Links for Keyword: Multiple Sclerosis

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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

Scientists have identified a way of prompting nerve system repair in multiple sclerosis (MS). Studies on rats by Cambridge and Edinburgh University researchers identified how to help stem cells in the brain regenerate myelin sheath, needed to protect nerve fibres. MS charities said the "exciting" Nature Neuroscience work offered hope of restoring physical functions. But they cautioned it would be some years before treatments were developed. MS is caused by a defect in the body's immune system, which turns in on itself, and attacks the fatty myelin sheath. It is thought to affect around 100,000 people in the UK. Around 85% have the relapsing/remitting form of the condition, in which "flare-ups" which cause disability, are followed by a recovery of a level of the lost physical function. In this form of MS, there does appear to be some natural myelin repair. However, around 10% of people are diagnosed with a progressive form of MS, where the decline continues without any periods of remission. BBC © MMX

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: 14746 - Posted: 12.06.2010

By DENISE GRADY For her first appointment with Dr. Daniel Simon, Neelima Raval showed up with a rolling file cabinet full of documents. She had downloaded every word written by or about Dr. Paolo Zamboni, a vascular surgeon from Italy with a most unorthodox theory about multiple sclerosis. Dr. Zamboni believes that the disease, which damages the nervous system, may be caused by narrowed veins in the neck and chest that block the drainage of blood from the brain. He has reported in medical journals that opening those veins with the kind of balloons used to treat blocked heart arteries—an experimental treatment he calls the “liberation procedure”— can relieve symptoms. The idea is a radical departure from the conventional belief that multiple sclerosis is caused by a malfunctioning immune system and inflammation. The new theory has taken off on the Internet, inspiring hope among patients, interest from some researchers and scorn from others. Supporters consider it an outside-the-box idea that could transform the treatment of the disease. Critics call it an outlandish notion that will probably waste time and money, and may harm patients. These critics warn that multiple sclerosis has unpredictable attacks and remissions that make it devilishly hard to know whether treatments are working — leaving patients vulnerable to purported “cures” that do not work. Copyright 2010 The New York Times Company

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: 14212 - Posted: 06.29.2010

Scientists have uncovered new evidence suggesting that damage to nerve cells in people with multiple sclerosis (MS) accumulates because the body’s natural mechanism for repairing the nerve coating called myelin stalls out. The new research, published by Howard Hughes Medical Institute investigator David H. Rowitch and colleagues in the July 2009 issue of the journal Genes & Development, shows that repair of nerve fibers is hampered by biochemical signals that inhibit cellular repair workers in the brain, called oligodendrocytes. The symptoms of MS, which range from tingling and numbness in the limbs to loss of vision and paralysis, develop when nerve cells lose their ability to transmit a signal. Axons, which are the fibrous cables radiating from nerve cells, transmit impulses to neighboring neurons. They are dependent on myelin, which protects nerve cells and helps transmit their electrical signals properly. In people with MS, immune cells attack and erode this protective layer of myelin. In the early stages of the disease, damage accumulates in the myelin sheath only, but it does not affect the nerve cells themselves. Later on, axons without myelin and the nerve cells themselves die. Although damaged myelin can usually be repaired, in some people with MS the repair effort is inefficient, said Rowitch, who is at the University of California, San Francisco. This could be because oligodendrocytes themselves might not work properly, or they may be killed off by the disease. Rowitch explained that in chronically demyelinated areas of the central nervous system, oligodendrocyte precursor cells have been found, but they appear stalled in development and never become fully functional oligodendrocytes. © 2009 Howard Hughes Medical Institute.

Related chapters from BP7e: Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 15: Emotions, Aggression, and Stress
Related chapters from MM:Chapter 4: The Chemistry of Behavior: Neurotransmitters and Neuropharmacology; Chapter 11: Emotions, Aggression, and Stress
Link ID: 13010 - Posted: 06.24.2010

ATLANTA - Tests of the first two oral drugs developed for treating multiple sclerosis show that both cut the frequency of relapses and may slow progression of the disease, but with side effects that could pose a tough decision for patients. Two experts not involved in the studies said the drugs appear effective but with potentially dangerous side effects. It’s too soon to know if the pills will be approved by the government or widely adopted by physicians, they said. About 2.5 million people around the world have multiple sclerosis, a neurological disease that can cause muscle tremors, paralysis and problems with speech, memory and concentration. The studies involve the most common form of the disease, in which people are well for a while and then suffer periodic relapses. Current treatments can reduce the duration and severity of symptoms but require daily or regular shots or infusions. The new studies tested two types of pills. Cladribine, made by Merck Serono, is already sold to treat a rare blood cancer. For MS, it would be taken eight to 10 days a year. Fingolimod is a daily MS pill being developed by Novartis. The research found that patients on the pills were about half as likely to suffer relapses of symptoms as those who took dummy pills or a commonly prescribed shot for MS. © 2010 The Associated Press.

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: 13697 - Posted: 06.24.2010

Depression, coordination and speech problems, muscle weakness and disability are just a few of the symptoms of Multiple Sclerosis (MS). Researchers from the Mouse Biology Unit of the European Molecular Biology Laboratory (EMBL) in Italy and the Department of Neuropathology at the Faculty of Medicine, University of Göttingen, Germany, have now discovered that these symptoms are aggravated by a specific signal in cells in the nervous system. The study, which will appear in this week's online issue of Nature Immunology, suggests that blocking the proteins that regulate the signal might be an efficient strategy for new therapies against MS. Nerve cells in our brain and spinal cord communicate with each other using electrical signals. This communication is fast and efficient because - just like wires in an electrical circuit - the axons of our nerves are surrounded by an insulating layer. In MS this protective sheath, made up of a mixture of lipids and proteins called myelin, gets destroyed by cells of our own immune system, and the communication between nerve cells gets disrupted. A central player in the molecular mechanisms behind MS is a signaling molecule called NF-kB. "We have known for a long time that NF-kB is crucially involved in MS," says Manolis Pasparakis, a former Group Leader at EMBL's Mouse Biology Unit who now works as a Professor at the Institute for Genetics at the University of Cologne, "but until now it was not clear if it was friend or foe. We were not sure whether it protects the brain cells against the consequences of the disease or actually aggravates the damage."

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: 9209 - Posted: 06.24.2010

Columbus, Ohio – A tiny difference in a gene may signal that a person is twice as susceptible to multiple sclerosis (MS) as normal. It could also foretell of a more rapidly progressing form of the disease, according to new research at The Ohio State University College of Medicine and Public Health. The study focused on a gene known as CD24, which directs the making of a protein found on immune cells and that plays an important role in immune responses. Specifically, the study looked at two different versions of the CD24 gene. The two versions differ because of a minute difference known as a single nucleotide polymorphism, or SNP (pronounced ‘snip’). A SNP is a difference of one so-called base, or nucleotide, in the gene’s DNA compared to the same gene in another person. SNPs are common and occur naturally. They may help give a unique pattern to each person’s DNA.

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: 4700 - Posted: 06.24.2010

By Nathan Seppa Ultraviolet radiation from sunshine seems to thwart multiple sclerosis, but perhaps not the way most researchers had assumed, a new study in mice suggests. If validated in further research, the finding could add a twist to a hypothesis that has gained credence in recent decades. The report appears online March 22 in the Proceedings of the National Academy of Sciences. Scientists have hypothesized that MS is rare in the tropics because people synthesize ample vitamin D from exposure to the UV radiation in equatorial sunlight. What’s more, MS is more common in the high latitudes of northern parts of Europe and North America than in regions farther south. That pattern has led to the assumption that higher levels of vitamin D might prevent people from developing MS, what became known as the latitude hypothesis. But a direct cause-and-effect relationship between vitamin D deficiency and MS has never been established. In past experiments, giving vitamin D supplements to mice with an MS-like disease required giving the animals harmful amounts of the nutrient, notes Hector DeLuca, a biochemist at the University of Wisconsin–Madison. “It just didn’t add up,” he says. “We decided to go back and see if maybe UV light by itself was doing something.” In MS, the fatty myelin sheaths that insulate nerves in the central nervous system are damaged by attacks by the immune system. In a series of experiments in mice, DeLuca and his team induced a condition comparable to human MS by injecting the animals with proteins that instigate similar myelin damage. © Society for Science & the Public 2000 - 2010

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: 13901 - Posted: 06.24.2010

Katharine Sanderson Human stem cells have been used to correct abnormal brain development in mice with fatal brain disorders, offering hope for treating a range of neurological disorders including some deadly childhood genetic diseases. Those behind the new treatment hope that human clinical trials could be just a few years away. The treatment uses human glial progenitor cells — cells that can differentiate into the glial cells that, among other things, make up myelin. Myelin, a protein that insulates the long 'arms' of nerve cells, called axons, helps the conduction of neural signals throughout the nervous system. A team led by Steven Goldman, at the University of Rochester in New York, took the progenitor cells from white matter in the fetal human brain and injected them into the spinal cords of mutant shiverer mice shortly after their birth. The mice, which shiver and shake as their name suggests, have severe neurological defects caused by a genetic mutation that stops them producing myelin. Without myelin, neural signals get stuck, causing potentially fatal disease. “There’s no way we’d be able to conduct a [neural] signal very far if it weren’t for myelin,” Goldman explains. As they develop, shiverer mice become unable to walk forwards, have increasing numbers of seizures, and typically die at just 18–21 weeks of age. © 2008 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: 11686 - Posted: 06.24.2010

Boston, MA – Researchers from the Harvard School of Public Health, Kaiser Permanente, and a team of collaborators have found further evidence implicating the Epstein-Barr virus (EBV) as a possible contributory cause to multiple sclerosis (MS). The study appears in the advance online edition of the June 2006 issue of Archives of Neurology. MS is a chronic degenerative disease of the central nervous system. Women are more likely than men to get the disease and it is the most common neurologically disabling disease in young adults. Although genetic predisposition plays an important role in determining susceptibility, past studies have shown that environmental factors are equally important. EBV is a herpes virus and one of the most common human viruses worldwide. Infection in early childhood is common and usually asymptomatic. Late age at infection, however, often causes infectious mononucleosis. In the U.S., upwards of 95% of adults are infected with the virus, but free of symptoms. EBV has been associated with some types of cancer and can cause serious complications when the immune system is suppressed, for example, in transplant recipients. There is no effective treatment for EBV. The study population was made up of more than 100,000 members of the Kaiser Permanente Northern California (KPNC) health plan, who provided blood specimens as part of medical examinations between 1965 and 1974.

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: 8769 - Posted: 06.24.2010

PORTLAND, Ore. – Oregon Health & Science University researchers have measured genetic changes reflecting a drop in the body's ability to suppress inflammatory cells that attack nerve fibers and promote progression of multiple sclerosis. In a study published in the July issue of the Journal of Neuroscience Research, OHSU scientists, in collaboration with The Immune Response Corp. of Carlsbad, Calif., found that MS patients have lower expression of the FOXP3 gene found in a subset of T-cells that may regulate defense against MS and other autoimmune diseases, such as diabetes and arthritis. They say that when FOXP3 is reduced due to abnormalities in its expression, the suppressive activity of regulatory T-cells, or T-regs, also plummets. "This is an important marker," said Arthur Vandenbark, Ph.D., professor of neurology and molecular microbiology and immunology, OHSU School of Medicine, and senior research career scientist at the Portland Veterans Affairs Medical Center. "This is the first publication that links FOXP3 with reduced suppression in MS." But there may be a solution to the FOXP3 loss. NeuroVax, a T-cell receptor peptide vaccine co-discovered by Vandenbark and colleagues at The Immune Response Corp., was shown in a separate study to increase FOXP3 expression levels among MS patients receiving injections of the drug for a year. "When we vaccinate with the T-cell receptor peptides – the NeuroVax – we can restore the FOXP3 levels," said Vandenbark, who presented the results of the NeuroVax and Journal of Neuroscience Research studies to the European Neurological Society this week in Vienna. "So not only have we identified the marker to show that there are fewer of these T-reg cells present in MS patients, but we're providing a solution for correcting the problem, at least in some patients."

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: 7562 - Posted: 06.24.2010

PORTLAND, Ore. – Oregon Health & Science University researchers have measured genetic changes reflecting a drop in the body's ability to suppress inflammatory cells that attack nerve fibers and promote progression of multiple sclerosis. In a study published in the July issue of the Journal of Neuroscience Research, OHSU scientists, in collaboration with The Immune Response Corp. of Carlsbad, Calif., found that MS patients have lower expression of the FOXP3 gene found in a subset of T-cells that may regulate defense against MS and other autoimmune diseases, such as diabetes and arthritis. They say that when FOXP3 is reduced due to abnormalities in its expression, the suppressive activity of regulatory T-cells, or T-regs, also plummets. "This is an important marker," said Arthur Vandenbark, Ph.D., professor of neurology and molecular microbiology and immunology, OHSU School of Medicine, and senior research career scientist at the Portland Veterans Affairs Medical Center. "This is the first publication that links FOXP3 with reduced suppression in MS." But there may be a solution to the FOXP3 loss. NeuroVax, a T-cell receptor peptide vaccine co-discovered by Vandenbark and colleagues at The Immune Response Corp., was shown in a separate study to increase FOXP3 expression levels among MS patients receiving injections of the drug for a year.

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: 7549 - Posted: 06.24.2010