Chapter 3. Neurophysiology: The Generation, Transmission, and Integration of Neural Signals

Follow us on Facebook and Twitter, or subscribe to our mailing list, to receive news updates. Learn more.


Links 81 - 100 of 614

David Cyranoski More than a decade of research hinting that magnesium supplements might boost your brain power is finally being put to the test in a small clinical trial. The research, led by biopharmaceutical company Magceutics of Hayward, California, began testing the ability of its product Magtein to boost magnesium ion (Mg2+) levels in the brain earlier this month. The trial will track whether the ions can decrease anxiety and improve sleep quality, as well as following changes in the memory and cognitive ability of participants. But critics caution that the trial in just 50 people is too small to draw definitive conclusions. Neuroscientist Guosong Liu of the Massachusetts Institute of Technology in Cambridge, who founded Magceutics, plans eventually to test whether Magtein can be used to treat a wider range of conditions, including attention deficit hyperactivity disorder (ADHD) and Alzheimer’s disease. But Liu knows that it will be difficult to convince other scientists that something as simple as a magnesium supplement can have such profound effects. It is almost “too good to be true”, he says. Many scientists contacted by Nature agreed with that sentiment. One clinical researcher cautioned against “over-excitement about a magic drug for a major disorder”. And others wonder whether the study will even be able to prove anything conclusively. “I am very sceptical that the proposed trial will provide the answer to the question being tested,” says Stephen Ferguson, a biochemist at the University of Western Ontario in London, Ontario. © 2012 Nature Publishing Group

Keyword: Learning & Memory; Aggression
Link ID: 17430 - Posted: 10.27.2012

by Emily Underwood Four young boys with a rare, fatal brain condition have made it through a dangerous ordeal. Scientists have safely transplanted human neural stem cells into their brains. Twelve months after the surgeries, the boys have more myelin—a fatty insulating protein that coats nerve fibers and speeds up electric signals between neurons—and show improved brain function, a new study in Science Translational Medicine reports. The preliminary trial paves the way for future research into potential stem cell treatments for the disorder, which overlaps with more common diseases such as Parkinson's disease and multiple sclerosis. "This is very exciting," says Douglas Fields, a neuroscientist at the National Institutes of Health in Bethesda, Maryland, who was not involved in the work. "From these early studies one sees the promise of cell transplant therapy in overcoming disease and relieving suffering." Without myelin, electrical impulses traveling along nerve fibers in the brain can't travel from neuron to neuron says Nalin Gupta, lead author of the study and a neurosurgeon at the University of California, San Francisco (UCSF). Signals in the brain become scattered and disorganized, he says, comparing them to a pile of lumber. "You wouldn't expect lumber to assemble itself into a house," he notes, yet neurons in a newborn baby's brain perform a similar feat with the help of myelin-producing cells called oligodendrocytes. Most infants are born with very little myelin and develop it over time. In children with early-onset Pelizaeus-Merzbacher disease, he says, a genetic mutation prevents oligodendrocytes from producing myelin, causing electrical signals to die out before they reach their destinations. This results in serious developmental setbacks, such as the inability to talk, walk, or breathe independently, and ultimately causes premature death. © 2010 American Association for the Advancement of Science

Keyword: Stem Cells; Aggression
Link ID: 17356 - Posted: 10.11.2012

by Michael Marshall THE human brain might be the most complex object in the known universe, but a much simpler set of neurons is also proving to be a tough nut to crack. A tiny wasp has brain cells so small, physics predicts they shouldn't work at all. These miniature neurons might harbour subtle modifications, or they might work completely differently from all other known neurons - mechanically. The greenhouse whitefly parasite (Encarsia formosa) is just half a millimetre in length. It parasitises the larvae of whiteflies and so it has long been used as a natural pest-controller. To find out how its neurons have adapted to miniaturisation, Reinhold Hustert of the University of Göttingen in Germany examined the insect's brain with an electron microscope. The axons - fibres that shuttle messages between neurons - were incredibly thin. Of 528 axons measured, a third were less than 0.1 micrometre in diameter, an order of magnitude narrower than human axons. The smallest were just 0.045 μm (Arthropod Structure & Development, doi.org/jfn). That's a surprise, because according to calculations by Simon Laughlin of the University of Cambridge and colleagues, axons thinner than 0.1 μm simply shouldn't work. Axons carry messages in waves of electrical activity called action potentials, which are generated when a chemical signal causes a large number of channels in a cell's outer membrane to open and allow positively charged ions into the axon. At any given moment some of those channels may open spontaneously, but the number involved isn't enough to accidentally trigger an action potential, says Laughlin - unless the axon is very thin. An axon thinner than 0.1 μm will generate an action potential if just one channel opens spontaneously (Current Biology, doi.org/frfwpz). © Copyright Reed Business Information Ltd

Keyword: Miscellaneous; Aggression
Link ID: 17335 - Posted: 10.06.2012

Analysis by Tracy Staedter From the department of "I hope this never happens to me," scientists have used a laser to manipulate the behavior of a worm. First, a research team from the Howard Hughes Medical Institute genetically engineered a tiny, transparent worm called Caenorhabditis elegans to have neurons that give off fluorescent light. This allowed the neurons to be tracked during experiments. The scientists also engineered the neurons to be sensitive to light, which made it possible to activate them with pulses of laser light. Next, they built a movable table for the worm to crawl on, keeping it aligned beneath a camera and laser. They used the laser to activate a single neuron at a time. By doing so, they were able to control a worm's behavior and its senses. In tests, which the researchers published in the journal Nature, the laser made the worm turn left or right and move through a loop. The laser also tricked the worm brain into thinking food was nearby. The worm, in turn, wiggled toward what it thought was a meal. The research, which on the surface seems like a bit of a circus, actually is important because it shows scientists which neurons are responsible for what. "If we can understand simple nervous systems to the point of completely controlling them, then it may be a possibility that we can gain a comprehensive understanding of more complex systems," said Sharad Ramanathan, an Assistant Professor of Molecular and Cellular Biology, and of Applied Physics. "This gives us a framework to think about neural circuits, how to manipulate them, which circuit to manipulate and what activity patterns to produce in them." © 2012 Discovery Communications, LLC

Keyword: Development of the Brain
Link ID: 17299 - Posted: 09.26.2012

By Nathan Seppa People with multiple sclerosis might soon have a new option for controlling their disease with pills instead of shots. Two studies in the Sept. 20 New England Journal of Medicine demonstrate that a variation on a drug used against psoriasis for years in Germany holds off MS relapses and has minimal side effects. “These data look good. Both studies show a reduction in relapses with really pretty robust effects,” says Clyde Markowitz, a neurologist at the University of Pennsylvania who wasn’t involved with the trials. The drug, called BG-12, has been submitted to the U.S. Food and Drug Administration for approval by the biotech company Biogen Idec. Markowitz expects it to get approved. “It would be a clear benefit to the MS population to have another option,” he says. If approved, BG-12 would be the third oral drug available to treat MS. The disease results when the immune system attacks the fatty myelin sheaths coating nerves in the central nervous system, leading to impaired muscle control, balance, vision and speech. BG-12, or dimethyl fumarate, has anti-inflammatory, cell-protective and antioxidant effects, which earlier work suggested could suppress the aberrant immune reactions in MS patients. Scientists in both studies recruited MS patients and randomly assigned some in each group to BG-12 or placebo tablets. In one of the studies, an additional group was randomly assigned to get an injectable MS drug called glatiramer acetate (Copaxone). In other respects the studies were nearly identical, each enrolling more than 1,000 MS patients, ages 18 to 55, in 28 countries apiece, for two years of treatment. Both trials included a mix of North American and European researchers. © Society for Science & the Public 2000 - 2012

Keyword: Multiple Sclerosis
Link ID: 17284 - Posted: 09.22.2012

by Douglas Heaven The versatile cannabis plant may have a new use: it could be used to control epileptic seizures with fewer side effects than currently prescribed anti-convulsants. Ben Whalley at the University of Reading, UK, and colleagues worked with GW Pharmaceuticals in Wiltshire, UK, to investigate the anti-convulsant properties of cannabidivarin (CBDV), a little-studied chemical found in cannabis and some other plants. There is "big, historical, anecdotal evidence" that cannabinoids can be used to control human seizures, says Whalley, but the "side-effect baggage" means there have been relatively few studies of its pharmaceutical effect on this condition. The team investigated the effectiveness of CBDV – one of around 100 non-psychoactive cannabinoids found in cannabis – as an anti-convulsant. They induced seizures in live rats and mice that had been given the drug. These animals experienced less severe seizures and lower mortality compared with animals given a placebo. The drug also had fewer side effects and was better tolerated than three of the most widely prescribed anticonvulsants. Epileptic seizures affect about one per cent of the population. Left uncontrolled, they can lead to depression, cognitive decline and death. If you control the seizures, says Whalley, "the chances of death drop away completely". The decision about whether to test the drug in humans will be made next year. © Copyright Reed Business Information Ltd

Keyword: Epilepsy; Aggression
Link ID: 17255 - Posted: 09.13.2012

Helen Shen Automated assistance may soon be available to neuroscientists tackling the brain’s complex circuitry, according to research presented last week at the Aspen Brain Forum in Colorado. Robots that can find and simultaneously record the activity of dozens of neurons in live animals could help researchers to reveal how connected cells interpret signals from one another and transmit information across brain areas — a task that would be impossible using single-neuron studies. The robots are designed to perform whole-cell patch-clamping, a difficult but powerful method that allows neuroscientists to access neurons' internal electrical workings, says Edward Boyden of the Massachusetts Institute of Technology in Cambridge, who is leading the work. Manually performing the method on live animals requires extensive training to perfect and, as a result, only a handful of neurophysiologists use the technique, says Boyden, who presented at the conference. He is developing the automated tool with Craig Forest at the Georgia Institute of Technology in Atlanta and others. “We think that it helps democratize procedures that require a lot of skill,” he says. In May, the group described how a basic version of the robot can record electrical currents in single neurons in the brains of anaesthetized mice1. The robot finds its target on the basis of characteristic changes in the electrical environment near neurons. Then, the device nicks the cell’s membrane and seals itself around the tiny hole to access the neuron's contents. On 24 August, Boyden presented results showing that a more advanced version of the robot could be used to identify and probe four neurons at once — and he says he wants to push the design further, perhaps to tap as many as 100 neurons at a time. © 2012 Nature Publishing Group

Keyword: Robotics
Link ID: 17215 - Posted: 08.29.2012

By Karen Weintraub Paul Barney had his first seizure four days after his fourth birthday. By the time he was 10, his mom worried that if they didn’t get the seizures under control soon, he might lose IQ points along with his ready smile. When Brian Manning, 11, had a seizure on the school playground – instead of in his bed as usual – his parents knew it was time for drastic action. He’d already had brain surgery once, but doctors said he might need five or six more operations. Or he could have one, to completely remove the right half of his brain. Both boys have epilepsy and recently underwent surgery at Boston Children’s Hospital. And both represent the promise and frustration of epilepsy treatment today. Patients have more options, and there is more awareness, less stigma, and a better understanding of epilepsy than there has ever been. But available medications can’t control seizures in about one-third of patients, including Paul and Brian, and while surgery is safer, it still comes with high risks. It also remains unclear what causes the electrical disturbance in patients’ brains that triggers seizures. Roughly 1 in 26 Americans will develop epilepsy at some point in life – more than will have autism, AIDS, or Parkinson’s disease. Some patients do fine between seizures and can function normally. In others, their brains are constantly being disrupted, like a radio station filled with static, according to Dr. Blaise Bourgeois the director of the Division of Epilepsy and Clinical Neurophysiology at Boston Children’s. © 2012 NY Times Co.

Keyword: Epilepsy
Link ID: 17156 - Posted: 08.13.2012

Duncan Graham-Rowe A skull implant that can detect an epileptic seizure and deliver therapeutic electrical impulses can reduce the length of these events by 60% in rats. The device, tested on nine rats with a ‘petit mal’ form of epilepsy, is described today in Science1. Most electrical stimulation devices, such as those that deliver deep-brain stimulation (DBS) to treat Parkinson’s disease and depression, operate continuously, delivering impulses regardless of the patient’s brain activity. But this can cause a range of undesirable side effects, such as headaches. Seizure-responsive versions of DBS devices are coming to market, such as the Responsive Neurostimulator System developed by NeuroPace, based in Mountain View, California. The system is awaiting approval by the US Food and Drug Administration and will be aimed at adults with certain types of partial-onset seizures, which tend to be localized to certain regions of the brain. But as the name implies, DBS uses electrodes that penetrate the brain, which can also carry certain risks, such as a worsening of epilepsy symptoms. In the latest study, György Buzsáki, a neuroscientist at the New York University School of Medicine, and his colleagues used a less invasive approach that involves transcranial electrical stimulation (TES) of neurons using electrodes implanted in the skull. This technique has been shown to be effective at modifying the brain's cortical (outermost) neurons, which become abnormally excited during epileptic seizures. To detect the onset of a seizure, recording electrodes that detect neural activity were implanted on the brain's surface. © 2012 Nature Publishing Group,

Keyword: Epilepsy
Link ID: 17148 - Posted: 08.11.2012

By Julie Appleby, An increasing number of psychiatrists and hospitals — as well as entrepreneurs opening rTMS centers around the country — are betting that there are millions of people like Curtis, discouraged by depression treatments that have proved unsuccessful and willing to pony up thousands of dollars for the possibility of relief. The treatment, which has been approved by the Food and Drug Administration, is covered by Medicare in five states, but few private insurers pay for it routinely. While rTMS has ardent supporters, its effectiveness is still debated, and there is little evidence showing how long the results last. The technique has been shown to work better than a placebo, but the proportion of patients who show complete relief ranges widely, from as few as 10 percent to as many as 57 percent, according to various studies. The debate has huge implications, not just for many of the 14 million Americans who suffer from major depression every year but also for businesses eyeing a potentially lucrative market and insurers weighing whether to cover it. About half of those 14 million Americans seek relief through psychotherapy and prescription drug treatment, according to an evaluation by the federal Agency for Healthcare Research and Quality. But studies show that antidepressants provide complete cessation of symptoms only about a third of the time. Magnetic stimulation is aimed at patients with such “treatment-resistant depression.” Supporters say rTMS is worth the cost — between $6,000 and $12,000 for the four-to-six-week treatment — because it enables people such as Curtis to resume productive lives. Skeptics question the price tag in light of uncertain benefits. © 1996-2012 The Washington Post

Keyword: Depression
Link ID: 17139 - Posted: 08.08.2012

By Laura Sanders A much-maligned molecule that is devastating in the brain may have therapeutic potential outside it. The sticky amyloid-beta protein, which piles up in the brains of people with Alzheimer’s disease, actually reverses paralysis in mice with symptoms of multiple sclerosis. The unexpected finding, published in the Aug. 1 Science Translational Medicine, could mean that A-beta or molecules like it may one day form the basis of a treatment for multiple sclerosis in people. In MS, rogue immune cells penetrate the brain and spinal cord and attack myelin, a substance that is necessary to keep neural impulses moving at full speed. Damage and inflammation from this attack can leave a person with paralysis, numbness, vision problems and extreme fatigue. A-beta is found in the brains of people with MS, but scientists do not know precisely what effect it has there, if any. To investigate that question, study coauthor Lawrence Steinman of Stanford University and colleagues tried injecting A-beta into mice’s abdomens, thinking it would worsen symptoms. “We expected that either nothing would happen or the disease would worsen because this is an infamous, villainous molecule,” he says. Instead, the mice got better. In several different kinds of mice designed to have symptoms similar to the human disease, A-beta injections into the body reduced paralysis and lowered brain inflammation. “The outcome was unmistakable,” Steinman says. © Society for Science & the Public 2000 - 2012

Keyword: Multiple Sclerosis; Aggression
Link ID: 17122 - Posted: 08.04.2012

By RODNEY MUHUMUZA KITGUM, Uganda — Augustine Languna's eyes welled up and then his voice failed as he recalled the drowning death of his 16-year-old daughter. The women near him looked away, respectfully avoiding the kind of raw emotion that the head of the family rarely displayed. "What is traumatizing us," he said after regaining his composure, "is that the well where she died is where we still go for drinking water." Joyce Labol was found dead about three years ago. As she bent low to fetch water from a pond a half mile from Languna's compound of thatched huts, an uncontrollable spasm overcame her. The teen was one of more than 300 young Ugandans who have died as a result of the mysterious illness that is afflicting more and more children across northern Uganda and in pockets of South Sudan. The disease is called nodding syndrome, or nodding head disease, because those who have it nod their heads and sometimes go into epileptic-like fits. The disease stunts children's growth and destroys their cognition, rendering them unable to perform small tasks. Some victims don't recognize their own parents. Ugandan officials say some 3,000 children in the East African country suffer from the affliction. Some caregivers even tie nodding syndrome children up to trees so that they don't have to monitor them every minute of the day. Beginning Monday, Uganda hosts a four-day international conference on nodding syndrome that health officials believe will lead to a clearer understanding of the mysterious disease. © 2012 NBCNews.com

Keyword: Development of the Brain; Aggression
Link ID: 17102 - Posted: 07.30.2012

by Andy Coghlan Treating disease by stimulating brain cells with light is a step closer to reality following the first demonstration that the technique can improve mental performance in monkeys. Two monkeys performed better on simple computer tasks after light was used to boost the activity of brain cells necessary for the task. "For the first time, we were able to change behaviour in primates with our technique," says Wim Vanduffel of Massachusetts General Hospital in Charlestown, who is head of the group that performed the experiment. Known as optogenetics, the method has the potential to treat conditions such as epilepsy, where the light could temporarily deactivate the brain cells that cause seizures, or Parkinson's disease, where it can activate cells that make dopamine, the neurotransmitter vital for controlling mobility that those with Parkinson's lack. Previously, it has been used in nematode worms to trigger them to lay eggs, and mice to relieve depression and paralysis. Researchers have also used it in monkeys, but only on single, isolated neurons. Vanduffel and his colleagues wanted to see if they could extend this to entire networks of cells, boosting a monkey's ability to perform a simple computer-based task. Natural performance enhancers First, Vanduffel's team scanned the two monkeys' brains using functional magnetic resonance imaging while they followed a green dot on a computer screen. From the scans, the researchers could tell that the monkeys relied on an area of the brain called the arcuate sulcus to do the task. © Copyright Reed Business Information Ltd.

Keyword: Vision
Link ID: 17098 - Posted: 07.28.2012

A widely prescribed drug for multiple sclerosis may not slow the disease from progressing, a British Columbia study shows. Beta interferons are prescribed for the relapse-remitting form of MS, which affects about 85 per cent of people with the disease in Canada. As the name suggests, people with relapsing-remitting MS have flare-ups when new symptoms appear or olds ones return or worsen. There are also periods of remission with partial or full recovery. "In clinical trial situations, it has been quite evident for years that patients receiving beta interferon treatment have reduced frequency of relapses as well as reduced frequency of new lesions seen on MRI," Dr. Joel Oger, who is also a neurologist with the UBC Hospital MS Clinic, said in a release. "This study following a large number of patients for a long time in 'real life situation' does not show an association of the beta interferons with long term disability and tends to confirm a more modern way of understanding MS: relapses may not be responsible for long term disability in all patients and another mechanism might be at work as well." The study in Wednesday's issue of the Journal of the American Medical Association compared 868 people prescribed the drug with 829 who were untreated as well as 959 who were treated before interferon beta was approved. © CBC 2012

Keyword: Multiple Sclerosis
Link ID: 17058 - Posted: 07.18.2012

By Dwayne Godwin and Jorge Cham In 1953, Henry Molaison underwent radical surgery in an attempt to stop his epileptic seizures... © 2012 Scientific American,

Keyword: Learning & Memory; Aggression
Link ID: 17046 - Posted: 07.16.2012

Analysis by Sheila Eldred If you've seen "Silence of the Lambs," you probably remember the scene where the lights go out on Jodie Foster and the unseen Buffalo Bill reaches out to her. That's because at that moment, your brain was probably at its peak of engagement, according to a study by a team of researchers from The City College of New York and Columbia University. "Peak correlations of neural activity across viewings can occur in remarkable correspondence with arousing moments of the film," the researchers wrote in the journal "Moreover, a significant reduction in neural correlation occurs upon a second viewing of the film or when the narrative is disrupted by presenting its scenes scrambled in time." Tense scenes present prime conditions for peak brain activity. They usually contain at least two of the three components identified by the researchers as most engaging: powerful visual cues, ominous music, and meaningful scene changes. To make the correlation, the researchers hooked 20 subjects up to EEG devices (electroencephalography measures electrical activity across the scalp) as they showed scenes from three films: Alfred Hitchcock's "Bang! You're Dead," Sergio Leone's "The Good, the Bad and the Ugly," and an amateur film of people walking on a college campus as a control. © 2012 Discovery Communications, LLC

Keyword: Emotions; Aggression
Link ID: 17038 - Posted: 07.14.2012

Ewen Callaway A genetic test could help to determine whether a multiple sclerosis patient would benefit from a promising therapy. Like diabetes, most forms of cancer and other common diseases, there is no single gene that causes the autoimmune condition multiple sclerosis (MS). Dozens of genetic variations act in concert with environmental factors to cause the debilitating neurological disease. Yet a single genetic variant may explain why drugs that treat other autoimmune diseases tend to make MS symptoms worse, and could identify other MS patients who might benefit from the therapies. Researchers say that the findings, which are published online in Nature1, also highlight how genome-wide association studies (GWAS) can yield useful medical insights. GWAS compare thousands of people who have a particular disease, detailing hundreds of thousands of genetic variations between them. The goal is to identify variations that are more common in people with the condition than in healthy people. Most such studies uncover scores of genetic variants associated with the disease in question, each increasing a person’s chances of developing the condition by a small percentage. Such is the case for a DNA letter in the gene that encodes the protein called tumour necrosis factor receptor 1 (TNFR1). The protein senses a potent immune molecule called tumour necrosis factor (TNF) that destroys cancerous cells but that is also implicated in autoimmune disease. People of European ancestry who have two ‘A’s at that particular spot on the genome are 12% more likely to develop MS than those with two ‘G’s at that spot. © 2012 Nature Publishing Group

Keyword: Multiple Sclerosis; Aggression
Link ID: 17015 - Posted: 07.10.2012

Scientists have identified why a once-promising class of drugs do not help people with multiple sclerosis. An Oxford University team say an genetic variant linked to MS means the drugs which work for patients with other autoimmune diseases will not work for them. The team, writing in Nature, say the drugs can actually make symptoms worse. Experts say the work shows how a person's genetic make-up could affect how they responded to treatment. The drugs, called anti-TNFs, work for patients with rheumatoid arthritis and inflammatory bowel disease, but they have not done so for patients with MS and researchers were unsure why. The Oxford University team looked at one particular genetic variant, found in a gene called TNFRSF1A, which has previously been associated with the risk of developing MS. The normal, long version of the protein sits on the surface of cells and binds the TNF signalling molecule, which is important for a number of processes in the body. But the team discovered the variant caused the production of an altered, shortened version which "mops up" TNF, preventing it from triggering signals - essentially the same thing that TNF blocking drugs do. BBC © 2012

Keyword: Multiple Sclerosis; Aggression
Link ID: 17011 - Posted: 07.09.2012

Analysis by Jesse Emspak The phrase, "use your brainpower" may soon become literal. Engineers at MIT have developed a tiny prototype fuel cell that creates electricy from the body's natural sugars. The fuel cell could be used to power brain implants for treating epilepsy, Parkinson's diseases and paralysis. Currently, devices implanted in the body are typically powered by lithium-ion batteries, but they have a limited lifetime and need to be replaced. Opening up the body to replace a battery is not something doctor like to do, but doing it in the brain is even less desirable. The researchers, led by Rahul Sarpeshkar, an associate professor of electrical engineering and computer science, built the fuel cell using a platinum catalyst at one end and a layer of carbon nanotubes at the other. It rests on a silicon chip, allowing it to be connected to electronics that would be used in brain implants. coughing robot As glucose passes over the platinum, electrons and hydrogen ions are stripped off as it is oxidized. That's what makes the current. At the other end of the cell, oxygen mixes with the hydrogen to make water when it hits the layer of single-walled carbon nanotubes. The cell produces up to 180 microwatts, enough to power a brain implant that might send signals to bypass damaged region, or stimulate part of the brain (a treatment used in disorders such as Parkinson's). © 2012 Discovery Communications, LLC.

Keyword: Robotics
Link ID: 16982 - Posted: 06.28.2012

A diet high in cholesterol may help people with a fatal genetic disease which damages the brain, according to early studies in mice. Patients with Pelizaeus-Merzbacher disease struggle to produce a fatty sheath around their nerves, which is essential for function. A study, published in Nature Medicine, showed that a high-cholesterol diet could increase production. The authors said the mice "improved dramatically". Pelizaeus-Merzbacher disease (PMD) is one of many leukodystrophies in which patients struggle to produce the myelin sheath. It protects nerve fibres and helps messages pass along the nerves. Without the sheath, messages do not travel down the nerve - resulting in a range of problems including movement and cognition. Researchers at the Max Planck Institute of Experimental Medicine, in Germany, performed a trial on mice with the disease and fed them a high cholesterol diet. The first tests were on mice when they were six weeks old, after signs of PMD had already emerged. Those fed a normal diet continued to get worse, while those fed a cholesterol-enriched diet stabilised. BBC © 2012

Keyword: Multiple Sclerosis; Aggression
Link ID: 16940 - Posted: 06.20.2012