Mitochondria: a therapeutic target in neurodegeneration.
Mitochondrial dysfunction has long been associated with neurodegenerative disease. Therefore, mitochondrial protective agents represent a unique direction for the development of drug candidates that can modify the pathogenesis of neurodegeneration. This review discusses evidence showing that mitochondrial dysfunction has a central role in the pathogenesis of Alzheimer's, Parkinson's and Huntington's diseases and amyotrophic lateral sclerosis. We also debate the potential therapeutic efficacy of metabolic antioxidants, mitochondria-directed antioxidants and Szeto-Schiller (SS) peptides. Since these compounds preferentially target mitochondria, a major source of oxidative damage, they are promising therapeutic candidates for neurodegenerative diseases. Furthermore, we will briefly discuss the novel action of the antihistamine drug Dimebon on mitochondria.
Center for Neuroscience and Cell Biology, University of Coimbra, Coimbra, Portugal.
Paula I
PI
Moreira
Xiongwei
X
Zhu
Xinglong
X
Wang
Hyoung-Gon
HG
Lee
Akihiko
A
Nunomura
Robert B
RB
Petersen
George
G
Perry
Mark A
MA
Smith
D000544:Alzheimer Disease / Q000188:drug therapy / Q000378:metabolism; D000818:Animals; D000975:Antioxidants / Q000378:metabolism / Q000627:therapeutic use; D006801:Humans; D008928:Mitochondria / Q000187:drug effects* / Q000378:metabolism*; D024101:Mitochondrial Proteins / Q000378:metabolism; D008954:Models, Biological; D019636:Neurodegenerative Diseases / Q000188:drug therapy* / Q000378:metabolism; D018384:Oxidative Stress; D010300:Parkinson Disease / Q000188:drug therapy / Q000378:metabolism
D000975:Antioxidants; D024101:Mitochondrial Proteins