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On elucidation of the role of mitochondria dysfunction and oxidative stress in multiple sclerosis
Author(s) -
Tobore Tobore Onojighofia
Publication year - 2019
Publication title -
neurology and clinical neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.125
0ISSN - 2049-4173
DOI - 10.1111/ncn3.12335
Subject(s) - multiple sclerosis , astrogliosis , medicine , oxidative stress , inflammation , disease , neuroscience , pathogenesis , mitochondrion , central nervous system , neurodegeneration , immunology , bioinformatics , pathology , biology , microbiology and biotechnology
Multiple sclerosis (MS) is a complex human neurodegenerative dysimmune disease of the central nervous system (CNS) which is characterized by chronic inflammation, demyelination, loss of blood‐brain barrier (BBB) integrity, neuronal loss, reactive astrogliosis, and oligodendrocyte depletion. It can result in physical disability and severe neurological and cognitive deficits. Research indicates that MS prevalence has significantly increased in many regions around the world since 1990. The specific elements that trigger MS remain unknown. In this paper, the critical role played by mitochondria dysfunction and oxidative stress in MS pathogenesis, progression, and clinical symptoms are elucidated. Their interactions with the key factors in the disease, as well as treatment strategies, are discussed.