title: Is multiple sclerosis a mitochondrial disease?
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.
authors.affiliation: Neurogenetics Laboratory, Neuroscience Division, Oregon National Primate Research Center, West Campus, Oregon Health & Science University, 505 NW 185th Avenue, Beaverton, OR 97006, USA.
authors.forename: Peizhong
authors.initials: P
authors.lastname: Mao
authors.forename: P Hemachandra
authors.initials: PH
authors.lastname: Reddy
mesh_terms: D000818:Animals; D006801:Humans; D028361:Mitochondrial Diseases / Q000378:metabolism* / Q000473:pathology; D008954:Models, Biological; D009103:Multiple Sclerosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D017382:Reactive Oxygen Species / Q000378:metabolism
chemical_list: D017382:Reactive Oxygen Species