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Academic Press Mechanisms of Disease Pathogenesis in Multiple Sclerosis

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Description

Multiple Sclerosis (MS) is an autoimmune disease which targets the central nervous system (CNS). MS is the most common cause of non-traumatic neurological disability in young adults with a prevalence of around 1 in 1000 and evidence that the incidence is increasing. Peripheral immune cells recruited to the CNS are thought to play central roles in disease pathogenesis, including monocytes and T cells, as well as multiple antigen presenting cells such as dendritic cells and B cells involved in the activation of autoimmune T cells. Neurodegeneration driven by CNS resident cells such as astrocytes and microglia is also known to contribute to disease pathogenesis, particularly to disease progression and the irreversible accumulation of neurologic disability. Genetic and environmental factors such as pollutants, viral infections and the microbiome play an important role in MS pathogenesis. Indeed, recent studies suggest that the course of MS is influenced by the effects of the commensal microbiome on the gut-CNS axis. Mechanisms of Disease Pathogenesis in Multiple Sclerosis summarizes our current understanding on MS, its clinical features and monitoring with available biomarkers, focusing on mechanisms that drive disease pathogenesis, and their control by genetic, environmental factors, and novel therapies for disease management. This book is written for neurologists, neuroimmunologists and clinical, translational and basic researchers interested in mechanisms of neurodegeneration. Review Comprehensive summary of mechanisms that drive disease pathogenesis in Multiple Sclerosis From the Back Cover <p>Multiple Sclerosis (MS) is an autoimmune disease which targets the central nervous system (CNS). MS is the most common cause of non-traumatic neurological disability in young adults with a prevalence of around 1 in 1000 and evidence that the incidence is increasing. Peripheral immune cells recruited to the CNS are thought to play central roles in disease pathogenesis, including monocytes and T cells, as well as multiple antigen presenting cells such as dendritic cells and B cells involved in the activation of autoimmune T cells. Neurodegeneration driven by CNS resident cells such as astrocytes and microglia is also known to contribute to disease pathogenesis, particularly to disease progression and the irreversible accumulation of neurologic disability. Genetic and environmental factors such as pollutants, viral infections and the microbiome play an important role in MS pathogenesis. Indeed, recent studies suggest that the course of MS is influenced by the effects of the commensal microbiome on the gut-CNS axis.</p> <p><i>Mechanisms of Disease Pathogenesis in Multiple Sclerosis</i> summarizes our current understanding on MS, its clinical features and monitoring with available biomarkers, focusing on mechanisms that drive disease pathogenesis, and their control by genetic, environmental factors, and novel therapies for disease management. This book is written for neurologists, neuroimmunologists and clinical, translational and basic researchers interested in mechanisms of neurodegeneration.</p> About the Author Francisco J. Quintana, PhD, is an Associate Professor of Neurology at the Center for Neurologic Diseases, at Brigham and Women’s Hospital, Harvard Medical School, and an Associate Member at the Broad Institute of Harvard and MIT. Dr. Quintana’s research investigates signaling pathways that control the immune response and neurodegeneration, with the ultimate goal of identifying novel therapeutic targets and biomarkers for immune-mediated disorders. Dr. Quintana has published over 140 peer reviewed articles and book chapters. He is the recipient of the Lady Anne Chain Prize for Academic Excellence and Scientific Achievements, the Junior Investigator Award from the National Multiple Sclerosis Society, the Pathway to Independence Award of the National Institute of Allergy an

Product Specifications

Format
paperback
Domain
Amazon UK
Release Date
28 June 2024
Listed Since
23 February 2022

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