Titlebook: Advances in Multiple Sclerosis and Experimental Demyelinating Diseases; Moses Rodriguez Book 2008 The Editor(s) (if applicable) and The Au

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https://doi.org/10.1007/BFb0011119 injury and promotes maximal remyelination within 5 weeks after a single low dose (25 μg/kg). The IgM isoform of this reparative antibody is required for in vivo function. We hypothesize that the IgM clusters membrane domains and associated signaling molecules on the surface of target cells. Current

pulmonary

https://doi.org/10.1007/BFb0011119 axonal damage, and remyelination, and studies utilizing in vivo T1 and T2 relaxometry, provide insight into the pathology of demyelinating diseases at previously unprecedented details. The technical challenges of small voxel in vivo MR spectroscopy and the biologically relevant information obtained

motor-unit

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0070-217X etic tools for identifying patients who are most likely to experience spontaneous remyelination. Epidemiology studies offer additional avenues of treatment. Exa978-3-642-43783-0978-3-540-73677-6Series ISSN 0070-217X Series E-ISSN 2196-9965

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Advances in Multiple Sclerosis and Experimental Demyelinating Diseases

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Benign Multiple Sclerosis: A Distinct Clinical Entity with Therapeutic Implications,clerosis. Based on the Olmsted County population prevalence cohort study performed at the Mayo Clinic, MS patients with EDSS scores of 2 or lower followed for a period of 5–10 years have a very small risk of developing disability over the next 10–20 years. Based on these findings, this chapter revie