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Multiple Sclerosis and Cerebral Endothelial Dysfunction: Mechanisms Publisher



Alexander JS1 ; Zivadinov R2 ; Maghzi AH3, 4 ; Ganta VC1 ; Harris MK5 ; Minagar A5
Authors
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Authors Affiliations
  1. 1. Department of Cellular and Molecular Physiology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, United States
  2. 2. Buffalo Neuroimaging Analysis Center, The Jacobs Neurological Institute, Department of Neurology, School of Medicine and Biomedical Sciences, State University of New York at Buffalo, Buffalo, NY, United States
  3. 3. Isfahan Research Committee of Multiple Sclerosis (IRCOMS), Isfahan University of Medical Sciences, Isfahan, Iran
  4. 4. Neuroimmunology Unit, Neuroscience Center, Institute of Cell and Molecular Science, Barts and the London School of Medicine and Dentistry, London, United Kingdom
  5. 5. Department of Neurology, Louisiana State University Health Sciences Center, Shreveport, LA 71130, 1501 Kings Highway, United States

Source: Pathophysiology Published:2011


Abstract

Multiple sclerosis (MS) is believed to be an immune-mediated neurodegenerative disorder of the human central nervous system which usually affects younger adults with certain genetic backgrounds. The causes and cure for MS remain elusive. Based on the recent advances in our understanding of the pathogenic mechanisms of MS, it appears to represents a heterogeneous group of disorders with dissimilar pathophysiology and neuropathology. Currently, there is no unifying hypothesis to explain the pathogenesis of this complex disease. The three prevailing concepts on the pathogenesis of MS include viral, immunological, and vascular hypotheses. This review presents MS as a neuroinflammatory disease with a significant vascular component and examines the existing evidence for the role of cerebral endothelial cell dysfunction in the pathogenesis of this progressive central nervous system (CNS) inflammatory disorder. © 2010 Elsevier Ireland Ltd.
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