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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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发表于 2025-3-28 15:45:43 | 显示全部楼层
Statins and Demyelination,n order to reduce atherogenesis and cardiovascular morbidity. Moreover, statins have been shown to exert pleiotropic immunomodulatory effects that might be of therapeutic benefit in autoimmune disorders. Statins appear to alter immune function largely independent of lipid lowering and rather through
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W. James Catallo,Jay L. Comeaux,Thomas Junknts purported to promote or enhance remyelination. This chapter reviews the technology of imaging of the brain, its application to MS, and the current state of imaging techniques for measuring remyelination and the health of the associated neurons in the setting of MS.
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Lecture Notes in Earth Sciencesdulators and may influence diseases such as multiple sclerosis (MS) or may be used therapeutically to modulate the immune response. More recently identified hormones, such as leptin and gherlin, may also influence the course of disease. This chapter reviews some of the evidence that supports a role for hormones in MS.
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Lecture Notes in Earth Sciencesderate success. Several recent studies have reported lower levels of uric acid (UA), a major scavenger of reactive nitrogen species, in MS patients, while other studies found no such correlation. Here, we discuss these studies as well as current efforts to manipulate serum UA levels in MS patients.
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Book 2008tory response is the primary contributor to demyelination, Dr. Rodriguez and colleagues take a fresh, bold look at the causes and possible treatments of MS....Assuming oligodendrocyte injury as a prerequisite to MS, the authors explore viruses, toxins and genetic defects as possible culprits. They p
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The Handbook of Environmental ChemistryS from the expression consequences of MS. The use of new methodologies and technologies to refine the phenotype, such as brain spectroscopy, PET and functional magnetic resonance imaging combined with novel computational tools and a better understanding of the human genome architecture, may help resolve the genetic causes of MS.
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https://doi.org/10.1007/BFb0011119w they can be used to study different aspects of remyelination. We also describe the optimal use of these models, highlighting potential pitfalls in interpretation, and how remyelination can be unequivocally recognized. Finally, we discuss the role of toxin models alongside viral and immune-mediated models of demyelination.
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