Is multiple sclerosis a mitochondrial disease?

被引:183
作者
Mao, Peizhong [1 ]
Reddy, P. Hemachandra [1 ,2 ]
机构
[1] Oregon Hlth & Sci Univ, Oregon Natl Primate Res Ctr, Neurogenet Lab, Div Neurosci, Beaverton, OR 97006 USA
[2] Oregon Hlth & Sci Univ, Dept Physiol & Pharmacol, Portland, OR 97201 USA
来源
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE | 2010年 / 1802卷 / 01期
关键词
Multiple sclerosis; Experimental autoimmune encephalomyelitis; Mitochondria; Oxidative stress; Myelin; Neuroprotection; NO; Gender difference; EXPERIMENTAL AUTOIMMUNE ENCEPHALOMYELITIS; APPEARING WHITE-MATTER; CENTRAL-NERVOUS-SYSTEM; EXPERIMENTAL ALLERGIC ENCEPHALOMYELITIS; PROGRAMMED CELL-DEATH; NITRIC-OXIDE SYNTHASE; MYELIN BASIC-PROTEIN; EPSTEIN-BARR-VIRUS; OXIDATIVE STRESS; REACTIVE OXYGEN;
D O I
10.1016/j.bbadis.2009.07.002
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
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. (C) 2009 Elsevier B.V. All rights reserved.
引用
收藏
页码:66 / 79
页数:14
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