Chapter 11. Motor Control and Plasticity
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By Abby Phillip Jan Scheuermann, who has quadriplegia, brings a chocolate bar to her mouth using a robot arm guided by her thoughts. Research assistant Elke Brown watches in the background. (University of Pittsburgh Medical Center) Over at the Defense Advanced Research Projects Agency, also known as DARPA, there are some pretty amazing (and often top-secret) things going on. But one notable component of a DARPA project was revealed by a Defense Department official at a recent forum, and it is the stuff of science fiction movies. According to DARPA Director Arati Prabhakar, a paralyzed woman was successfully able use her thoughts to control an F-35 and a single-engine Cessna in a flight simulator. It's just the latest advance for one woman, 55-year-old Jan Scheuermann, who has been the subject of two years of groundbreaking neurosignaling research. First, Scheuermann began by controlling a robotic arm and accomplishing tasks such as feeding herself a bar of chocolate and giving high fives and thumbs ups. Then, researchers learned that -- surprisingly -- Scheuermann was able to control both right-hand and left-hand prosthetic arms with just the left motor cortex, which is typically responsible for controlling the right-hand side. After that, Scheuermann decided she was up for a new challenge, according to Prabhakar.
Link ID: 20647 - Posted: 03.04.2015
by Hal Hodson Video: Bionic arm trumps flesh after elective amputation Bionic hands are go. Three men with serious nerve damage had their hands amputated and replaced by prosthetic ones that they can control with their minds. The procedure, dubbed "bionic reconstruction", was carried out by Oskar Aszmann at the Medical University of Vienna, Austria. The men had all suffered accidents which damaged the brachial plexus – the bundle of nerve fibres that runs from the spine to the hand. Despite attempted repairs to those nerves, the arm and hand remained paralysed. "But still there are some nerve fibres present," says Aszmann. "The injury is so massive that there are only a few. This is just not enough to make the hand alive. They will never drive a hand, but they might drive a prosthetic hand." This approach works because the prosthetic hands come with their own power source. Aszmann's patients plug their hands in to charge every night. Relying on electricity from the grid to power the hand means all the muscles and nerves need do is send the right signals to a prosthetic. Before the operation, Aszmann's patients had to prepare their bodies and brains. First he transplanted leg muscle into their arms to boost the signal from the remaining nerve fibres. Three months later, after the nerves had grown into the new muscle, the men started training their brains. © Copyright Reed Business Information Ltd.
Link ID: 20617 - Posted: 02.26.2015
By Michelle Roberts Health editor, BBC News online Scientists have proposed a new idea for detecting brain conditions including Alzheimer's - a skin test. Their work, which is at an early stage, found the same abnormal proteins that accumulate in the brain in such disorders can also be found in skin. Early diagnosis is key to preventing the loss of brain tissue in dementia, which can go undetected for years. But experts said even more advanced tests, including ones of spinal fluid, were still not ready for clinic. If they were, then doctors could treatment at the earliest stages, before irreversible brain damage or mental decline has taken place. Brain biomarker Investigators have been hunting for suitable biomarkers in the body - molecules in blood or exhaled breath, for example, that can be measured to accurately and reliably signal if a disease or disorder is present. Dr Ildefonso Rodriguez-Leyva and colleagues from the University of San Luis Potosi, Mexico, believe skin is a good candidate for uncovering hidden brain disorders. Skin has the same origin as brain tissue in the developing embryo and might, therefore, be a good window to what's going on in the mind in later life - at least at a molecular level - they reasoned. Post-mortem studies of people with Parkinson's also reveal that the same protein deposits which occur in the brain with this condition also accumulate in the skin. To test if the same was true in life as after death, the researchers recruited 65 volunteers - 12 who were healthy controls and the remaining 53 who had either Parkinson's disease, Alzheimer's or another type of dementia. They took a small skin biopsy from behind the ear of each volunteer to test in their laboratory for any telltale signs of disease. Specifically, they looked for the presence of two proteins - tau and alpha-synuclein. © 2015 BBC.
By JON PALFREMAN EUGENE, Ore. — FOUR years ago, I was told I had Parkinson’s disease, a condition that affects about one million Americans. The disease is relentlessly progressive; often starting with a tremor in one limb on one side of the body, it spreads. The patient’s muscles become more rigid, frequently leading to a stooped posture, and movements slow down and get smaller and less fluid. As the disease advances — usually over a number of years — the patient becomes more and more disabled, experiencing symptoms from constipation to sleep disorders to cognitive impairment. Can Parkinson’s be slowed, stopped or even reversed? Can the disease be prevented before it starts, like polio and smallpox? More than at any time in history, success seems possible. Having sequenced the human genome, biomedical researchers have now set their sights on the ultimate frontier — the human brain. The formidable puzzle is to figure out how a three-pound lump of mostly fatty matter enables us to perform a seemingly endless number of tasks, like walking, seeing, hearing, smelling, tasting, touching, thinking, loving, hating, speaking and writing ... and why those awesome abilities break down with neurological disease. Many scientists view Parkinson’s as a so-called pathfinder. If they can figure out what causes Parkinson’s, it may open the door to understanding a host of other neurodegenerative diseases — and to making sense of an organ of incredible complexity. In Parkinson’s, the circuitry in a tiny region of the brain called the basal ganglia becomes dysfunctional. Along with the cerebellum, the basal ganglia normally acts as a kind of adviser that helps people learn adaptive skills by classic conditioning — rewarding good results with dopamine bursts and punishing errors by withholding the chemical. Babies rely on the basal ganglia to learn how to deploy their muscles to reach, grab, babble and crawl, and later to accomplish many complex tasks without thinking. For example, when a tennis player practices a stroke over and over again, the basal ganglia circuitry both rewards and “learns” the correct sequence of activities to produce, say, a good backhand drive automatically. © 2015 The New York Times Company
Link ID: 20606 - Posted: 02.24.2015
By Sandra G. Boodman Catherine Cutter’s voice was her livelihood. A professor of food science at Penn State University, the microbiologist routinely lectured to large classes about food safety in the meat and poultry industries. But in 2008, after Cutter’s strong alto voice deteriorated into a raspy whisper, she feared her academic career might be over.How could she teach if her students could barely hear her? The classroom wasn’t the only area of Cutter’s life affected by her voicelessness. The mother of two teenagers, Cutter, now 52, recalls that she “couldn’t yell — or even talk” to her kids and would have to knock on a wall or countertop to get their attention. Social situations became increasingly difficult as well, and going to a restaurant was a chore. Using the drive-through at her bank or dry cleaner was out of the question because she couldn’t be heard. “I just retreated,” said Cutter, who sought assistance from nearly two dozen specialists for her baffling condition. The remedies doctors prescribed — when they worked at all — resulted in improvement that was temporary at best. For two years Cutter searched in vain for help. It arrived in the form of a neurosurgeon she consulted for a second opinion about potentially risky surgery to correct a different condition. He suggested a disorder that had never been mentioned, a diagnosis that proved to be correct — and correctable. Until then, “everyone had been looking in the wrong place,” Cutter said.
Keyword: Movement Disorders
Link ID: 20605 - Posted: 02.24.2015
By Gary Stix Everyone knows that ALS is a very bad disease, an awareness underscored by the recent Ice Bucket Challenge. The death of neurons that results in paralysis can be caused by specific genetic mutations. But in most cases, single genes are not the culprit. So researchers have looked for other risk factors that might play a role. Studies have tagged cigarette smoking as a definite danger. Alcohol, another plausible suspect, has yielded equivocal results in previous investigations. To get a better read on ethanol (some earlier studies were small), researchers from Sweden’s Lund University looked at giant medical registries from that country, compiled at various times between 1973 and 2010. They found that individuals who were classified as problem drinkers were a little more than half as likely to be diagnosed with ALS as those who didn’t have “alcohol use disorder.” More than 420,000 problem drinkers were registered during the period surveyed—and there were 7965 patients who received an ALS diagnosis. The study, just reported in The European Journal of Neurology, controlled for gender, education and place of birth, among other factors. But it was unable to tell why drinking might help. It did lead, though, to a number of intriguing speculations. The researchers cited studies in rats, done by other groups, that indicated that ingestion of alcohol decreased the number of brain cells called astrocytes that bore high levels of a certain protein linked to the pathology of ALS. © 2015 Scientific American
By Nick Lavars Keeping ourselves upright is something most of us shouldn't need to think a whole lot about, given we've been doing it almost our entire lives. But when it comes to dealing with more precarious terrain, like walking on ice or some sort of tight rope, you might think some pretty significant concentration is required. But researchers have found that even in our moments of great instability, our subconsciousness is largely responsible for keeping us from landing on our backsides. This is due to what scientists are describing as a mini-brain, a newly mapped bunch of neurons in the spinal cord which processes sensory information and could lead to new treatment for ailing motor skills and balance. "How the brain creates a sensory percept and turns it into an action is one of the central questions in neuroscience," says Martin Goulding, senior author of the research paper and professor at the Salk Institute. "Our work is offering a really robust view of neural pathways and processes that underlie the control of movement and how the body senses its environment. We’re at the beginning of a real sea change in the field, which is tremendously exciting.” The work of Goulding and his team focuses on how the body processes light touch, in particular the sensors in our feet that detect changes in the surface underfoot and trigger a reaction from the body. "Our study opens what was essentially a black box, as up until now we didn’t know how these signals are encoded or processed in the spinal cord," says Goulding. "Moreover, it was unclear how this touch information was merged with other sensory information to control movement and posture."
Keyword: Movement Disorders
Link ID: 20561 - Posted: 02.07.2015
By Angelina Fanous After the height of the Ice Bucket Challenge last fall, I found myself at a dinner party where the conversation turned to A.L.S. — amyotrophic lateral sclerosis — the disease for which millions were dousing themselves to raise awareness and money. “Would you rather have A.L.S., Alzheimer’s, or Parkinson’s?” someone asked. All those diseases are devastating, but A.L.S. is unique in that it usually kills within two to three years of diagnosis. It was just a game to my friends, all of whom are in their 20s. Everyone chose A.L.S., agreeing that it would be the fastest and therefore easiest death. But I stayed silent. I hadn’t yet told my friends that I had been diagnosed with A.L.S. in July — two months after my 29th birthday. Had I been healthy, I might have answered A.L.S., too. But since my diagnosis, all I have wanted is more time. When I first noticed I couldn’t type with my left hand, the doctors narrowed down it down to two options: a treatable autoimmune disease or A.L.S. They initially began treating me for the autoimmune disease. About once a month, we shut down my immune system so it would stop attacking my central nervous system. But with no immune system I made regular visits to the E.R. “At least it’s not A.L.S.,” I consoled myself. When the treatment didn’t work and the weakness spread to my left leg and right hand, A.L.S. was the only remaining possibility. Still, I did that socially acceptable but also borderline insane thing where I sought second, third and fourth opinions. I voluntarily subjected myself to excruciating medical tests. I got shocked with electricity, had my spinal fluid drained, and underwent a surgery to remove a piece of my muscles and nerves, all in the hopes of finding a different diagnosis. All of the tests confirmed the diagnosis of A.L.S. © 2015 The New York Times Company
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20556 - Posted: 02.05.2015
by Bethany Brookshire The windup before the pitch. The take-away before the golf swing. When you learn to pitch a softball, swing a golf club or shoot a basketball, you learn that preparation is important. You also learn about follow-through — the upswing of the golf club or the bend in the elbow after a softball pitch. It’s the preparation and the execution that get the ball across the plate, so why should we care about follow-through? In theory, once the ball has left your hands or sailed away from your club or racket, there’s no movement you could make that could affect what happens next. So while some follow-through might be important to diffuse the energy you just put into your shot, it shouldn’t really matter whether you swing your golf club up in an arc, whip it off to the side or club your opponent over the head with it. But follow-through is in fact quite important, and not just as an extension of the movements that preceded it. Consistent follow-through actually helps performance, reports neuroscientist Ian Howard and colleagues at the University of Plymouth in England. The finding gives coaches some science to back up their training, and helps scientists understand how the brain accesses motor memories. Howard has always been interested in how the brain learns movement tasks. “The first study we did looked at the preparation movement — you move backwards and then you move forwards [as in a golf swing],” he says. His lab found that the preparation before a particular motion had a strong effect on how our brains learn and recall motor movements. © Society for Science & the Public 2000 - 2015.
Keyword: Movement Disorders
Link ID: 20549 - Posted: 02.05.2015
By Lenny Bernstein Parkinson's Disease patients secretly treated with a placebo instead of their regular medication performed better when told they were receiving a more expensive version of the "drug," researchers reported Wednesday in an unprecedented study that involved real patients. The research shows that the well-documented "placebo effect" -- actual symptom relief brought about by a sham treatment or medication -- can be enhanced by adding information about cost, according to the lead author of the study. It is the first time that concept has been demonstrated using people with a real illness, in this case Parkinson's, a progressive neurological disease that has no cure, according to an expert not involved in the study. "The potentially large benefit of placebo, with or without price manipulations, is waiting to be untapped for patients with [Parkinson's Disease], as well as those with other neurologic and medical diseases," the authors wrote in a study published online Wednesday in the journal Neurology. But deceiving actual patients in a research study raised ethical questions about violating the trust involved in a doctor-patient relationship. Most studies in which researchers conceal their true aims or other information from subjects are conducted with healthy volunteers. This one was subjected to a lengthy review before it was allowed to proceed, and, in an editorial that accompanied the article, two other physicians wrote that "the authors do not mention whether there was any possible effect (reduction) on trust in doctors or on willingness to engage in future clinical research."
Ewen Callaway Since August 2014, more than 100 children and young adults in the United States have developed a mysterious paralysis. Many of them had fevers before losing strength in one or more limbs, and the cases coincided with a wider epidemic of a little-known respiratory pathogen. That virus, enterovirus D68 (EV-D68), is the leading candidate for the cause of the paralysis, which few children have recovered from. Yet researchers have not definitively linked the two, or determined how the virus could cause the children’s symptoms. A study published on 28 January in The Lancet1 that describes a cluster of cases from Denver, Colorado, strengthens the link, but falls short of providing a 'smoking gun'. Here is what we know about the virus — and what scientists are trying to find out. It belongs to the enterovirus family, which includes poliovirus and the pathogens that cause common colds; it is most similar to the rhinoviruses that cause respiratory infections. Although EV-D68 was first isolated in the 1960s, it is relatively uncommon among enteroviruses circulating worldwide. However, since August 2014, the virus has been linked to more than 1,000 respiratory infections in the United States, some of them severe, and France has seen cases, too. John Watson, a medical epidemiologist at the US Centers for Disease Control and Prevention (CDC) in Atlanta, Georgia, says that last year, EV-D68 was the predominant type of enterovirus circulating in the country. “That’s a first,” he says. Genome sequencing2 of viruses recovered from respiratory cases in St Louis, Missouri, shows that the EV-D68 strain circulating in the United States is most closely related to viruses that caused a pneumonia-like illness in three children in Thailand in 20113. What is the evidence that links EV-D68 to the cases of paralysis? © 2015 Nature Publishing Group
Keyword: Movement Disorders
Link ID: 20533 - Posted: 01.29.2015
By SAM ROBERTS When he was just 5 years old, Thomas Graboys declared that he intended to become a doctor. As a young physician, he visited a nephew serving in the Peace Corps in Mauritania and remained for two months, treating dozens of patients a day. He skied and played tennis and joined fellow cardiologists as the drummer in a rock band called the Dysrhythmics. In Boston, he was famous as a member of the team that diagnosed the Celtics star Reggie Lewis’s heart defect before he died abruptly on a basketball court. In short, “he was a medical version of one of Tom Wolfe’s masters of the universe,” one reviewer concluded after Dr. Graboys (pronounced GRAY-boys) published his autobiography. But barely 60, after experiencing horrific nightmares, frequently flailing in bed, losing his memory, suffering tremors and finally collapsing on his wedding day, he acknowledged that he was suffering from Parkinson’s disease and the onset of dementia. He informed his patients that he had no choice but to close his practice. “My face is often expressionless, though I still look younger than my 63 years,” he recalled in the autobiography, “Life in the Balance: A Physician’s Memoir of Life, Love, and Loss With Parkinson’s Disease and Dementia,” which was published in 2008. “I am stooped,” he continued. “I shuffle when I walk, and my body trembles. My train of thought regularly runs off the rails. There is no sugarcoating Parkinson’s. There is no silver lining here. There is anger, pain, and frustration at being victimized by a disease that can to some extent be managed but cannot be cured.” After managing for more than a decade, Dr. Graboys died on Jan. 5 at his home in Chestnut Hill, Mass., his daughter, Penelope Graboys Blair, said. The cause was complications of Lewy Body Dementia, which was diagnosed after his Parkinson’s. He was 70. © 2015 The New York Times Company
Link ID: 20485 - Posted: 01.15.2015
By Peter Holley "Lynchian," according to David Foster Wallace, "refers to a particular kind of irony where the very macabre and the very mundane combine in such a way as to reveal the former's perpetual containment within the latter." Perhaps no other word better describes the onetime fate of Martin Pistorius, a South African man who spent more than a decade trapped inside his own body involuntarily watching "Barney" reruns day after day. "I cannot even express to you how much I hated Barney," Martin told NPR during the first episode of a new program on human behavior, "Invisibilia." The rest of the world thought Pistorius was a vegetable, according to NPR. Doctors had told his family as much after he'd fallen into a mysterious coma as a healthy 12-year-old before emerging several years later completely paralyzed, unable to communicate with the outside world. The nightmarish condition, which can be caused by stroke or an overdose of medication, is known as "total locked-in syndrome," and it has no cure, according to the National Institute of Neurological Disorders and Stroke. In a first-person account for the Daily Mail, Pistorius described the period after he slipped into a coma: I was completely unresponsive. I was in a virtual coma but the doctors couldn’t diagnose what had caused it. When he finally did awaken in the early 1990s, around the age of 14 or 15, Pistorius emerged in a dreary fog as his mind gradually rebooted itself.
By CATHERINE SAINT LOUIS A nationwide outbreak of a respiratory virus last fall sent droves of children to emergency departments. The infections have now subsided, as researchers knew they would, but they have left behind a frightening mystery. Since August, 103 children in 34 states have had an unexplained, poliolike paralysis of an arm or leg. Each week, roughly three new cases of so-called acute flaccid myelitis are still reported to the Centers for Disease Control and Prevention. Is the virus, called enterovirus 68, really the culprit? Experts aren’t certain: Unexplained cases of paralysis in children happen every year, but they are usually scattered and unrelated. After unusual clusters of A.F.M. appeared this fall, enterovirus 68 became the leading suspect, and now teams of researchers are racing to figure out how it could have led to such damage. “It’s unsatisfying to have an illness and not know what caused it,” said Dr. Samuel Dominguez, an epidemiologist and an infectious disease specialist at Children’s Hospital Colorado, which has had the largest cluster of patients. For many families, the onset of persistent limb paralysis has been a bewildering experience. Roughly two thirds of the children with A.F.M. have reported some improvement, according to the C.D.C. About a third show none. Only one child has fully recovered. In August, Jack Wernick, a first grader in Kingsport, Tenn., developed a “crummy little cold,” said his father, Dan Wernick, who works for a paper company. It seemed ordinary, until Jack complained that his right arm was heavy, his face began drooping and pain started shooting down his right leg. © 2015 The New York Times Company
Keyword: Movement Disorders
Link ID: 20477 - Posted: 01.13.2015
By James Gallagher Health editor, BBC News website An elastic implant that moves with the spinal cord can restore the ability to walk in paralysed rats, say scientists. Implants are an exciting field of research in spinal cord injury, but rigid designs damage surrounding tissue and ultimately fail. A team at Ecole Polytechnique Federale de Lausanne (EPFL) has developed flexible implants that work for months. It was described by experts as a "groundbreaking achievement of technology". The spinal cord is like a motorway with electrical signals rushing up and down it instead of cars. Injury to the spinal cord leads to paralysis when the electrical signals are stuck in a jam and can no longer get from the brain to the legs. The same group of researchers showed that chemically and electrically stimulating the spinal cord after injury meant rats could "sprint over ground, climb stairs and even pass obstacles". Rat walks up stairs Previous work by the same researchers But that required wired electrodes going directly to the spinal cord and was not a long-term option. Implants are the next step, but if they are inflexible they will rub, causing inflammation, and will not work properly. The latest innovation, described in the journal Science, is an implant that moves with the body and provides both chemical and electrical stimulation. When it was tested on paralysed rats, they moved again. One of the scientists, Prof Stephanie Lacour, told the BBC: "The implant is soft but also fully elastic to accommodate the movement of the nervous system. "The brain pulsates with blood so it moves a lot, the spinal cord expands and retracts many times a day, think about bending over to tie your shoelaces. "In terms of using the implant in people, it's not going to be tomorrow, we've developed dedicated materials which need approval, which will take time. © 2015 BBC.
Link ID: 20465 - Posted: 01.10.2015
|William Mullen, Tribune reporter Researchers at Northwestern University say they have discovered a common cause behind the mysterious and deadly affliction of amyotrophic lateral sclerosis, or Lou Gehrig's disease, that could open the door to an effective treatment. Dr. Teepu Siddique, a neuroscientist with Northwestern's Feinberg School of Medicine whose pioneering work on ALS over more than a quarter-century fueled the research team's work, said the key to the breakthrough is the discovery of an underlying disease process for all types of ALS. The discovery provides an opening to finding treatments for ALS and could also pay dividends by showing the way to treatments for other, more common neurodegenerative diseases such as Alzheimer's, dementia and Parkinson's, Siddique said. The Northwestern team identified the breakdown of cellular recycling systems in the neurons of the spinal cord and brain of ALS patients that results in the nervous system slowly losing its ability to carry brain signals to the body's muscular system. Without those signals, patients gradually are deprived of the ability to move, talk, swallow and breathe. "This is the first time we could connect (ALS) to a clear-cut biomedical mechanism," Siddique said. "It has really made the direction we have to take very clear and sharp. We can now test for drugs that would regulate this protein pathway or optimize it, so it functions as it should in a normal state."
Keyword: ALS-Lou Gehrig's Disease
Link ID: 20459 - Posted: 01.08.2015
|By Lindsey Konkel For 28 years, Bill Gilmore lived in a New Hampshire beach town, where he surfed and kayaked. “I’ve been in water my whole life,” he said. “Before the ocean, it was lakes. I’ve been a water rat since I was four.” Now Gilmore can no longer swim, fish or surf, let alone button a shirt or lift a fork to his mouth. Earlier this year, he was diagnosed with amyotrophic lateral sclerosis (ALS), or Lou Gehrig’s disease. In New England, medical researchers are now uncovering clues that appear to link some cases of the lethal neurological disease to people’s proximity to lakes and coastal waters. About five years ago, doctors at a New Hampshire hospital noticed a pattern in their ALS patients—many of them, like Gilmore, lived near water. Since then, researchers at Dartmouth-Hitchcock Medical Center have identified several ALS hot spots in lake and coastal communities in New England, and they suspect that toxic blooms of blue-green algae—which are becoming more common worldwide—may play a role. Now scientists are investigating whether breathing a neurotoxin produced by the algae may raise the risk of the disease. They have a long way to go, however: While the toxin does seem to kill nerve cells, no research, even in animals, has confirmed the link to ALS. As with all ALS patients, no one knows what caused Bill Gilmore’s disease. He was a big, strong guy—a carpenter by profession. One morning in 2011, his arms felt weak. “I couldn’t pick up my tools. I thought I had injured myself,” said Gilmore, 59, who lived half his life in Hampton and now lives in Rochester, N.H. © 2014 Scientific American
by Andy Coghlan To catch agile prey on the wing, dragonflies rely on the same predictive powers we use to catch a ball: that is, anticipating by sight where the ball will go and readying body and hand to snatch it from mid-air. Until now, dragonflies were thought to catch their prey without this predictive skill, instead blindly copying every steering movement made by their prey, which can include flies and bees. Now, sophisticated laboratory experiments have tracked the independent body and eye movements of dragonflies as they pursue prey, showing for the first time that dragonflies second guess where their prey will fly to next and then steer their flight accordingly. Throughout the pursuit, they lock on to their target visually while they orient their bodies and flight path for ultimate interception, rather than copying each little deviation in their prey's flight path in the hope of ultimately catching up with it. "The dragonfly lines up its body axis in the flight direction of the prey, but keeps the eyes in its head firmly fixed on the prey," says Anthony Leonardo of the Howard Hughes Medical Institute in Ashburn, Virginia. "It enables the dragonfly to catch the prey from beneath and behind, the prey's blind spot," he says. © Copyright Reed Business Information Ltd.
Link ID: 20412 - Posted: 12.13.2014
Injections of a new drug may partially relieve paralyzing spinal cord injuries, based on indications from a study in rats, which was partly funded by the National Institutes of Health. The results demonstrate how fundamental laboratory research may lead to new therapies. “We’re very excited at the possibility that millions of people could, one day, regain movements lost during spinal cord injuries,” said Jerry Silver, Ph.D., professor of neurosciences, Case Western Reserve University School of Medicine, Cleveland, and a senior investigator of the study published in Nature. Every year, tens of thousands of people are paralyzed by spinal cord injuries. The injuries crush and sever the long axons of spinal cord nerve cells, blocking communication between the brain and the body and resulting in paralysis below the injury. On a hunch, Bradley Lang, Ph.D., the lead author of the study and a graduate student in Dr. Silver’s lab, came up with the idea of designing a drug that would help axons regenerate without having to touch the healing spinal cord, as current treatments may require. “Originally this was just a side project we brainstormed in the lab,” said Dr. Lang. After spinal cord injury, axons try to cross the injury site and reconnect with other cells but are stymied by scarring that forms after the injury. Previous studies suggested their movements are blocked when the protein tyrosine phosphatase sigma (PTP sigma), an enzyme found in axons, interacts with chondroitin sulfate proteoglycans, a class of sugary proteins that fill the scars.
Link ID: 20394 - Posted: 12.04.2014
Stem cells can be used to heal the damage in the brain caused by Parkinson's disease, according to scientists in Sweden. They said their study on rats heralded a "huge breakthrough" towards developing effective treatments. There is no cure for the disease, but medication and brain stimulation can alleviate symptoms. Parkinson's UK said there were many questions still to be answered before human trials could proceed. The disease is caused by the loss of nerve cells in the brain that produce the chemical dopamine ,which helps to control mood and movement. To simulate Parkinson's, Lund University researchers killed dopamine-producing neurons on one side of the rats' brains. They then converted human embryonic stem cells into neurons that produced dopamine. Parkinson's Disease Parkinson's is one of the commonest neurodegenerative diseases These were injected into the rats' brains, and the researchers found evidence that the damage was reversed. There have been no human clinical trials of stem-cell-derived neurons, but the researchers said they could be ready for testing by 2017. Malin Parmar, associate professor of developmental and regenerative neurobiology, said: "It's a huge breakthrough in the field [and] a stepping stone towards clinical trials." A similar method has been tried in a limited number of patients. It involved taking brain tissue from multiple aborted foetuses to heal the brain. Clinical trials were abandoned after mixed results, but about a third of the patients had foetal brain cells that functioned for 25 years. BBC © 2014
Link ID: 20292 - Posted: 11.08.2014