stave off this decline in brain blood flow and may even increase it. Delivering blood to our brains is one of those automatic internal processes that most of us seldom consider, although it is essential for life and cognition. Brain cells need the oxygen and nutrients that blood contains, and several large arteries constantly shuttle blood up to our skulls. Because this flow is so necessary, the brain tightly regulates it, tracking a variety of physiological signals, including the levels of carbon dioxide in our blood, to keep the flow rate within a very narrow range. But small fluctuations do occur, both sudden and lingering, and may have repercussions. Past studies in people and animals indicate that slight, short-term drops in brain blood flow can temporarily cloud thinking and memory, while longer-term declines are linked to higher risks for some neurodegenerative diseases, including dementia. Other research has shown that uninterrupted sitting dampens blood flow to various parts of the body. Most of those studies looked at the legs, which are affected the most by our postures, upright or not. Stay seated for several hours, and blood flow within the many blood vessels of the legs can slacken. Whether a similar decline might occur in the arteries carrying blood to our brains was not known, however. So for the new study, which was published in June in the Journal of Applied Physiology, researchers at Liverpool John Moores University in England gathered 15 healthy, adult, male and female office workers. © 2018 The New York Times Company

Keyword: Alzheimers
Link ID: 25338 - Posted: 08.16.2018

Michaeleen Doucleff My back hurts when I sit down. It's been going on for 10 years. It really doesn't matter where I am — at work, at a restaurant, even on our couch at home. My lower back screams, "Stop sitting!" To try to reduce the pain, I bought a kneeling chair at work. Then I got a standing desk. Then I went back to a regular chair because standing became painful. I've seen physical therapists, orthopedic surgeons and pain specialists. I've mastered Pilates, increased flexibility and strengthened muscles. At one point, my abs were so strong my husband nicknamed them "the plate." All these treatments helped a bit, at first. But the pain never really went away. So a few years ago, I decided to accept reality: Sitting down is — and will always be — painful for me. Then back in November, I walked into the studio of Jenn Sherer in Palo Alto, Calif. She is part of a growing movement on the West Coast to teach people to move and sit and stand as they did in the past — and as they still do in other parts of the world. I was interviewing Sherer for a story about bending. But she could tell I was in pain. So I told her my story. Her response left me speechless: "Sitting is a place where you can find heaven in your joints and in your back," she says. "It's not sitting that's causing the pain, it's how you're sitting. "Do you want me to show you how?" © 2018 npr

Keyword: Pain & Touch
Link ID: 25322 - Posted: 08.13.2018

Alison Abbott The two major neuroscience societies in the United States and Europe have joined forces to criticize the prestigious Max Planck Society (MPS) in Germany for its treatment of a world-renowned neuroscientist targeted by animal-rights activists. Nikos Logothetis, a director at the Max Planck Institute for Biological Cybernetics (MPI-Biocyb) in Tübingen who used to run a primate laboratory, has been charged with mistreatment of animals after allegations made by animal-rights groups. When Logothetis was indicted in February, the MPS removed many of his responsibilities relating to animal research — despite the fact that a court has not yet ruled on those charges. Logothetis, who studies how the brain makes sense of the world, denies the allegations. In a strongly worded statement posted online on 3 August, the US Society for Neuroscience (SfN) and the Federation of European Neuroscience Societies (FENS), which together represent more than 60,000 scientists, add to an outcry that has been gathering momentum since scientists at MPI-Biocyb made their concerns public in May. “FENS and SfN are extremely dismayed by the treatment of Professor Nikos Logothetis and his colleagues,” reads the joint statement. The MPS's actions set "an alarming precedent whereby institutions neglect to support affiliated scientists facing similar unproven accusations and disregard the presumption of innocence”, adds the statement. © 2018 Springer Nature Limited

Keyword: Animal Rights
Link ID: 25309 - Posted: 08.08.2018

By Emily Willingham Celebrity plays a role in increasing public awareness of Parkinson’s disease—and drums up funding. A foundation named after actor Michael J. Fox is the largest nonprofit funder of Parkinson’s research. Another actor, Alan Alda, generated global news coverage with his recent announcement that he received a diagnosis more than three years ago. Tech titan Sergey Brin carries a version of a gene that greatly increases risk for Parkinson’s (PD), but the gene has an unwieldy name that few would otherwise recognize. These high-profile associations call attention to PD and its causes, including mutations like the one Brin carries. A handful of gene mutations are linked to inherited PD, but they account for less than 15 percent of the one million U.S. cases and the five million worldwide. The most common of these is a mutated version of leucine-rich repeat kinase 2 (LRRK2), the one Brin carries. It is responsible for one to two percent of PD cases, but the percentage is much higher in certain groups, including those with Ashkenazi Jewish or Basque ancestry. LRRK2 has drawn the interest of pharmaceutical companies because it is an accessible drug target. The gene encodes a namesake protein that functions as a a type of enzyme called a kinase. The LRRK2 protein attaches chemical tags called phosphates to other proteins. Like a molecular switch, these phosphate tags activate or silence LRRK2’s targets. Dozens of drugs that inhibit the activity of kinases have been approved in the last 30 years, primarily for cancer. © 2018 Scientific American

Keyword: Parkinsons
Link ID: 25301 - Posted: 08.07.2018

By Alex Marshall Alan Alda has been living with Parkinson’s disease for over three years, the actor revealed Tuesday in an appearance on CBS’s “This Morning.” “The reason I want to talk about it in public is that I was diagnosed three-and-a-half years ago, and I’ve had a full life since,” he said. “I thought it’s probably only a matter of time before somebody does a story about this from a sad point of view,” he added, pointing out that one of his thumbs had been twitching in recent TV appearances. “But that’s not where I am.” Parkinson’s is a movement disorder with symptoms that include muscle tremors and stiffness, poor balance and coordination. It affects over a million Americans, according to the American Parkinson Disease Association, including Michael J. Fox and the Rev. Jesse L. Jackson, the longtime civil rights leader. Mr. Alda, who made his name in the TV series “M*A*S*H,” said he went to the doctors after reading an article in The New York Times, by Jane E. Brody, which said that acting out one’s dreams could be an early warning sign of the disorder. “By acting out your dreams, I mean I was having a dream that somebody was attacking me and I threw a sack of potatoes at them,” Mr. Alda, 82, said in the interview. “But what I was really doing is throwing a pillow at my wife.” He said he had no other symptoms, but a few months later noticed a thumb twitch. Mr. Alda said he was also speaking out to reassure people that they do not have to be fearful after a diagnosis. “You still have things you can do,” he said. Mr. Alda goes boxing three times a week, plays tennis and marches to John Philip Sousa music. “Marching to march music is good for Parkinson’s,” he explained. Mr. Alda was not trying to belittle people who have severe symptoms, he added. “That’s difficult,” he said. © 2018 The New York Times Company

Keyword: Parkinsons; Sleep
Link ID: 25277 - Posted: 08.01.2018

By Dennis Normile Researchers in Japan today announced the launch of a clinical trial to treat Parkinson’s disease with neurological material derived from induced pluripotent stem (iPS) cells, mature cells chemically manipulated to return to an early stage of development from which they can theoretically differentiate into any of the body’s specialized cells. The study team will inject dopaminergic progenitors, a cell type that develops into neurons that produce dopamine, directly into a region of the brain known to play a key role in the neural degeneration associated with Parkinson’s disease. The effort is being led by Jun Takahashi, a neurosurgeon at Kyoto University's Center for iPS Cell Research and Application (CiRA), in cooperation with Kyoto University Hospital. Parkinson’s disease results from the death of specialized cells in the brain that produce the neurotransmitter dopamine. A lack of dopamine leads to a decline in motor skills, resulting in difficulty walking and involuntary trembling. As the disease progresses it can lead to dementia. The trial strategy is to derive dopaminergic progenitors from iPS cells and inject them into the putamen, a round structure located at the base of the forebrain. Surgeons will drill two small holes through a patient’s skull and use a specialized device to inject roughly 5 million cells. © 2018 American Association for the Advancement of Science.

Keyword: Parkinsons; Stem Cells
Link ID: 25275 - Posted: 07.31.2018

NIH-funded researchers delayed signs of amyotrophic lateral sclerosis (ALS) in rodents by injecting them with a second-generation drug designed to silence the gene, superoxide dismutase 1 (SOD1). The results, published in the Journal of Clinical Investigation, suggest the newer version of the drug may be effective at treating an inherited form of the disease caused by mutations in SOD1. Currently, the drug is being tested in an ALS clinical trial (NCT02623699). ALS destroys motor neurons responsible for activating muscles, causing patients to rapidly lose muscle strength and their ability to speak, swallow, move, and breathe. Most die within three to five years of symptom onset. Previous studies suggested that a gene therapy drug, called an antisense oligonucleotide, could be used to treat a form of ALS caused by mutations in the gene SOD1. These drugs turned off SOD1 by latching onto versions the gene encoded in messenger RNA (mRNA), tagging them for disposal and preventing SOD1 protein production. Using rats and mice genetically modified to carry normal or disease-mutant versions of human SOD1, a team of researchers led by Timothy M. Miller, M.D., Ph.D., Washington University, St. Louis, MO, discovered that newer versions of the drug may be more effective at treating ALS than the earlier one that had been tested in a phase 1 clinical trial. For instance, injections of the newer versions were more efficient at reducing normal, human SOD1 mRNA levels in rats and mice and they helped rats, genetically modified to carry a disease-causing mutation in SOD1, live much longer than previous versions of the drug. Injections of the new drugs also delayed the age at which mice carrying a disease-mutant SOD1 gene had trouble balancing on a rotating rod and appeared to prevent muscle weakness and loss of connections between nerves and muscles, suggesting it could treat the muscle activation problems caused by ALS. These and other results were the basis for a current phase 1 clinical trial testing the next generation drug in ALS patients (NCT02623699).

Keyword: ALS-Lou Gehrig's Disease
Link ID: 25261 - Posted: 07.27.2018

Mutations in the gene LRRK2 have been linked to about three percent of Parkinson’s disease cases. Researchers have now found evidence that the activity of LRRK2 protein might be affected in many more patients with Parkinson’s disease, even when the LRRK2 gene itself is not mutated. The study was published in Science Translational Medicine and was supported in part by the National Institute of Neurological Disorders and Stroke (NINDS), a part of the National Institutes of Health (NIH). “This is a striking finding that shows how normal LRRK2 may contribute to the development of Parkinson’s disease,” said Beth-Anne Sieber, Ph.D., program director at NINDS. “This study also identifies LRRK2 as an integral protein in the neurobiological pathways affected by the disease.” More than 10 years ago, researchers linked mutations in the LRRK2 gene with an increased risk for developing Parkinson’s disease. Those mutations produce a version of LRRK2 protein that behaves abnormally and is much more active than it would be normally. Despite its importance in Parkinson’s disease, the very small amount of normal LRRK2 protein in nerve cells has made it difficult to study. In the current study, the authors developed a new method for observing LRRK2 cells that makes them glow fluorescently only when LRRK2 is in its activated state. They have also used detection of fluorescent signals to demonstrate loss of binding of an inhibitor protein to LRRK2 when LRRK2 is activated.

Keyword: Parkinsons
Link ID: 25259 - Posted: 07.27.2018

By Perri Klass, M.D. You probably remember the before and after of learning to ride a bicycle — and perhaps the joy of helping your children learn how. Riding together is a wonderful family activity — good exercise, outdoor time, and it even gets you places. But safety is a vital part of what parents should be teaching. A recent study looked at bicycle-related injuries in children treated in emergency departments in the United States over a 10-year period from the beginning of 2006 through the end of 2017. Over that time, there were more than two million such injuries in children from 5 to 17, which the researchers calculated meant more than 600 a day, or 25 an hour. “That’s a lot,” said Lara McKenzie, principal investigator in the Center for Injury Research and Policy at Nationwide Children’s Hospital. Given the age of the most-injured group, 10 to 14, she said, “I feel this is a group where the parents might view the child as an experienced rider, but perhaps they’re riding in places they shouldn’t ride.” The study did not include fatalities, since it was looking only at children in the emergency room and excluded the 12 who actually died there. Of the injuries, 36 percent were to the upper extremities, 25 percent to the lower extremities, 15 percent to the face, and 15 percent to the head and neck. Many were related to falling off bikes, or crashing into something, Dr. McKenzie said, and when cars were involved, whether stationary or moving, the risk of traumatic brain injury (11 percent) and hospitalization (4 percent) increased. So safety first and foremost: wear helmets. In the new study, “helmet use at the time of injury was associated with lower risk of head and neck injury, and of hospitalization — that’s protective, we know,” Dr. McKenzie said. And it isn’t just about making your children wear helmets; when parents wear helmets, they are not only protecting themselves, but research has shown that when parents model the safe behavior, it’s more likely that children will be putting those helmets on themselves. Make sure the child is riding a bike the right size, and make sure the helmet fits correctly. © 2018 The New York Times Company

Keyword: Brain Injury/Concussion
Link ID: 25235 - Posted: 07.23.2018

by Lynn Peterson Mobley We started our ascent of Italy’s Stromboli volcano at dusk, as the Tyrrhenian Sea darkened behind us. It was a long, steady trek upward, but not an exhausting one. At the crater’s rim, with fountains and bombs of glowing lava exploding into the night sky, we soon forgot the effort it had taken to get there. Going down, however, was unforgettably harder. The trail through the deep black sand blanketing the massive cone was impossible to follow by the paltry light of our helmet lamps. I had never witnessed my athletic husband struggle before. He stumbled down the mountain for two hours with borrowed walking sticks, falling more than once. We had been hiking along the Volcano Route: Vesuvius, Amalfi’s Trail of the Gods, Vulcano, Etna. Robert was a fit 70-year-old then, never sick in his life. But after Stromboli, things weren’t quite the same. Back in Rome for a few days before our flight home, he was aware of weakness in his feet and lower legs. His shoes slapped the sidewalks as if they were too big. It took forever to get back to our hotel after a day of sightseeing. He was tired, yes, but this was different. Later that year, in 2010, he was diagnosed with a disease that we had never heard of, and that he shared with millions of other Americans: peripheral neuropathy, or PN. As we were to learn, the nervous system is composed of two parts. The brain and spinal cord make up the central nervous system, while the nerves running from them form the peripheral nervous system. PN encompasses damage to the nerves that deliver messages to or from the brain. Damage to the sensory nerves can mean tingling or numbness in the hands, feet and legs; damage to motor nerves that control the muscles causes loss of strength and balance; damage to the autonomic nervous system, which regulates automatic functions, affects things such as heart rate, blood pressure, bladder control and digestion, along with a host of other involuntary responses. © 1996-2018 The Washington Post

Keyword: Movement Disorders
Link ID: 25186 - Posted: 07.09.2018

By Denise Gellene Dr. Arvid Carlsson, a Swedish scientist whose discoveries about the brain led to the development of drugs for Parkinson’s disease and earned him a Nobel Prize, died on Friday. He was 95. His death was announced by the Sahlgrenska Academy at the University of Gothenburg, where he had been a professor of pharmacology. It did not say where he died. When Dr. Carlsson started his research in the 1950s, dopamine, a chemical in the brain, was thought to have little significance. Dr. Carlsson discovered that it was, in fact, an important neurotransmitter — a brain chemical that passes signals from one neuron to the next. He then found that dopamine was concentrated in the basal ganglia, the portion of the brain that controls movement. He showed that rabbits lost their ability to move after they were given a drug that lowered their dopamine stores; their mobility was restored after they received L-dopa, a drug that is converted into dopamine in the brain. Noting that the movement difficulties of his rabbits were similar to those of people with Parkinson’s disease, Dr. Carlsson proposed that the illness was related to a loss of dopamine. Other scientists confirmed that dopamine is depleted in people with Parkinson’s disease, a degenerative condition that causes tremors and rigidity, and L-dopa soon became the standard treatment for the illness. Dr. Carlsson shared the 2000 Nobel Prize in Physiology or Medicine with two American researchers, Dr. Eric Kandel and Paul Greengard, who made their own discoveries about the transmission of chemical signals in the brain. In awarding the Nobel, the Karolinska Institute of Sweden said the contributions of the three scientists were “crucial for an understanding of the normal function of the brain” and for how signal disturbances could “give rise to neurological and psychiatric disorders.” © 2018 The New York Times Company

Keyword: ADHD
Link ID: 25162 - Posted: 07.02.2018

By Meredith Wadman Roughly once a day in the United States, a child is born with a fatal genetic disorder that destroys motor neurons in the brain stem and spinal cord. In its worst and most common form, spinal muscular atrophy (SMA) kills children when they are still toddlers, as their respiratory muscles fail. But 18 months ago, the Food and Drug Administration approved a first, promising treatment: a drug that restores production of a key protein missing in SMA. Now, SMA advocacy groups and members of Congress are urging Secretary of Health and Human Services (HHS) Alex Azar to recommend that all 4 million infants born in the United States each year be tested for SMA. They argue that affected children should be identified and treated when the new drug likely helps the most—before neurons die. By law, Azar faces an 8 July deadline, but such deadlines have been missed in the past. And although an advisory panel voted in February in favor of screening all newborns, some of its experts dissented. They noted that key studies of the new treatment—a drug called nusinersen (marketed as Spinraza by Biogen of Cambridge, Massachusetts)—are still ongoing, involve small numbers of children, and are unpublished. But delay "would be a tragedy for children born in the interim who may benefit from screening because they will miss the window for receiving treatment when it is most effective," 14 members of the House of Representatives wrote to Azar last month, urging speedy approval. An HHS spokesperson says Azar is "still reviewing this important issue." © 2018 American Association for the Advancement of Science.

Keyword: Movement Disorders
Link ID: 25156 - Posted: 06.29.2018

By Catherine Offord An experimental gene therapy for Duchenne Muscular Dystrophy has showed better-than-expected results in a three-patient trial, according to preliminary data presented by Cambridge, Massachusetts–based biotech Sarepta Therapeutics on Tuesday (June 19). Company shares jumped 60 percent following the news that the treatment dramatically boosted levels of microdystrophin, a muscle-protecting protein designed by researchers, and reduced levels of an enzyme associated with the disease. “I have spent my life wanting to make a real change in this disease,” principal investigator Jerry Mendell of Nationwide Children’s Hospital in Columbus tells STAT News. “Finally, we may be there. I am very hopeful. This is an emotional time for people in the field.” Duchenne Muscular Dystrophy (DMD) is a rare genetic disorder caused by loss-of-function mutations in the dystrophin gene. An X-linked condition, the disease mostly affects boys, and usually manifests itself in the form of muscle weakness in children between the ages of 3 and 5. There is no cure for DMD, and although steroids can slow the progression of symptoms, the disease eventually causes life-threatening damage to the heart muscles. Few patients live beyond their 30s. The US Food and Drug Administration (FDA) approved the first drug for DMD, Sarepta’s oligonucleotide therapeutic Exondys 51 (eteplirsen), in 2016. But the therapy was only effective in around 15 percent of DMD patients—those with a specific genetic mutation—and produced just marginal improvements in dystrophin levels. More-recent, preclinical approaches are experimenting with CRISPR to correct DMD-causing point mutations. © 1986-2018 The Scientist

Keyword: Muscles; Genes & Behavior
Link ID: 25125 - Posted: 06.22.2018

By Sukanya Charuchandra Researchers in China have taken cell therapy for Parkinson’s disease one step further. In research published in Stem Cell Reports on June 14, scientists report improvements in the motor abilities of monkeys with Parkinsonian symptoms after grafting dopamine neurons derived from embryonic stem cells (ESCs) into their brains. The findings will serve as preclinical data for China’s first ESC-based clinical study for the neurological disease. “Since there are a number of therapies being developed, there is no overwhelming theoretical support for a particular cell type, and actually studying them in advanced animal models and then even in patients makes sense to determine what works best,” D. Eugene Redmond Jr., a psychiatrist and neurosurgeon at Yale Stem Cell Center who was not involved in the study, writes in an email to The Scientist. See “Parkinson’s Disease Cell Therapy Relieves Symptoms in Monkeys” Parkinson’s disease is a neurological condition that originates from the death of dopamine-producing cells in the brain. Since the early 1990s, groups around the world have been developing cell-replacement therapies to counteract this depletion, with recent efforts focusing on stem cells. Scientists have conducted rodent and primate research using dopamine-producing neurons derived from adult stem cells, ESCs, and induced pluripotent stem cells to treat Parkinson’s disease. © 1986-2018 The Scientist

Keyword: Parkinsons; Stem Cells
Link ID: 25117 - Posted: 06.22.2018

Ian Sample Science editor Rats with spinal cord injuries have regained the use of their paws after being given a groundbreaking gene therapy that helps to mend damaged nerves in the spine. The new therapy works by dissolving the dense scar tissue that forms a thick barrier between severed nerves when the spinal column is broken. Animals that were given the treatment produced an enzyme called chondroitinase which breaks down scar tissue and allows the broken nerves to reconnect with each other. Tests showed that when the therapy was given for two months, rats relearned the kinds of skilled movements they needed to grab little sugar balls from a platform. “The gene therapy has enabled us to treat large areas of the spinal cord with only one injection,” said Elizabeth Bradbury, who led the research at King’s College London. “This is important because the spinal cord is long and the pathology spreads down its whole length after injury.” While more animal studies are needed before the therapy can go into human trials, researchers hope that ultimately the treatment will help people with spinal injuries who have lost the ability to perform daily tasks, such as using a knife and fork, picking up a mug, and writing. © 2018 Guardian News and Media Limited

Keyword: Regeneration
Link ID: 25095 - Posted: 06.16.2018

By James Gallagher Health and science correspondent, BBC News Scientists say they have taken a significant step towards the goal of giving paralysed people control of their hands again. The team at King's College London used gene therapy to repair damage in the spinal cord of rats. The animals could then pick up and eat sugar cubes with their front paws. It is early stage research, but experts said it was some of the most compelling evidence that people's hand function could one day be restored. The spinal cord is a dense tube of nerves carrying instructions from the brain to the rest of the body. The body repairs a wounded spinal cord with scar tissue. However, the scar acts like a barrier to new connections forming between nerves. How the gene therapy works The researchers were trying to dissolve components of the scar tissue in the rats' spinal cord. They needed to give cells in the cord a new set of genetic instructions - a gene - for breaking down the scar. The instructions they gave were for an enzyme called chondroitinase. And they used a virus to deliver them. Finally, a drug was used to activate the instructions. The animals regained use of their front paws after the gene therapy had been switched on for two months. Dr Emily Burnside, one of the researchers, said: "The rats were able to accurately reach and grasp sugar pellets. "We also found a dramatic increase in activity in the spinal cord of the rats, suggesting that new connections had been made in the networks of nerve cells." The researchers hope their approach will work for people injured in car crashes or falls. © 2018 BBC.

Keyword: Regeneration
Link ID: 25092 - Posted: 06.15.2018

by Cleve R. Wootson Jr. Kailyn Griffin, 5, experienced temporary paralysis following a tick bite in Grenada, Miss., discovered on June 6. (WLBT) As soon as Kailyn Griffin's feet hit the floor Wednesday morning, she collapsed in a heap. The 5-year-old kept trying to stand but fell every time. She was also struggling to speak, said her mother, Jessica Griffin. Her daughter had been fine when the family went out to a T-ball game the night before, NBC-affiliate WLBT in Jackson, Miss., reported. Maybe Kailyn was having a hard time waking up Wednesday morning, or perhaps her legs were asleep. Then Griffin saw the tick. She had gathered Kailyn's hair to put it in a ponytail when she spotted the arachnid, embedded in the girl's scalp, swelled with the girl's blood. She pulled the tick out and placed it in a plastic bag, then rushed to the hospital with Kailyn, WTXL reported. Doctors told Griffin it was an uncommon condition called tick paralysis. “After tons of bloodwork and a CT of the head UMMC has ruled it as tick paralysis! PLEASE for the love of god check your kids for ticks! It’s more common in children than it is adults!” Griffin, of Grenada, Miss., wrote in a Facebook post Wednesday that seemed a mixture of worry and relief. “Scary is a UNDERSTATEMENT!” Griffin could not be immediately reached for comment. It was unclear where or when she thought her daughter had acquired the tick, or how long it had been on her body. Ticks are most active from April through September, The Washington Post has reported. Tick paralysis is caused by female ticks on the verge of laying eggs. After the tick eats a blood meal and is engorged, it secretes a neurotoxin into the host, according to the American Lyme disease Foundation. The symptoms can occur five to seven days after the tick starts feeding. © 1996-2018 The Washington Post

Keyword: Movement Disorders
Link ID: 25081 - Posted: 06.12.2018

By Ruth Williams Four patients with chronic spinal damage and a complete loss of motor and sensory functions below their waists have received transplants of human neural stem cells in a first-of-its-kind clinical trial. A report in Cell Stem Cell today (June 1) documents the procedure and the subsequent clinical follow up of the patients, who exhibit no signs of untoward effects but rather tiny hints of improvement. “It’s an extremely interesting and important piece of work,” says neurologist Eva Feldman of the University of Michigan who was not involved with the work. “The rodent model results were very compelling and . . . laid the groundwork for this very small, proof-of-concept safety trial.” While these results seem tantalizing, “the numbers [of patients] are extremely small,” says Feldman, and “the patients themselves notice no change in function or quality of life.” Severe spinal injuries can have devastating consequences, often leaving patients with complete paralysis below the injury site and with little hope of recovery. While there is currently no therapy that can promote neuronal repair in such patients, evidence from animal studies, including those carried out in primates, has indicated that transplantation of human-derived neural stem cells to the site of injury can promote some functional recovery of downstream musculature. © 1986-2018 The Scientist

Keyword: Regeneration; Stem Cells
Link ID: 25059 - Posted: 06.05.2018

By Robert F. Service Prosthetics may soon take on a whole new feel. That’s because researchers have created a new type of artificial nerve that can sense touch, process information, and communicate with other nerves much like those in our own bodies do. Future versions could add sensors to track changes in texture, position, and different types of pressure, leading to potentially dramatic improvements in how people with artificial limbs—and someday robots—sense and interact with their environments. “It’s a pretty nice advance,” says Robert Shepherd, an organic electronics expert at Cornell University. Not only are the soft, flexible, organic materials used to make the artificial nerve ideal for integrating with pliable human tissue, but they are also relatively cheap to manufacture in large arrays, Shepherd says. Modern prosthetics are already impressive: Some allow amputees to control arm movement with just their thoughts; others have pressure sensors in the fingertips that help wearers control their grip without the need to constantly monitor progress with their eyes. But our natural sense of touch is far more complex, integrating thousands of sensors that track different types of pressure, such as soft and forceful touch, along with the ability to sense heat and changes in position. This vast amount of information is ferried by a network that passes signals through local clusters of nerves to the spinal cord and ultimately the brain. Only when the signals combine to become strong enough do they make it up the next link in the chain. © 2018 American Association for the Advancement of Science.

Keyword: Robotics; Pain & Touch
Link ID: 25048 - Posted: 06.01.2018

Deep brain stimulation has been used to treat Parkinson’s disease symptoms for 25 years, but limitations have led researchers to look for ways to improve the technique. This study describes the first fully implanted DBS system that uses feedback from the brain itself to fine-tune its signaling. The study was supported by the National Institutes of Health’s Brain Research through Advancing Innovative Technologies (BRAIN) Initiative and the National Institute of Neurological Disorders and Stroke (NINDS). “The novel approach taken in this small-scale feasibility study may be an important first step in developing a more refined or personalized way for doctors to reduce the problems patients with Parkinson’s disease face every day,” said Nick B. Langhals, Ph.D., program director at NINDS and team lead for the BRAIN Initiative. Deep brain stimulation is a method of managing Parkinson’s disease symptoms by surgically implanting an electrode, a thin wire, into the brain. Traditional deep brain stimulation delivers constant stimulation to a part of the brain called the basal ganglia to help treat the symptoms of Parkinson’s. However, this approach can lead to unwanted side effects, requiring reprogramming by a trained clinician. The new method described in this study is adaptive, so that the stimulation delivered is responsive in real time to signals received from the patient’s brain. “This is the first time a fully implanted device has been used for closed-loop, adaptive deep brain stimulation in human Parkinson’s disease patients,” said Philip Starr, M.D., Ph.D., professor of neurological surgery, University of California, San Francisco, and senior author of the study, which was published in the Journal of Neural Engineering.

Keyword: Parkinsons
Link ID: 25034 - Posted: 05.30.2018