Chapter 11. Motor Control and Plasticity
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By Maggie Fox, NBC News Seniors who fit in the most daily physical activity – from raking leaves to dancing – can have more gray matter in important brain regions, researchers reported on Monday. The scientists have images that show people who were the most active had 5 percent more gray matter than people who were the least active. Having more little gray brain cells translates into a lower risk of Alzheimer’s disease, other studies have shown. “People really want to know what they can do to reduce their risk of Alzheimer’s disease,” said Dr. Cyrus Raji of the University of California in Los Angeles, who presented his team’s findings to a meeting of the Radiological Society of North America. Raji’s team looked at the records of 876 adults, who were recruited into a larger study on heart health starting in 1989. They all got magnetic resonance imaging (MRI) brain scans in 1998 and 1999, when they were on average 78 years old, and filled out detailed questionnaires on exercise and other types of activity. Most of them were a little overweight – with a body mass index or BMI of 27. People with BMIs above 25 are considered overweight and at 30 they are considered clinically obese. The researchers found a huge difference in the amount of activity people reported. They were asked about everything from cycling to yard work, dancing and bicycle riding. © 2012 NBCNews.com
Link ID: 17543 - Posted: 11.27.2012
David Perlman With an ultimate goal to help paralyzed patients achieve a degree of independence, Stanford brain researchers report they have taken a promising step forward in efforts to link nerve centers in the human brain with computers controlled by only a person's thought. In their latest development, the Stanford scientists have successfully enabled a pair of rhesus monkeys to move a virtual cursor across a computer screen merely by thinking about their response to human commands. The monkeys' ability to manipulate a cursor without using a mouse is based on a powerful new algorithm, a mathematical computing program devised by Vikash Gilja, a Stanford electrical engineer and computer scientist. Four years ago, neurosurgeons at Brown University and Massachusetts General Hospital had demonstrated a simpler version of an algorithm that enabled completely paralyzed humans with implanted sensors in their brains to command a cursor to move erratically toward targets on a computer screen. But with Gilja's algorithm, called ReFit, the monkeys showed they could aim their virtual cursor, a moving dot of light, at another bright light on a computer screen, and hold it steadily there for 15 seconds - far more precisely than the humans four years ago. With the new algorithm, they were able to perform their thinking tasks faster and more accurately as they sat comfortably in a chair facing the computer. The development is "a big step toward clinically useful brain-machine technology that has faster, smoother, and more natural movements" than anything before it, said James Gnadt of the National Institute of Neurological Disorders and Stroke. © 2012 Hearst Communications Inc.
Link ID: 17537 - Posted: 11.26.2012
By David Pogue Okay, great: we can control Our phones with speech recognition and our television sets with gesture recognition. But those technologies don't work in all situations for all people. So I say, forget about those crude beginnings; what we really want is thought recognition. As I found out during research for a recent NOVA episode, it mostly appears that brain-computer interface (BCI) technology has not advanced very far just yet. For example, I tried to make a toy helicopter fly by thinking “up” as I wore a $300 commercial EEG headset. It barely worked. Such “mind-reading” caps are quick to put on and noninvasive. They listen, through your scalp, for the incredibly weak remnants of electrical signals from your brain activity. But they're lousy at figuring out where in your brain they originated. Furthermore, the headset software didn't even know that I was thinking “up.” I could just as easily have thought “goofy” or “shoelace” or “pickle”—whatever I had thought about during the 15-second training session. There are other noninvasive brain scanners—magnetoencephalography, positron-emission tomography and near-infrared spectroscopy, and so on—but each also has its trade-offs. Of course, you can implant sensors inside someone's skull for the best readings of all; immobilized patients have successfully manipulated computer cursors and robotic arms using this approach. Still, when it comes to controlling everyday electronics, brain surgery might be a tough sell. © 2012 Scientific American,
Link ID: 17518 - Posted: 11.21.2012
Scientists have reversed paralysis in dogs after injecting them with cells grown from the lining of their nose. The pets had all suffered spinal injuries which prevented them from using their back legs. The Cambridge University team is cautiously optimistic the technique could eventually have a role in the treatment of human patients. The study is the first to test the transplant in "real-life" injuries rather than laboratory animals. The only part of the body where nerve fibres continue to grow in adults is the olfactory system. Found in the at the back of the nasal cavity, olfactory ensheathing cells (OEC) surround the receptor neurons that both enable us to smell and convey these signals to the brain. The nerve cells need constant replacement which is promoted by the OECs. For decades scientists have thought OECs might be useful in spinal cord repair. Initial trials using OECs in humans have suggested the procedure is safe. In the study, funded by the Medical Research Council and published in the neurology journal Brain, the dogs had olfactory ensheathing cells from the lining of their nose removed. These were grown and expanded for several weeks in the laboratory. BBC © 2012
By Laura Sanders The insidious spread of an abnormal protein may be behind Parkinson’s disease, a study in mice suggests. A harmful version of the protein crawls through the brains of healthy mice, killing brain cells and damaging the animals’ balance and coordination, researchers report in the Nov. 16 Science. If a similar process happens in humans, the results could eventually point to ways to stop Parkinson’s destruction in the brain. “I really think that this model will increase our ability to come up with Parkinson’s disease therapies,” says study coauthor Virginia Lee of the University of Pennsylvania Perelman School of Medicine in Philadelphia. The new study targets a hallmark of Parkinson’s disease — clumps of a protein called alpha-synuclein. The clumps, called Lewy bodies, pile up inside nerve cells in the brain and cause trouble, particularly in cells that make dopamine, a chemical messenger that helps control movement. Death of these dopamine-producing cells leads to the characteristic tremors and muscle rigidity seen in people with Parkinson’s. Lee and her team injected alpha-synuclein into the brains of healthy mice. After 30 days, the protein had spread to connected brain regions, suggesting that rouge alpha-synuclein moves from cell to cell, the scientists found. Months later, the spreading was even more extensive. © Society for Science & the Public 2000 - 2012
Link ID: 17499 - Posted: 11.17.2012
By Ben Thomas In the early 1990s, a team of neuroscientists at the University of Parma made a surprising discovery: Certain groups of neurons in the brains of macaque monkeys fired not only when a monkey performed an action – grabbing an apple out of a box, for instance – but also when the monkey watched someone else performing that action; and even when the monkey heard someone performing the action in another room. In short, even though these “mirror neurons” were part of the brain’s motor system, they seemed to be correlated not with specific movements, but with specific goals. Over the next few decades, this “action understanding” theory of mirror neurons blossomed into a wide range of promising speculations. Since most of us think of goals as more abstract than movements, mirror neurons confront us with the distinct possibility that those everyday categories may be missing crucial pieces of the puzzle – thus, some scientists propose that mirror neurons might be involved in feelings of empathy, while others think these cells may play central roles in human abilities like speech. Some doctors even say they’ve discovered new treatments for mental disorders by reexamining diseases through the mirror neuron lens. For instance, UCLA’s Marco Iacoboni and others have put forth what Iacoboni called the “broken mirror hypothesis” of autism – the idea that malfunctioning mirror neurons are likely responsible for the lack of empathy and theory of mind found in severely autistic people. © 2012 Scientific American,
Danish researchers Krogh and colleagues randomly 115 assigned depressed people to one of two exercise programs. One was a strenuous aerobic workout - cycling for 30 minutes, 3 times per week, for 3 months. The other was various stretching exercises. The idea was that stretching was a kind of placebo control group on the grounds that, while it is an intervention, it's not the kind of exercise that gets you fit. It doesn't burn many calories, it doesn't improve your cardiovascular system, etc. Aerobic exercise is the kind that's most commonly been proposed as having an antidepressant effect. So what happened? Not much. Both groups got less depressed but there was zero difference between the two conditions. The cyclists did get physically fitter than the stretchers, losing more weight and improving on other measures. But they didn't feel any better. If this is true, it might mean that the antidepressant effects of aerobic exercise are psychological rather than physical - it's about the idea of 'exercising', not the process of becoming fitter. While many trials have found modest beneficial effects of exercise vs a "control condition", the control condition was often just doing nothing much - such as being put on a waiting-list. So the placebo effect or the motivational benefits of 'doing something', rather than the effects of exercise per se, could be behind it. In the current study though the stretching avoided that problem.
Link ID: 17463 - Posted: 11.07.2012
By Meghan Rosen Michael McAlpine’s shiny circuit doesn’t look like something you would stick in your mouth. It’s dashed with gold, has a coiled antenna and is glued to a stiff rectangle. But the antenna flexes, and the rectangle is actually silk, its stiffness melting away under water. And if you paste the device on your tooth, it could keep you healthy. The electronic gizmo is designed to detect dangerous bacteria and send out warning signals, alerting its bearer to microbes slipping past the lips. Recently, McAlpine, of Princeton University, and his colleagues spotted a single E. coli bacterium skittering across the surface of the gadget’s sensor. The sensor also picked out ulcer-causing H. pylori amid the molecular medley of human saliva, the team reported earlier this year in Nature Communications. At about the size of a standard postage stamp, the dental device is still too big to fit comfortably in a human mouth. “We had to use a cow tooth,” McAlpine says, describing test experiments. But his team plans to shrink the gadget so it can nestle against human enamel. McAlpine is convinced that one day, perhaps five to 10 years from now, everyone will wear some sort of electronic device. “It’s not just teeth,” he says. “People are going to be bionic.” McAlpine belongs to a growing pack of tech-savvy scientists figuring out how to merge the rigid, brittle materials of conventional electronics with the soft, curving surfaces of human tissues. Their goal: To create products that have the high performance of silicon wafers — the crystalline material used in computer chips — while still moving with the body. © Society for Science & the Public 2000 - 2012
Link ID: 17455 - Posted: 11.05.2012
By Katherine Harmon With a juicy insect dinner perched on a leaf above the water, what is a hungry little archer fish down below to do? Knock it down with a super-powered, super-precise jet of water that packs six times the power the fish could generate with its own muscles, according to new findings published online October 24 in PLoS ONE. The stunning spitting power of the amazing archer fish (Toxotes jaculatrix) was first described in the 18th century. The creature lives in mostly in mangrove forests and estuaries where insects are prevalent—above water, that is. And these tasty treats are not easily knocked off of the plants that hang over the archer fish’s territory. The insects, such as grasshoppers, can hang on with a force some 10 times their own body weight. So the archer fish has developed an impressive strategy for fetching food that not many other fish can reach. Its water jet can target and dislodge a single insect so that it falls into the water for the fish to eat. Just how the fish manages to do this—and in less than a second—had remained a mystery. Many scientists figured that the source must be a special organ in the fish’s body. “The origin of the effectiveness of the jet squirted by the archer fish has been searched for inside of the fish for nearly 250 years,” Alberto Vailati, a physicist at the University of Milan and co-author of the new paper, said in a prepared statement. © 2012 Scientific American
By ANAHAD O'CONNOR Remaining physically active as you age, a new study shows, may help protect parts of your brain from shrinking, a process that has been linked to declines in thinking and memory skills. Physical exercise not only protected against such age-related brain changes, but also had more of an effect than mentally and socially stimulating activities. In the new report, published in the journal Neurology, a team at the University of Edinburgh followed more than 600 people, starting at age 70. The subjects provided details on their daily physical, mental and social activities. Three years later, using imaging scans, the scientists found that the subjects who engaged in the most physical exercise, including walking several times a week, had less shrinkage and damage in the brain’s white matter, which is considered the “wiring” of the brain’s communication system. The relationship remained even after the researchers controlled for things like age, health status, social class and I.Q. As far as mental exercise, “we can only say we found no benefit in our sample,” said Dr. Alan J. Gow, an author of the study and a senior research fellow at Edinburgh. He added: “There might be associations earlier in the life course. Such activities also have important associations with well-being and quality of life, so we would certainly agree it is important for older adults to continue to pursue them.” Copyright 2012 The New York Times Company
Link ID: 17427 - Posted: 10.27.2012
by Helen Thomson Paralysis may no longer mean life in a wheelchair. A man who is paralysed from the trunk down has recovered the ability to stand and move his legs unaided thanks to training with an electrical implant. Andrew Meas of Louisville, Kentucky, says it has changed his life (see "I suddenly noticed I can move my pinkie", below). The stimulus provided by the implant is thought to have either strengthened persistent "silent" connections across his damaged spinal cord or even created new ones, allowing him to move even when the implant is switched off. The results are potentially revolutionary, as they indicate that the spinal cord is able to recover its function years after becoming damaged. Previous studies in animals with lower limb paralysis have shown that continuous electrical stimulation of the spinal cord below the area of damage allows an animal to stand and perform locomotion-like movements. That's because the stimulation allows information about proprioception – the perception of body position and muscle effort – to be received from the lower limbs by the spinal cord. The spinal cord, in turn, allows lower limb muscles to react and support the body without any information being received from the brain (Journal of Neuroscience, doi.org/czq67d). Last year, Susan Harkema and Claudia Angeli at the Frazier Rehab Institute and University of Louisville in Kentucky and colleagues tested what had been learned on animals in a man who was paralysed after being hit by a car in 2006. He was diagnosed with a "motor complete" spinal lesion in his neck, which means that no motor activity can be recorded below the lesion. © Copyright Reed Business Information Ltd
Link ID: 17420 - Posted: 10.25.2012
By Michelle Roberts Health editor, BBC News online Exercising in your 70s may stop your brain from shrinking and showing the signs of ageing linked to dementia, say experts from Edinburgh University. Brain scans of 638 people past the age of retirement showed those who were most physically active had less brain shrinkage over a three-year period. Exercise did not have to be strenuous - going for a walk several times a week sufficed, the journal Neurology says. But giving the mind a workout by doing a tricky crossword had little impact. The study found no real brain-size benefit from mentally challenging activities, such as reading a book, or other pastimes such as socialising with friends and family. When the researchers examined the brain's white matter - the wiring that transmits messages round the brain - they found that the people over the age of 70 who were more physically active had fewer damaged areas than those who did little exercise. And they had more grey matter - the parts of the brain where the messages originate. Experts already know that our brains tend to shrink as we age and that this shrinkage is linked to poorer memory and thinking. BBC © 2012
Link ID: 17410 - Posted: 10.23.2012
By Dan Cossins There’s a new suspect in the search for the causes of Parkinson’s disease—deformities in the nuclear membrane of neural stem cells. Scientists observed the same defects, caused by a single gene mutation, in brain tissue samples from deceased Parkinson’s patients, suggesting that nuclear deterioration—and the mutation that drives it—could play a role in the pathology of the disease. The study, published today (October 17) in Nature, also shows that correcting the mutation reverses this phenotype, pointing to new ways to treat this cause of neurodegeneration. “I don’t recall anyone ever suggesting this as a major phenotype [for Parkinson’s], so that’s really quite a big new direction for the field,” said Mark Cookson, a neuroscientist at the National Institutes of Health in Bethesda, Maryland, who did not participate in the study. Parkinson’s disease has traditionally been attributed to a loss of dopamine-generating neurons, which leads to the degenerative muscle control that is characteristic of the disease. But Parkinson’s also causes many other sensory problems, which cannot be explained by a dopaminergic mechanism. Over the past 5 years, several groups have shown that disruption of the structure of the nuclear envelope—the lipid bilayer that separates nucleus from cytoplasm—is correlated with aging and certain age-related pathologies in the human brain, though the precise role of nuclear defects in the diseases remained unclear. Meanwhile, since 2004 scientists including Cookson have demonstrated that a mutation in the luceine-rich repeat kinase 2 (LRRK2) gene is correlated with Parkinson’s. However, the molecular and cellular mechanisms by which the LRRK2 mutation might drive disease progression remained a mystery. © 1986-2012 The Scientist
Link ID: 17392 - Posted: 10.20.2012
By Tina Hesman Saey The 2012 Nobel Prize in physiology or medicine was awarded for the discovery that adult cells can be reprogrammed, as scientists did to these neurons, created from skin cells reprogrammed into a type of primordial stem cell and then coaxed into brain cells that control movement.G. Croft and M. Weygandt/The Cell: An Image Library Two scientists who showed that a cell's fate is reversible have won the 2012 Nobel Prize in physiology or medicine. The Nobel committee announced October 8 that John Gurdon and Shinya Yamanaka are being honored for showing that cells once thought to be locked into a specific identity could remember and revert to the supremely flexible state they have in an early embryo. Gurdon’s 1962 work forever changed the view that adult cells are stuck in their fate. In a series of experiments, he transplanted the nucleus — the cellular compartment that contains DNA — from an intestinal cell of an adult frog into a frog egg cell from which the nucleus had been removed. The cell developed into a normal tadpole, demonstrating that DNA contains all the information necessary to make an embryo. More than four decades later, Yamanaka, of Kyoto University in Japan, changed the debate over stem cells when he created induced pluripotent stem cells, which are capable of becoming nearly any cell in the body. He was trying to understand the factors that make stem cells isolated from embryos so malleable; many genes seemed to be involved. Yamanaka used viruses to insert combinations of candidate genes into skin cells, and found that only four genes are required to turn a mouse skin cell into a stem cell. The technique has since been used to convert adult human cells into embryonic-like cells and even to convert skin cells directly into heart or brain cells. © Society for Science & the Public 2000 - 2012
Two pioneers of stem cell research have shared the Nobel prize for medicine or physiology. John Gurdon from the UK and Shinya Yamanaka from Japan were awarded to prize for transforming specialised cells into stem cells.
By ANDREW POLLACK An experimental drug preserved and even improved the walking ability of boys with Duchenne muscular dystrophy in a clinical trial, raising hopes that the first effective treatment for the disease may be on the horizon. Boys with the disease who received the highest dose of the drug had a slightly improved ability to walk after 48 weeks of treatment, the drug’s developer, Sarepta Therapeutics, announced Wednesday. By contrast, the boys who received a placebo suffered a sharp decline in how well they could walk. The drug, called eteplirsen, also appeared to restore levels of the crucial protein that muscular dystrophy patients lack to about half of normal levels, Sarepta said. “I think this changes the entire playing field for muscular dystrophy,” said Dr. Jerry R. Mendell, director of the gene therapy and muscular dystrophy programs at Nationwide Children’s Hospital in Columbus, Ohio, and the lead investigator in the trial. There are many caveats. The trial had only 12 patients, with only four receiving the high dose and four the placebo, and the data has not been reviewed by experts. It is also unclear how long the effects of the drug would last or if safety issues would arise with longer treatment. Also, eteplirsen would be appropriate for only about 13 percent to 15 percent of Duchenne patients, those with the particular genetic mutation the drug is meant to counteract. However, a similar approach might work for some other mutations. © 2012 The New York Times Company
By Gary Stix 14 inSharHuntington’ disease, which killed folk singer Woody Guthrie, seems to put into overdrive the main chemical that turns on brain cells, ultimately leading to their death. The normal function of the neurotransmitter glutamate, the chemical overproduced in Huntington’s, is also intimately involved with learning. Researchers from Ruhr University and the University of Dortmund in Germany have been intrigued by the question of whether the neurodegeneration initiated by glutamate in this genetic disorder is all bad. Is it simply burning out brain circuits? Or might an excess of the chemical also help presymptomatic carriers of the Huntington’s gene or even patients with the disease itself, learn some things faster or better? “Neurotransmission causes cell death but we know from the vast amount of literature that learning processes very much depend on glutamate neurotransmission; so there may be two effects of one and the same process,” says Christian Beste of Ruhr University. “On the one hand this process may lead to neurodegeneration. But on the other hand, it may augment a cognitive process that depends on glutamate transmission.” Beste is the lead author on a paper published this month in Current Biology that found that those who have the genetic mutation for Huntington’s but who have yet to develop inevitable symptoms of the disease perform better on a learning task than a control group that lacks the mutation. The 29 Huntington’s gene carriers learned to detect twice as fast as the 45 controls a change in brightness of a small bar as its orientation on a computer screen altered. In fact, the Huntington’s carriers with the most pronounced mutations—the number of repetitions of a short DNA segment determines how early disease onset occurs—logged the best performance. © 2012 Scientific American,
Link ID: 17311 - Posted: 09.29.2012
By GRETCHEN REYNOLDS Can you improve your body’s ability to remember by making it move? That rather odd-seeming question stimulated researchers at the University of Copenhagen to undertake a reverberant new examination of just how the body creates specific muscle memories and what role, if any, exercise plays in the process. To do so, they first asked a group of young, healthy right-handed men to master a complicated tracking skill on a computer. Sitting before the screen with their right arm on an armrest and a controller similar to a joystick in their right hand, the men watched a red line squiggle across the screen and had to use the controller to trace the same line with a white cursor. Their aim was to remain as close to the red squiggle as possible, a task that required input from both the muscles and the mind. The men repeated the task multiple times, until the motion necessary to track the red line became ingrained, almost automatic. They were creating a short-term muscle memory. The term “muscle memory” is, of course, something of a misnomer. Muscles don’t make or store memories. They respond to signals from the brain, where the actual memories of any particular movement are formed and filed away. But muscle memory — or “motor memory,” as it is more correctly referred to among scientists — exists and can be quite potent. Learn to ride a bicycle as a youngster, abandon the pastime and, 20 years later, you’ll be able to hop on a bicycle and pedal off. Copyright 2012 The New York Times Company
Keyword: Learning & Memory
Link ID: 17304 - Posted: 09.26.2012
by Andy Coghlan Muscles that burn energy without contracting have yielded new clues about how the body retains a constant temperature – and they may provide new targets for combating obesity. Traditionally, the body's main thermostat was thought to be brown fat. It raids the body's white fat stores in cold conditions to burn energy and keep the body warm. Muscles also play a role in keeping the body warm by contracting and triggering the shiver response – but this is only a short-term fix because prolonged shivering damages muscles. Now it seems that muscles have another way to turn up the heat. "Our findings demonstrate for the first time that muscle, which accounts for 40 per cent of body weight in humans, can generate heat independent of shivering," says Muthu Periasamy of Ohio State University in Columbus. Surviving the chill Through experiments on mice that had their usual thermostat – brown fat – surgically removed, Periasamy and his colleagues proved that a protein called sarcolipin helps muscle cells keep the body warm by burning energy, almost like an idling motor car, even if the muscles do not contract. All of the mice had their brown fat removed, but some of them had been genetically engineered to lack sarcolipin too. These rodents could not survive when held at 4 °C, and died of hypothermia within 10 hours. By contrast, mice that could make sarcolipin were able to survive the chilly temperatures and maintained their core body temperature – despite having no brown fat. © Copyright Reed Business Information Ltd.
By Miguel A. L. Nicolelis In 2014 billions of viewers worldwide may remember the opening game of the World Cup in Brazil for more than just the goals scored by the Brazilian national team and the red cards given to its adversary. On that day my laboratory at Duke University, which specializes in developing technologies that allow electrical signals from the brain to control robotic limbs, plans to mark a milestone in overcoming paralysis. If we succeed in meeting still formidable challenges, the first ceremonial kick of the World Cup game may be made by a paralyzed teenager, who, flanked by the two contending soccer teams, will saunter onto the pitch clad in a robotic body suit. This suit—or exoskeleton, as we call it—will envelop the teenager's legs. His or her first steps onto the field will be controlled by motor signals originating in the kicker's brain and transmitted wirelessly to a computer unit the size of a laptop in a backpack carried by our patient. This computer will be responsible for translating electrical brain signals into digital motor commands so that the exoskeleton can first stabilize the kicker's body weight and then induce the robotic legs to begin the back-and-forth coordinated movements of a walk over the manicured grass. Then, on approaching the ball, the kicker will visualize placing a foot in contact with it. Three hundred milliseconds later brain signals will instruct the exoskeleton's robotic foot to hook under the leather sphere, Brazilian style, and boot it aloft. This scientific demonstration of a radically new technology, undertaken with collaborators in Europe and Brazil, will convey to a global audience of billions that brain control of machines has moved from lab demos and futuristic speculation to a new era in which tools capable of bringing mobility to patients incapacitated by injury or disease may become a reality. © 2012 Scientific American
Link ID: 17220 - Posted: 08.30.2012