TY - JOUR
T1 - Is multiple sclerosis a mitochondrial disease?
AU - Mao, Peizhong
AU - Reddy, P. Hemachandra
N1 - Funding Information:
This work was supported by grants from NIH (AG028072 AG026051) and Vertex Pharmaceuticals to P.H.R. and by American Heart Association Award 0565527Z to P.M.
PY - 2010/1
Y1 - 2010/1
N2 - 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.
AB - 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.
KW - Experimental autoimmune encephalomyelitis
KW - Gender difference
KW - Mitochondria
KW - Multiple sclerosis
KW - Myelin
KW - NO
KW - Neuroprotection
KW - Oxidative stress
UR - http://www.scopus.com/inward/record.url?scp=71849083196&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=71849083196&partnerID=8YFLogxK
U2 - 10.1016/j.bbadis.2009.07.002
DO - 10.1016/j.bbadis.2009.07.002
M3 - Review article
C2 - 19607913
AN - SCOPUS:71849083196
SN - 0925-4439
VL - 1802
SP - 66
EP - 79
JO - Biochimica et Biophysica Acta - Molecular Basis of Disease
JF - Biochimica et Biophysica Acta - Molecular Basis of Disease
IS - 1
ER -