Advances in multiple Sclerosis and Experimental Demyelinating Diseases /
Rodriguez, Moses.
Advances in multiple Sclerosis and Experimental Demyelinating Diseases / edited by Moses Rodriguez. - recurso en línea. - Current Topics in Microbiology and Immunology, 318 0070-217X ; .
Springer eBooks
Benign Multiple Sclerosis: A Distinct Clinical Entity with Therapeutic Implications -- Pathological Heterogeneity of Idiopathic Central Nervous System Inflammatory Demyelinating Disorders -- Multiple Sclerosis Genetics -- Imaging of Remyelination and Neuronal Health -- Immunological Aspects of Axon Injury in Multiple Sclerosis -- The Multiple Sclerosis Degradome: Enzymatic Cascades in Development and Progression of Central Nervous System Inflammatory Disease -- Genetic Analysis of CNS Remyelination -- Remyelination in Experimental Models of Toxin-Induced Demyelination -- Remyelination-Promoting Human IgMs: Developing a Therapeutic Reagent for Demyelinating Disease -- Neuroimaging of Demyelination and Remyelination Models -- Hormonal Influences in Multiple Sclerosis -- Statins and Demyelination -- Role of Uric Acid in Multiple Sclerosis -- Neuromyelitis Optica: Clinical Syndrome and the NMO-IgG Autoantibody Marker.
"There is a need for a paradigm shift in our thinking about the pathogenesis of multiple sclerosis." Challenging Charcot’s hypothesis that inflammatory 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 present novel methods to interrupt and reverse demyelination. This book examines the correlation between axonal loss and clinical deficits, including the implied role of the CD8+ T cell and perforin. It assesses proteases, specifically, kallikrein 6, which are strongly associated with active demyelination. By directing natural autoantibodies against oligodendrocytes that demonstrate remyelination in animal models, the authors envision clinical trials for remyelination enhancement. As internationally recognized specialists in a wide range of MS disciplines, the authors explore genetic tools for identifying patients who are most likely to experience spontaneous remyelination. Epidemiology studies offer additional avenues of treatment. Examples include uric acid, statin drugs, estrogen and progesterone. MS affects nearly 400,000 people in the United States, many of whom are between18 and 40 years of age. With their novel, multifaceted approach to basic science—and their applications in understanding cause and treatment—the authors offer help to clinicians and hope to patients.
9783540736776
10.1007/9783540736776 doi
QR180-189.5
Advances in multiple Sclerosis and Experimental Demyelinating Diseases / edited by Moses Rodriguez. - recurso en línea. - Current Topics in Microbiology and Immunology, 318 0070-217X ; .
Springer eBooks
Benign Multiple Sclerosis: A Distinct Clinical Entity with Therapeutic Implications -- Pathological Heterogeneity of Idiopathic Central Nervous System Inflammatory Demyelinating Disorders -- Multiple Sclerosis Genetics -- Imaging of Remyelination and Neuronal Health -- Immunological Aspects of Axon Injury in Multiple Sclerosis -- The Multiple Sclerosis Degradome: Enzymatic Cascades in Development and Progression of Central Nervous System Inflammatory Disease -- Genetic Analysis of CNS Remyelination -- Remyelination in Experimental Models of Toxin-Induced Demyelination -- Remyelination-Promoting Human IgMs: Developing a Therapeutic Reagent for Demyelinating Disease -- Neuroimaging of Demyelination and Remyelination Models -- Hormonal Influences in Multiple Sclerosis -- Statins and Demyelination -- Role of Uric Acid in Multiple Sclerosis -- Neuromyelitis Optica: Clinical Syndrome and the NMO-IgG Autoantibody Marker.
"There is a need for a paradigm shift in our thinking about the pathogenesis of multiple sclerosis." Challenging Charcot’s hypothesis that inflammatory 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 present novel methods to interrupt and reverse demyelination. This book examines the correlation between axonal loss and clinical deficits, including the implied role of the CD8+ T cell and perforin. It assesses proteases, specifically, kallikrein 6, which are strongly associated with active demyelination. By directing natural autoantibodies against oligodendrocytes that demonstrate remyelination in animal models, the authors envision clinical trials for remyelination enhancement. As internationally recognized specialists in a wide range of MS disciplines, the authors explore genetic tools for identifying patients who are most likely to experience spontaneous remyelination. Epidemiology studies offer additional avenues of treatment. Examples include uric acid, statin drugs, estrogen and progesterone. MS affects nearly 400,000 people in the United States, many of whom are between18 and 40 years of age. With their novel, multifaceted approach to basic science—and their applications in understanding cause and treatment—the authors offer help to clinicians and hope to patients.
9783540736776
10.1007/9783540736776 doi
QR180-189.5