Links for Keyword: Multiple Sclerosis

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


Links 21 - 40 of 191

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

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
Link ID: 17122 - Posted: 08.04.2012

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

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 17058 - Posted: 07.18.2012

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

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
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

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 17011 - Posted: 07.09.2012

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

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 16940 - Posted: 06.20.2012

By Nathan Seppa By delving into the components of protective nerve coatings that get damaged in multiple sclerosis, scientists have identified a handful of lipid molecules that appear to be attacked by an immune system run amok. Bolstering the supply of these lipids might help preserve these nerve coatings and, in the process, knock back the inflammation that contributes to their destruction, researchers report in the June 6 Science Translational Medicine. In MS patients, rogue antibodies assault myelin, the fatty sheath that insulates nerves and facilitates signaling. Inflammation exacerbates the attack on myelin and the cells that make it. But other details of MS, including the roles of myelin lipids, have been less clearly understood. “I think this is a very good study,” says Francisco Quintana, an immunologist at Harvard Medical School. “Overall, there are not many papers on lipids in MS. Technically, they are challenging and require a lot of expertise.” To explore the role of lipids, the researchers studied spinal fluid from people with MS, healthy people and patients with other neurological disorders. Tests on the fluid showed that antibodies targeted four lipids more often in MS patients than in the other groups. Examination of autopsied brains from MS patients and people without MS revealed that, in the MS patients, these four lipids were depleted at the sites where the nerve coatings were damaged. © Society for Science & the Public 2000 - 2012

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 16886 - Posted: 06.07.2012

Smoking marijuana may help relieve the muscle tightness and pain of multiple sclerosis, a small U.S. study suggests. Many people with MS often suffer from spasticity, an uncomfortable and disabling condition in which the muscles become tight and difficult to control. Spasticity can be controlled with medications but the symptoms may continue or the anti-spasticity drugs may carry adverse effects such as drowsiness, sedation, and muscle weakness. The medical marijuana used in the study the strength of cigarettes most commonly available in the community at the time of the research. Most trials testing medical marijuana have focused on oral forms. Now a randomized trial has put smoked cannabis to the test against placebo for 30 people with MS whose spasticity resisted treatment. "Using an objective measure, we saw a beneficial effect of inhaled cannabis on spasticity among patients receiving insufficient relief from traditional treatment," Dr. Jody Corey-Bloom, of the department of neuroscience at University of California, San Diego and her co-authors concluded in Monday's issue of the Canadian Medical Association Journal. In the study, the average age of participants was 50 and 63 per cent were female. More than half of the participants needed walking aids and 20 per cent used wheelchairs. Copyright © CBC 2012

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology
Link ID: 16791 - Posted: 05.15.2012

Hundreds of Canadian MS patients have gone out of country for a controversial neck vein treatment in recent years. Hundreds of Canadian MS patients have gone out of country for a controversial neck vein treatment in recent years. (CBC) Saskatchewan multiple sclerosis patients hoping to take part in a clinical trial of a controversial treatment may soon get a call from the ministry of health. But only around 10 per cent of those who applied will actually get that call. Deb Jordan, a ministry spokeswoman, said 670 people had signed up as of Thursday, just ahead of the Friday midnight deadline for applications to be part of a two-year, double-blind trial of what has been dubbed liberation therapy. Jordan said patient names will be randomly drawn to determine who will fill 86 spots in the test, which will take place in Albany, N.Y. A successful candidate must be a Saskatchewan resident, under the age of 60 and not had liberation treatment. "Once we verify that information, then the applicant will be forwarded to the folks who are involved in the clinical trial," said Jordan. "I want to also emphasize that the fact that a patient may be drawn does not necessarily mean that they will move on to the clinical trial. © CBC 2012

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 16438 - Posted: 02.27.2012

By Jennifer LaRue Huget Multiple sclerosis has long been understood to be an autoimmune disease in which the body’s immune system, for reasons poorly understood, responds destructively to antigens in the central nervous system. But research published in December in The Quarterly Review of Biology posits a different way of looking at MS. Angelique Corthals, a forensic anthropologist at the John Jay College of Criminal Justice in New York, suggests that MS may result from problems with the way the body metabolizes lipids, or fats in the blood, which in turn cause inflammation and spark a series of damaging events. Corthals, in her lengthy review and analysis of existing research, notes that MS shares that underlying mechanism with atherosclerosis. (“Sclerosis” refers to hardening or scarring such as the build-up of plaque in arteries and the development of plaques in the brain associated with MS.) She concludes that viewing MS in this light helps explain many mysteries that the autoimmune model leaves unanswered, including the role genetics play in MS risk, the environmental elements or pathogens that may trigger disease onset, and the reasons MS strikes twice as many women as men. (Atherosclerosis affects men more commonly than women; Carthals suggests gender differences in lipid metabolism may play a big role in determining who gets which condition.) Because anti-inflammatory drugs such as statins commonly used to fight cardiovascular disease have also been used to treat symptoms of MS, she writes, such drugs may become part of more comprehensive and effective MS treatments than currently exist. © 1996-2012 The Washington Post

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 11: Emotions, Aggression, and Stress
Link ID: 16208 - Posted: 01.03.2012

(HealthDay News) -- New research suggests that in addition to the disabling lesions it's known to cause, multiple sclerosis also damages the part of the brain that affects thinking skills, motor function and the senses. "The thalamus is a central area that relates to the rest of the brain and acts as the 'post office,'" study co-author Khader Hasan, an associate professor at University of Texas Health Science Center at Houston, said in a university news release. "It also is an area that has the least amount of damage from lesions in the brain, but we see volume loss, so it appears other brain damage related to the disease is also occurring." Hasan and colleagues published their observations in a recent issue of the Journal of Neuroscience. The study authors noted that aging alone can bring about changes in the size of the thalamus region, resulting in some shrinkage after age 70. However, the research team wanted to see if multiple sclerosis (MS) -- which is often associated with the onset of dementia -- accelerates such structural shifts. The radiology researchers used cutting-edge MRI scanning equipment to analyze brain structure in 109 MS patients, compared to 255 healthy men and women. The result: MS patients had greater volume loss in the thalamus region than healthy patients, after accounting for age. And the greater the loss in thalamus volume, the more disabled the patient was, the investigators noted. © 2011 U.S.News & World Report LP

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 2: Functional Neuroanatomy: The Nervous System and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 2: Cells and Structures: The Anatomy of the Nervous System
Link ID: 16195 - Posted: 12.31.2011

By LAURIE TARKAN Three years ago, Kristie Salerno Kent, a singer-songwriter, was standing in a security line at the airport on her way home from a gig when her legs went numb. “From the waist down, it felt as though I was trying to walk through a bowl of oatmeal,” said the 38-year-old musician, who has multiple sclerosis. She inched her way to a security officer, who called for a wheelchair and helped remove her shoes and belt to get her through security. Frightened and embarrassed, she was taken to her gate in a wheelchair. Three months later, she experienced another flare-up. While giving a live television interview about a short film she had made on living with M.S., she suddenly lost her ability to speak. “It was as if my mouth was packed with marbles,” she said. “I kept trying to say, ‘I’m sorry,’ to the reporter, but nothing came out that made sense.” The medication she was taking to prevent these attacks was losing its effect, so her doctor suggested she switch to Tysabri, one of the newer, more potent “disease-modifying drugs,” which reduce the severity and frequency of relapses. She also began taking Ampyra, which early last year became the first drug approved to treat any M.S. symptom. She hasn’t had a flare-up since. After decades of basic research on M.S., the last five years have brought a rapid rollout of new and sophisticated drugs that are changing how this disease is managed and offering patients new hope. © 2011 The New York Times Company

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 16190 - Posted: 12.27.2011

A rare genetic variant which causes reduced levels of vitamin D appears to be directly linked to multiple sclerosis, says an Oxford University study. UK and Canadian scientists identified the mutated gene in 35 parents of a child with MS and, in each case, the child inherited it. Researchers say this adds weight to suggestions of a link between vitamin D deficiency and MS. The study is in Annals of Neurology. Multiple sclerosis is an inflammatory disease of the central nervous system (the brain and spinal cord). Although the cause of MS is not yet conclusively known, both genetic and environmental factors and their interactions are known to be important. Oxford University researchers, along with Canadian colleagues at the University of Ottawa, University of British Columbia and McGill University, set out to look for rare genetic changes that could explain strong clustering of MS cases in some families in an existing Canadian study. They sequenced all the gene-coding regions in the genomes of 43 individuals selected from families with four or more members with MS. The team compared the DNA changes they found against existing databases, and identified a change in the gene CYP27B1 as being important. When people inherit two copies of this gene they develop a genetic form of rickets - a disease caused by vitamin D deficiency. BBC © 2011

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
Link ID: 16134 - Posted: 12.10.2011

By Tina Hesman Saey The spark that ignites multiple sclerosis may come from within. A new study in mice points to normal intestinal bacteria as a trigger for the immune disorder. In patients with multiple sclerosis, the body’s immune system attacks the brain, stripping away a protective sheath called myelin from nerve cells. This causes inflammation that leads to the disease. Although the exact causes of MS are not known, scientists generally agree that a genetic predisposition combines with one or more environmental triggers to set off the attack on the brain. The new study provides evidence that friendly bacteria may be one of those triggers. Mice genetically engineered to develop multiple sclerosis–like symptoms don’t get the disease when raised without any bacteria in their guts, a research team from Germany reports online October 26 in Nature. But germ-free mice that were then colonized with intestinal bacteria quickly developed the disease, the team found. About 80 percent of mice with intestinal bacteria developed MS-like symptoms, but none of the germ-free mice did. The result is not a total surprise. Previous reports had indicated that gut bacteria might be involved in autoimmune disorders such as MS, juvenile diabetes and arthritis, says Simon Fillatreau, an immunologist at the German Rheumatism Research Center in Berlin. “So maybe it was expected, but that it is really such a black-and-white response? Probably not,” says Fillatreau, who was not involved in the study. “It’s very big news.” © Society for Science & the Public 2000 - 2011

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Homeostasis: Active Regulation of the Internal Environment
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 9: Homeostasis: Active Regulation of the Internal Environment
Link ID: 15950 - Posted: 10.27.2011

Duncan Graham-Rowe The first drug to show signs of not just halting multiple sclerosis (MS), but actually reversing the nerve damage caused by the condition, has taken a significant step towards clinical approval. The results of a phase III trial, presented on 22 October at the 5th Joint Triennial Congress of the European and Americas Committees for Treatment and Research in Multiple Sclerosis, in Amsterdam, found that 78% of patients treated with the monoclonal antibody alemtuzumab remained free from relapse after two years — and half the relapse rate of one of the standard therapies, interferon β-1a (marketed as Rebif, among other names). However, alemtuzumab did not perform quite as well as it had in earlier trials1. There was some evidence that it had reversed damage to nerves, but the result was not statistically significant, says Alasdair Coles, a neuroscientist at the University of Cambridge, UK, and the UK chief investigator of the Comparison of Alemtuzumab and Rebif Efficacy in Multiple Sclerosis (CARE-MS) I trial. Coles told the meeting that magnetic resonance imaging showed that subjects taking alemtuzumab had also lost less brain volume than those taking Rebif, a proxy measure for overall tissue damage. "Alemtuzumab has eliminated the loss of brain tissue," he says. Just 8% of patients taking alemtuzumab experienced a worsening in disability according to standard measures, in comparison with 11% taking Rebif. There was no statistical difference between the two groups, but Coles puts this down to Rebif performing better than expected. "The patients recruited in this trial showed very little worsening of disability," he says. © 2011 Nature Publishing Group,

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 15947 - Posted: 10.25.2011

Multiple sclerosis might be connected to a lack of steroids in the brain, Alberta researchers have found. MS attacks the brain and spinal cord, causing inflammation and damage that can lead to paralysis and sometimes blindness. In the September issue of the journal Brain, neurologist Dr. Chris Power of the University of Alberta Hospital in Edmonton and his colleagues describe a new potential avenue for treating MS. There are some drugs related to neurosteroids that are actively in clinical trials, Dr. Chris Power said.There are some drugs related to neurosteroids that are actively in clinical trials, Dr. Chris Power said. CBC The discovery centres on neurosteroids, which help brain cells to talk, grow and repair themselves. The findings open up a brain process "that we might be able to direct so that we can prevent damage and maybe even repair the damaged brain," Power said Wednesday. Brains of people who died with multiple sclerosis showed lower levels of neurosteroids, the researchers found. The team believes that by replacing neurosteroids, it might be possible to alleviate symptoms or even prompt recovery, based on the results of their test tube and mouse modeling studies. "We've actually jumped the queue a little bit because there are some drugs related to neurosteroids that are actively in clinical trials," Power said. "This certainly provides fertile ground." © CBC 2011

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 5: Hormones and the Brain
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 8: Hormones and Sex
Link ID: 15828 - Posted: 09.22.2011

Researchers at the University of Calgary have documented serious health complications in multiple sclerosis patients who travelled outside of Canada to undergo a controversial treatment for their disease. Many MS patients have travelled overseas to find clinics willing to provide the treatment invented by Italian physician Paolo Zamboni, which uses balloon angioplasty to open up blocked veins in the necks of those who suffer from the disease. The new study followed five patients who had the vein opening therapy and were treated in Calgary hospitals in October and November last year after complications from their surgeries. The lead author of the paper, Dr. Jodie Burton, admits that it is difficult to draw conclusions since there were only five patients involved and it's not known how many Canadians went to locations like the United States, Mexico, India, and Poland to have the procedure done. But she says the seriousness of the complications should serve as a — quote — "cautionary tale" to anyone considering having the procedure done. Burton says patients shouldn't be afraid to let their doctors know they had the treatment and physicians need to know what to watch for as a result. In June, the federal government announced it will hold early-stage clinical trials into the treatment. © The Canadian Press, 2011 © CBC 2011

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 15722 - Posted: 08.25.2011

By Steve Connor, Science Editor One of the biggest studies ever undertaken into multiple sclerosis has identified 29 new genetic factors that are implicated in the development of the disease. The nature of the genes that have been linked with MS has demonstrated with a high degree of certainty that the root causes of the illness can be traced to the faulty functioning of the body's immune system, scientists said. Nearly 10,000 individuals with multiple sclerosis took part in the study and their genomes were scanned to find the genetic differences with the DNA of over 17,000 healthy people. The total number of genetic faults linked with the disease now amounts to 57. Alastair Compston, of the University of Cambridge, one of the lead authors of the study published in Nature, said there have been rival theories about what are the important factors implicated in triggering the disease, one of the most common neurological conditions affecting young adults. "Our research settles a long-standing debate on what happens first in the complex sequences of events that leads to disability in multiple sclerosis," he said. "This has important implications for future treatment strategies. It puts immunology right at the front end of the disease, absolutely." The study involved a relatively new technique called genome-wide scanning, which involves analysing the entire length of a patient's DNA for anomalies that appear not to exist in healthy people and could therefore be linked with the disease. Previous research had established that multiple sclerosis has a strong genetic component. ©independent.co.uk

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 15664 - Posted: 08.11.2011

By Tia Ghose Blocking a death receptor causes damaged myelin, the protective coating surrounding nerve cells, to repair itself, according to a study published Sunday (July 3) in Nature Medicine. The finding suggests that drugs targeting the receptor could help treat multiple sclerosis by reversing the myelin damage characteristic of the disease. “Showing remyelination, as they do in vivo and in vitro, is a pretty cool result,” said Richard Ransohoff, a Cleveland Clinic neuroscientist who was not involved in the work. The new receptor is a novel first step in potentially repairing damaged nerves of multiple sclerosis patients, he said. Current multiple sclerosis drugs slow the disease’s progression by quieting the inflammatory response of the immune system, which attacks the myelin surrounding nerve cells and kills oligodendrocytes, brain cells that make and repair myelin. Without their myelin, nerve cells gradually lose their ability to send electrical signals. But because they suppress the immune response, these drugs make patients more susceptible to rare infections such as viral brain inflammation and diseases such as leukemia. They also cannot undo existing damage, leading scientists to seek out approaches that stimulate the growth of new myelin or the restoration of existing myelin. Though research has identified several candidate molecules that promote myelin survival, none have yet proven to do so successfully in patients. © 1986-2011 The Scientist

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 7: Life-Span Development of the Brain and Behavior
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals; Chapter 13: Memory, Learning, and Development
Link ID: 15532 - Posted: 07.07.2011

People with multiple sclerosis may show blocked neck veins as a result of the disease rather than as a cause, a large study published Wednesday suggests. The findings cast doubt on the theory that blocked or narrowed veins are a main cause of MS, study author Dr. Robert Zivadinov of the University of Buffalo said. The findings published in the journal Neurology were consistent with thinking that the condition — also known as chronic cerebrospinal venous insufficiency, or CCSVI — is more common in patients with multiple sclerosis but not to the degree first reported by the Italian doctor Paolo Zamboni. "These findings indicate that CCSVI does not have a primary role in causing MS," said Zivadinov, who has worked with Zamboni. Zamboni proposed that multiple sclerosis may be linked with vascular problems, and that using angioplasty, or ballooning, to open blocked neck veins can help treat MS symptoms by changing blood flow patterns. Patients eager for surgery For more than a year, Canadians with MS have been leaving the country to get the surgery, despite reluctance from neurologists at home. An ultrasound technician, who did not know which group the subjects were in, did the test. The team found 56 per cent of people in the MS group met the criteria for CCSVI, as did 23 per cent of the healthy controls and 46 per cent of people with other neurological diseases. © CBC 2011

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 15213 - Posted: 04.14.2011

An oral drug for multiple sclerosis has been approved for some MS patients in Canada. Until Thursday's announcement, drug treatment options for MS patients in this country were limited to medications taken regularly by injection or infusion. Gilenya, also called fingolimod, is a capsule taken once a day for people with the relapsing-remitting form of MS. These patients have relapses that continue to worsen in severity, disability level, or who are unable to tolerate injections. "It's a very long awaited type of medication for our patients," said Dr. Heather MacLean, a neurologist at the Ottawa Hospital who specializes in MS. Needle injections under the skin are painful and are associated with itching and lumpy skin reactions, and the weekly intramuscular medication can also cause muscle pain, noted MacLean, who has treated patients with the new drug as part of early clinical trials. From her experience, MacLean estimated that 10 to 20 per cent of relapsing-remitting MS patients currently on treatment stand to benefit from Gilenya. "It always surprises me how patients really require different modalities of treatment based on their own personal disease course and their own treatment goals. To have another available option for them, I think they'll be thrilled." Gilenya's manufacturer, Novartis, submitted clinical trial data to Health Canada to get the approval. © CBC 2011

Related chapters from BP7e: Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Related chapters from MM:Chapter 3: Neurophysiology: The Generation, Transmission, and Integration of Neural Signals
Link ID: 15097 - Posted: 03.11.2011