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    You are here : Home » MS Research News » New Discoveries » Oligodendrocytes and Astrocytes

    Oligodendrocytes and Astrocytes

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    Researchers report potential MS breakthrough

    LIFCaltech researchers report a possible breakthrough in multiple sclerosis medicine in the latest issue of the Journal of Neuroscience.

    Scientists led by Paul Patterson, the Biaggini Professor of Biological Sciences at Caltech, have found a way to use tissue from the brain to help heal neurons damaged by the disease. The scientists developed a gene therapy to stimulate production of specialized nerve cells called oligodendrocytes that make material that protects neurons.

    The therapy uses leukemia inhibitory factor (LIF), a naturally occurring protein.

    “We're using the brain's own progenitor cells as a way to boost repair," Benjamin Deverman, a postdoctoral biology student at Caltech and lead author of the paper, said in a statement.

    "This new application of LIF is an avenue of therapy that has not been explored in human patients with MS," Deverman said, adding the therapy might also help spinal-cord injury patients. Patterson and Deverman, who’ve done their initial research on mice, plan to develop their research to bring it closer to potential human clinical trials.

    More information: The work done in this study, "Exogenous Leukemia Inhibitory Factor Stimulates Oligodendrocyte Progenitor Cell Proliferation and Enhances Hippocampal Remyelination," was funded by the California Institute for Regenerative Medicine, the National Institutes of Neurological Disorders and Stroke, and the McGrath Foundation.

    Source: Pasadena Sun © Copyright Pasadena Sun 2012 (10/02/12)

    Research overturns theories about Multiple Sclerosis

    Brain CellsThe trigger for multiple sclerosis could be completely different to what scientists have believed, say Australian researchers who made the breakthrough discovery that could overturn decades of MS research.

    Their work, which suggests the past 40 years of MS research has been looking at the wrong parts of the central nervous system, could eventually lead to new treatments.

    About 15,000 Australians have MS, which is a notoriously difficult disease to diagnose and treat.

    Up until now it was thought to begin with the disintegration of protective coverings around neurons in the central nervous system, although why that occurred was not known.

    John Prineas and his colleague John Parratt discovered that before the protective coverings disintegrate other vital cells, known as astrocytes, die. "Astrocytes are very common and important cells … their role in the central nervous system is basically to look after everything else," Professor Prineas, from the University of Sydney, said.

    Earlier research by Vanda Lennon, an Australian working at the Mayo Clinic in the US, had discovered an antibody which attacked astrocytes in a subtype of MS called neuromyelitis optica, but up until now it had not been shown astrocytes were damaged in patients who had died with MS or neuromyelitis optica.

    "There is the possibility that the discovery … of that antibody may turn out to be the most important breakthrough in the last 40 years or so," Professor Prineas said.

    MS is one of a number of diseases such as type 1 diabetes and rheumatoid arthritis where a person's immune system over-reacts and starts attacking them. Researchers have been unable to discover why the body would attack the protective coating of cells. But now they could begin to investigate why it was attacking the astrocytes, potentially laying the path for new methods of diagnosis and treatment for the condition.

    Dr Parratt, a lecturer at the University of Sydney and research fellow at Multiple Sclerosis Research Australia, said the antibody attacking the astrocytes has only been found in patients with neuromyelitis optica. There was now a chance to look for a similar antibody which was behind the astrocyte damage in MS patients.

    The research is published in the journal Multiple Sclerosis.

    Source: The Sydney Morning Herald Copyright © 2010 Fairfax Media (27/09/10)

    Multiple Sclerosis research may benefit from new findings

    OligodendrocyteMyelin, which insulates axons in the central nervous system is produced by oligodendrocytes. But not all oligodendrocytes are equal.

    Led by Dr. Jonathan Vinet of the University Laval in Quebec, scientists have identified three different types of oligodendrocytes in the mouse hippocampus: “ramified,” “stellar,” and “smooth.”

    Each type displayed varying morphological characteristics, mainly in shape, volume, and branching behavior, which led the researchers to believe that the three types represent different stages of maturation.

    As described in the paper, “Subclasses of oligodendrocytes populate the mouse hippocampus,” published in the European Journal of Neuroscience, the “smooth,” or most simple type possibly morphs into the “stellar,” which eventually develops into the most complex of the three, the “ramified” oligodendrocyte.

    The identification of these morphologically distinct oligodendrocyte populations in the hippocampus may help researchers determine which specific types of oligodendrocytes are affected in diseases such as schizophrenia and multiple sclerosis.

    Using a Neurolucida system with an Olympus AX-50 microscope, the scientists formed 3D reconstructions of the hippocampal oligodendrocytes integral to their study. They then analyzed their tracings with Neurolucida Explorer.

    “Without Neurolucida we couldn’t have carried out this study,” said Dr. Attila Sik, “it was an essential component. Nice piece of equipment, for sure.”

    Source: MBF Mindset (13/05/10)

    Myelin oligodendrocyte glycoprotein antibodies and multiple sclerosis in healthy young adults

    Background: It remains uncertain whether the presence of serum anti-myelin oligodendrocyte glycoprotein (MOG) antibodies in healthy individuals contributes to predict their risk of developing multiple sclerosis (MS).

    Methods: Prospective, nested case-control study of more than 7 million US military personnel who have serum samples stored in the Department of Defense Serum Repository. A total of 126 MS cases and 252 controls matched by age, sex, race/ethnicity, and dates of blood collection were included in the analysis. An ELISA was used to detect IgM and IgG antibodies to MOG. Analyses were conducted with and without adjustment for serum titers of antibodies to the Epstein-Barr nuclear antigen (EBNA), which are an established risk factor for MS.

    Results: The presence of anti-MOG IgG antibodies in serum was associated with an increase in risk of developing MS (relative risk for anti-MOG IgG+/IgM– vs seronegativity to both anti-MOG IgM and IgG: 2.03; 95% CI: 1.19–3.46; p = 0.01). This association, however, was attenuated and no longer significant after adjustment for titers of antibodies to EBNA, which were higher among individuals positive for anti-MOG antibodies.

    Conclusion: Our findings suggest that although individuals with anti-myelin oligodendrocyte glycoprotein (MOG) antibodies have an increased risk of developing multiple sclerosis, this association may at least in part reflect cross-reactivity between MOG and Epstein-Barr nuclear antigen.

    H. Wang, MD, PhD, K. L. Munger, MSc, M. Reindl, PhD, E. J. O’Reilly, MSc, L. I. Levin, PhD, MPH, T. Berger, MD, MSc and A. Ascherio, MD, DrPH

    From the Departments of Nutrition (H.W., K.L.M., E.J.O., A.A.) and Epidemiology (A.A.), Harvard School of Public Health, Boston; Channing Laboratory, Department of Medicine, Brigham and Women’s Hospital, and Harvard Medical School (A.A.), Boston, MA; Clinical Department of Neurology (M.R., T.B.), Innsbruck Medical University, Austria; and Division of Preventive Medicine (L.I.L.), Walter Reed Army Institute of Research, Silver Spring, MD.

    Source: NEUROLOGY 2008;71:1142-1146 © 2008 American Academy of Neurology (07/10/08)

    Multiple Sclerosis :: Stress response prevents neurodegeneration
    Multiple sclerosis (MS) is a debilitating immune-mediated disease of the brain and spinal cord (the central nervous system [CNS]).

    It is characterised by infiltration of the CNS by inflammatory cells and destruction of cells that reside in the CNS, known as oligodendrocytes (ODCs). The soluble factor IFN-gamma has a detrimental effect on disease in patients with MS. However, studies using the mouse model of MS, known as EAE, indicate that IFN-gamma can also have a protective effect. In a study appearing in the February issue of the Journal of Clinical Investigation, researchers from the University of Chicago describe a mechanism by which IFN-gamma protects mice from developing EAE.

    Brian Popko and colleagues showed that if IFN-gamma is expressed in the brain before EAE is induced it protects mice from neurodegeneration. IFN-gamma–mediated protection was associated with an increased survival of ODCs and activation of the integrated stress response in ODCs. The ODC integrated stress response, which is triggered in cells by non-optimal environmental conditions, was mediated by PERK, as the beneficial effects of IFN-gamma were lost in PERK-deficient mice.

    This study describes a mechanism by which IFN-gamma can protect mice from developing EAE and leads the authors to suggest that the timing of IFN-gamma expression in the brain and the extent of the stress response in the ODCs are factors determining whether or not IFN-gamma has a protective or detrimental effect on EAE.

    Furthermore, they suggest that therapies designed to activate the integrated stress response in ODCs might be beneficial to individuals with MS. However, in an accompanying commentary, Jason Lees and Anne Cross sound a note of warning, saying that "an understanding of these relationships [between the level of IFN-gamma in the brain and the extent of the integrated stress response in ODCs] would be required before attempting to alter ODC stress responses in MS patients for therapeutic benefit."

    Source: ©2002-2007 (05/02/07)

    Time-Lapse Movies Reveal Surprisingly Dynamic Process Of Insulating Nerves
    Much like the electrical wiring in your house, the nerves in your body need to be completely covered by a layer of insulation to work properly.

    Instead of red, white or black plastic, however, the wiring in the nervous system is protected by layers of an insulating protein called myelin. These layers increase the speed that nerve impulses travel throughout the brain and the body. The critical role they play is dramatically illustrated by the symptoms of multiple sclerosis, which is caused by lesions that destroy myelin. These include: blindness, muscle weakness and paralysis, loss of coordination, stuttering, pain and burning sensations, impotence, memory loss, depression and dementia.

    The formation of myelin sheaths during development requires a complex choreography generally considered to be one of nature's most spectacular examples of the interaction between different kinds of cells. Now, a group of Vanderbilt researchers has successfully produced movies that provide the first direct view of the initial stage of this process: the period when the cells that ultimately produce the myelin sheathing spread throughout the developing nervous system. The results were published online in the journal Nature Neuroscience on Nov. 12 and should aid in the design of new therapies to promote the repair of this protective layer following disease or injury.

    "We discovered that this process is far more dynamic than anyone had dreamed," says Bruce Appel, the associate professor of biological sciences and Kennedy Center investigator who headed up the study.

    In the central nervous system, the myelin membranes are produced by cells called oligodendrocytes. These cells must be distributed uniformly along axons — the long, wire-like extensions from neurons that carry nerve impulses — so that the membranes, which wrap the nerve fibers like millions of microscopic pieces of electrician's tape, can cover the axons completely and uniformly. The wrapping process takes place near the end of fetal development and actually continues for some time after birth.

    In order to study this process, Appel and his research group — graduate students Brandon Kirby and Jimann Shin along with post doctoral fellows Norio Takada and Andrew Latimer — created a transgenic zebrafish which incorporates fluorescent proteins in the cells involved in myelination. The zebrafish is a small tropical fish that has become a popular species for studying the process of development in vertebrates (animals with backbones). Because zebrafish embryos are transparent and develop within a few days, they allow biologists to watch developmental processes as they take place: something they cannot do with mice or other mammals. These characteristics allowed the Vanderbilt researchers to obtain images of the cells involved in myelination using a confocal microscope and edit them into time-lapse movies.

    The oligodendrocytes that produce the myelin membranes arise from mobile, dividing cells called "oligodentrocyte progenitor cells" or OPCs. OPCs are made in special locations in the brain and spinal cord. These cells seek out axons and spread out along them. Then, at a certain point, a fraction of the OPCs transform themselves into oligodentrocytes and begin wrapping axons. Each of these cells can wrap portions of several different axons and each axon is wrapped by a large number of oligodentrocytes.

    Before the Vanderbilt study, there were a number of different theories about how OPCs space themselves along axons. One was that the axons themselves produce some kind of positional cues that the OPCs follow. Another was that the OPCs sense each other and adjust their position accordingly: a mechanism somewhat similar to that which soldiers on the parade ground use to align a formation by extending their right arm and adjusting their position until their outstretched fingers touch the shoulder of the person on the right.

    Previous studies of OPCs grown in tissue culture had seen that they could generate small pseudopods, called filopodia, but no one knew what their purpose might be. So, when the researchers began viewing their movies, they were excited to observe that the cells were continually sending out filopodia in different directions. They found that OPCs not only generate these tiny tentacles, but keep them extending and contracting in a fashion reminiscent of the party noise-makers called blow-outs that unroll when you blow on them and snap back when you stop. They observed that when one of these tiny tentacles touches a neighboring OPC, the cells react by moving in the opposite direction. This caused a surprising amount of movement as the OPCs repeatedly readjusted their positions.

    "This could serve as a surveillance mechanism that allows the OPCs to determine the presence or absence of nearby cells of the same type," says Appel, "and could explain how they distribute themselves along the axons."

    The researchers used the same system to see how the OPCs respond to injuries and conditions like multiple sclerosis. They did so by using a laser to destroy the OPCs along a short length of the embryo's spine a day before the axon-wrapping stage begins. They found that the OPCs in the vicinity of the gap start dividing to produce additional cells that move into the gap. After a day, the number of OPCs in the gap had grown to 50 percent of normal and after four days it had risen to 70 percent.

    "Now that we have a better understanding of OPC and oligodendrocyte behaviors, we are in a much better position to identify and study the genes that are necessary for myelination," says Appel, "and having these genes in hand should aid in the design of drugs to promote remyelination following disease or injury."

    Robert Kelsh from the University of Bath and Thomas Carney now at the Max-Planck Insitute for Immunobiology also contributed to the study. The research was supported by funding from the National Institutes of Health, the National Multiple Sclerosis Foundation and Vanderbilt University.

    Source: ScienceDaily Copyright © 1995-2006 ScienceDaily LLC (21/11/06)

    Central nervous system beckons attack in MS-like disease
    It may sound like a case of blame the victim, but researchers at Washington University School of Medicine in St. Louis have shown that cells in the central nervous system can sometimes send out signals that invite hostile immune system attacks. In mice the researchers studied, this invitation resulted in damage to the protective covering of nerves, causing a disease resembling multiple sclerosis.

    "It's been clear for quite a while that our own lymphocytes (white blood cells) have the ability to enter the central nervous system and react with the cells there," says John Russell, Ph.D., professor of molecular biology and pharmacology. "Under normal circumstances, the brain and the immune system cooperate to keep out those cells that might harm the brain. But in people with multiple sclerosis, they get in."

    The researchers found that they could prevent destructive immune cells from entering nervous system tissue by eliminating a molecular switch that sends "come here" messages to immune cells. Ordinarily, flipping that switch would cause immune cells to rush to the vicinity of the cells that sent the signals and destroy whatever they consider a danger — including nerve cell coatings.

    But in the mice in which the switch was removed, the researchers saw that immune cells previously primed by the scientists to attack the central nervous system (CNS) did not enter the CNS, and the mice stayed healthy.

    In contrast, normal mice treated with the same hostile immune cells had numerous immune cells in their CNS tissue and developed symptoms similar to multiple sclerosis.

    "What allows the primed lymphocytes into the CNS are signals from the CNS asking them in," Russell says. "We determined that the astrocytes, the specialized cells that provide nutrients to neurons, are among the cells most active in sending signals to attract lymphocytes."

    The molecular switch that sends the call to immune cells is termed the tumor necrosis factor receptor (TNFR). When TNFR is activated, it causes cells to send out signal molecules called chemokines that direct immune cells to the site of damage or infection. The researchers found that astrocytes in mice were producing chemokines in response to activation of their TNFR molecules.

    TNFR activation also makes the astrocytes bristle with specific adhesion molecules that act like Velcro to bind to similar molecules on the surface of the immune cells. That allows the immune cells that are attracted by the chemokines to stick around and do more harm.

    One of the most promising new drugs for treating multiple sclerosis, natalizumab (tradename Tysabri), works by blocking the ability of the immune cells to stick in the CNS through this Velcro mechanism, Russell notes. Natalizumab is being tested in clinical trials and appears to be much better at preventing the nerve cell destruction associated with multiple sclerosis than previous therapies.

    "Experiments by others suggested that natalizumab prevented immune cells from crossing the blood-brain barrier — it was thought to prevent the cells from leaving the blood stream," Russell says. "We are working on that question, and we think that it doesn't necessarily prevent them from getting out of the blood, but it does keep them from getting further into the brain. The immune cells pile up in the space around the blood vessels. This space, the perivascular space, serves as a gatekeeper to determine what gets in and what doesn't."

    Next, the research team will study various regions of the brain to determine the types of signals sent to and from different areas of the CNS to the immune system.

    Gimenez MA, Sim J, Archambault AS, Klein RS, Russell JH. A tumor necrosis factor dependent receptor 1-dependent conversation between central nervous system-specific T cells and the central nervous system is required for inflammatory infiltration of the spinal cord. American Journal of Pathology 2006;168(4):1200-1209.

    Source: Washington University in St. Louis Copyright 2000-2006, Washington University in St. Louis (09/06/06)

    The pathology of multiple sclerosis: a paradigm shift?

    PURPOSE OF REVIEW: Detailed immunopathological assessment of multiple sclerosis tissue remains the research tool most likely to elucidate the major processes involved in disease pathogenesis and tissue injury. Such studies steer and provide the impetus for refining cellular/molecular investigations and developing more relevant disease models in animals.

    RECENT FINDINGS: Recent observations in early multiple sclerosis lesions challenge the traditional hypothesis that multiple sclerosis arises as the result of a primary autoimmune process that specifically targets myelin antigen(s).

    A new multiple sclerosis paradigm proposes that oligodendrocyte apoptosis is the earliest change in newly forming lesions and that tissue injury is amplified by the subsequent recruitment of a systemic immune response. Over months to years the pathology of multiple sclerosis is transformed and the changes which accompany the late phase of the disease suggest that the inflammatory response becomes progressively 'compartmentalised' and therefore largely isolated from systemic influence with time.

    SUMMARY: Recent pathological studies raise important questions regarding the aetiology of oligodendrocyte apoptosis, the mechanisms by which the accompanying inflammatory response amplifies tissue injury and the regulation of central nervous system immunity. An improved understanding of these processes is essential for advancing therapeutic interventions applicable to different stages of the disease.

    Authors Barnett MH, Sutton I.

    Source: PubMed - PMID: 16702829 (19/05/06)

    New 'stars' in formation of nerve cell insulation
    The insulating myelin sheath enwrapping the cable-like axons of nerve cells is the major target of attack of the immune system in multiple sclerosis. Such attack causes neural short-circuits that give rise to the muscle weakness, loss of coordination, and speech and visual loss in the disease.

    Now, Douglas Fields of the National Institute of Child Health and Human Development and his colleagues have reported in the March 16, 2006, issue of Neuron that supporting cells called astrocytes in the central nervous system (CNS) promote myelination by releasing an immune system molecule that triggers myelin-forming cells to action. The finding, they say, "may offer new approaches to treating demyelinating diseases."

    Astrocytes, so named because of their star-like shape, are the most prominent supporting cells in the nervous system. They provide critical regulatory molecules that enable nerve cells to develop and connect properly.

    In their studies, Fields and his colleagues sought to understand other research findings indicating that the electrical activity of nerve cells somehow triggers myelin-producing cells, called oligodendrocytes, to form the myelin membrane surrounding the nerve cells.

    In their studies, the researchers cultured rat and mice neurons together with oligodendrocytes and conducted experiments to understand the mechanism of myelin formation. They found that electrical stimulation of the neurons caused production of the energy molecule ATP, and this ATP increases myelination.

    Drawing on other researchers' findings that an immune signaling molecule called leukemia inhibitory factor (LIF) might be involved, they explored whether LIF was a key molecule in the ATP-triggered myelination machinery. Their experiments revealed LIF's central role in the machinery, and further studies showed that astrocytes were the source of that LIF.

    Indeed, when they tested directly whether astrocytes were important in promoting myelination in the cell cultures, they found the cells to be potent promoters of the process.

    "Taken together, these results reveal a new mechanism by which electrical activity promotes myelination of CNS axons at a later developmental stage and possibly into postnatal life," concluded the researcher. They wrote that the "new findings may provide novel approaches to understanding and treating myelin disorders in the CNS" after the immature oligodendrocytes have matured into myelinating cells.

    The researchers include Tomoko Ishibashi, Kelly A. Dakin, Beth Stevens, Philip R. Lee, and R. Douglas Fields of the National Institute of Child Health and Human Development in Bethesda, MD; Serguei V. Kozlov and Colin L. Stewart of the National Cancer Institute in Bethesda, MD. This work was supported by the intramural research program at National Institutes of Health, National Institute of Child Health and Human Development.

    Ishibashi et al.: "Astrocytes Promote Myelination in Response to Electrical Impulses." Publishing in Neuron 49, 823–832, March 16, 2006. DOI 10.1016/j.neuron.2006.02.006

    Source: Cell Press (16/03/06)

    Netrin acts as a repellent cue for migrating oligodendrocytes

    A new discovery by scientists at the Montreal Neurological Institute at McGill University may provide insights into Multiple Sclerosis.

    In a study published in the May issue of the Journal of Neuroscience (J. Neuroscience 2003 23: 3735-3744), Dr. Tim Kennedy and colleagues have discovered that a protein called netrin-1 directs the normal movement of the cells that become oligodendrocytes in the developing spinal cord. Oligodendrocytes are the cells that provide critical support for the nerve cells – they make myelin, the electrical insulation of the central nervous system. They are also the cells that degenerate and die in Multiple Sclerosis (MS). Although oligodendrocytes play an essential role in the nervous system, many aspects of their basic cell biology are not well understood, which is one of the reasons why MS is such a mystery. This research finding identifies a fundamental mechanism that directs migrating oligodendrocyte precursor cells. This has implications for understanding demyelinating diseases such as MS, where even a small myelin deficit can lead to functional impairment of the nerve cell.

    An estimated 50,000 people have MS [in Canada], which is most often diagnosed in young adults. Its devastating effects last a lifetime and may include problems in seeing or speaking, difficulty with balance and coordination, and even paralysis. "Dr. Kennedy's research will contribute to the growing body of knowledge which is developing new therapies for MS," said Dr. William McIlroy, MS Society of Canada national medical advisor.

    "In order to treat a disease in the most effective way possible, it is necessary to understand the manner in which proteins function," said Dr. Alan Bernstein, President of the Canadian Institutes of Health Research. "Dr. Kennedy's discovery is a vital step in understanding the root causes of MS and will play a role in one day developing an entirely new generation of drugs to combat this condition."

    It is widely known that netrins are proteins that guide nerve cell axons to their target in the developing nervous system leading them to their target. In the embryo, this can involve axons travelling long distances. "In addition to this long-range function, last year we reported that netrin-1 may have a short-range function associated with the cell surface that contributes to the maintenance of nerve cell-oligodendrocyte interactions in the mature nervous system. This prompted us to study the possibility that netrin-1 might contribute to oligodendrocyte development," says Dr. Tim Kennedy, MNI researcher and co-discoverer of netrins.

    The researchers showed that netrin acts as a repellent cue for migrating oligodendrocytes- directing them to move away from sources of netrin. "This result was very exciting for us because netrins are ancient signposts in developing nervous systems," says Dr. Kennedy. "They've been pointing axons in the right direction for at least 500 million years. Although 500 million years ago very simple animals did exist -like little worms, oligodendrocytes had not yet evolved. Evolution has been suggested to work like someone who tinkers with bits and pieces to make new things, like pasting together bits and pieces of other pictures to make a new image. In the natural history of oligodendrocyte cell biology, netrin is an example of something that was already there doing other things, that got picked up along the way and applied to a new purpose."

    "Understanding the basic biology of oligodendrocytes is very important for MS. If we can understand what stimulates them to function, then perhaps we can develop new targets for therapy," explained Dr. Jack Antel, a neurologist at the Montreal Neurological Institute specializing in the research and treatment of MS.

    This research was supported by the Canadian Institutes of Health Research (CIHR) and the Multiple Sclerosis Society of Canada.

    This study is available online at

    Dr. Tim Kennedy is Associate Professor in McGill University's Faculty of Medicine. His research laboratory is at the Montreal Neurological Institute. Dr. Kennedy completed his doctoral studies at Columbia University (1992) with Dr. Eric Kandel, winner of the 2000 Nobel Prize in Medicine, and his conducted his post-graduate with Dr. Marc Tessier-Lavigne, at the University of California, San Francisco. Dr. Kennedy's research has led to several fundamental discoveries in neurobiology including the discovery of netrins. Dr. Kennedy is the author of more than 30 scientific papers.

    The CIHR  is Canada's premier agency for health research. Its objective is to excel, according to internationally accepted standards of scientific excellence, in the creation of new knowledge and its translation into improved health for Canadians, more effective health services and products and a strengthened health care system. CIHR's Institute of Neurosciences, Mental Health and Addiction supports research to enhance mental health, neurological health, vision, hearing, and cognitive functioning and to reduce the burden of related disorders through prevention strategies, screening, diagnosis, treatment, support systems, and palliation.

    The Multiple Sclerosis Society of Canada ( is the only national voluntary organization in Canada to support both MS research and services for people with MS, an unpredictable often disabling disease of the central nervous system. May is MS Awareness Month.

    The Montreal Neurological Institute ( is a McGill University ( research and teaching institute, dedicated to the study of the nervous system and neurological diseases. Since its founding in 1934 by the renowned Dr. Wilder Penfield, the MNI has helped put Canada on the international map. It is one of the world's largest institutes of its kind; MNI researchers are world leaders in biotechnology, brain imaging, cognitive neuroscience and the study and treatment of epilepsy, multiple sclerosis and neuromuscular disorders.

    Source: The Montreal Neurological Institute (31/05/05)

    © Multiple Sclerosis Resource Centre

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