期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE
卷 1802, 期 1, 页码 66-79出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbadis.2009.07.002
关键词
Multiple sclerosis; Experimental autoimmune encephalomyelitis; Mitochondria; Oxidative stress; Myelin; Neuroprotection; NO; Gender difference
资金
- NIH [AG028072, AG026051]
- Vertex Pharmaceuticals
- American Heart Association [0565527Z]
- NATIONAL INSTITUTE ON AGING [R03AG026051, R01AG028072] Funding Source: NIH RePORTER
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.
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