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      Is multiple sclerosis a mitochondrial disease?

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          Abstract

          Multiple sclerosis (MS) is a relatively common and etiologically unknown disease with no cure. It is the leading cause of neurological disability in young adults, affecting over two million people worldwide. Traditionally, MS has been considered a chronic, inflammatory disorder of the central white matter in which ensuing demyelination results in physical disability. Recently, MS has become increasingly viewed as a neurodegenerative disorder in which axonal injury, neuronal loss, and atrophy of the central nervous system leads to permanent neurological and clinical disability. In this article, we discuss the latest developments on MS research, including etiology, pathology, genetic association, EAE animal models, mechanisms of neuronal injury and axonal transport, and therapeutics. In this article, we also focus on the mechanisms of mitochondrial dysfunction that are involved in MS, including mitochondrial DNA defects, and mitochondrial structural/functional changes.

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          Most cited references178

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          Angiogenesis in life, disease and medicine.

          The growth of blood vessels (a process known as angiogenesis) is essential for organ growth and repair. An imbalance in this process contributes to numerous malignant, inflammatory, ischaemic, infectious and immune disorders. Recently, the first anti-angiogenic agents have been approved for the treatment of cancer and blindness. Angiogenesis research will probably change the face of medicine in the next decades, with more than 500 million people worldwide predicted to benefit from pro- or anti-angiogenesis treatments.
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            Multiple Sclerosis

            New England Journal of Medicine, 343(13), 938-952
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              Multiple sclerosis--the plaque and its pathogenesis.

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                Author and article information

                Contributors
                Journal
                Biochim Biophys Acta Mol Basis Dis
                Biochim Biophys Acta Mol Basis Dis
                Biochimica et Biophysica Acta. Molecular Basis of Disease
                Elsevier B.V.
                0925-4439
                1879-260X
                14 July 2009
                January 2010
                14 July 2009
                : 1802
                : 1
                : 66-79
                Affiliations
                [a ]Neurogenetics Laboratory, Neuroscience Division, Oregon National Primate Research Center, West Campus, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA
                [b ]Department of Physiology and Pharmacology, Oregon Health & Science University, Portland, OR 97201, USA
                Author notes
                [* ]Corresponding author. Neurogenetics Laboratory, Neuroscience Division, Oregon National Primate Research Center, West Campus, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA. Tel.: +1 503 418 2625; fax: +1 503 418 2501. reddyh@ 123456ohsu.edu
                Article
                S0925-4439(09)00146-X
                10.1016/j.bbadis.2009.07.002
                2790545
                19607913
                45765eb6-5ae6-4c04-ac21-253c0ef4763c
                Copyright © 2009 Elsevier B.V. All rights reserved.

                Since January 2020 Elsevier has created a COVID-19 resource centre with free information in English and Mandarin on the novel coronavirus COVID-19. The COVID-19 resource centre is hosted on Elsevier Connect, the company's public news and information website. Elsevier hereby grants permission to make all its COVID-19-related research that is available on the COVID-19 resource centre - including this research content - immediately available in PubMed Central and other publicly funded repositories, such as the WHO COVID database with rights for unrestricted research re-use and analyses in any form or by any means with acknowledgement of the original source. These permissions are granted for free by Elsevier for as long as the COVID-19 resource centre remains active.

                History
                : 30 May 2009
                : 30 June 2009
                : 1 July 2009
                Categories
                Article

                multiple sclerosis,experimental autoimmune encephalomyelitis,mitochondria,oxidative stress,myelin,neuroprotection,no,gender difference

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