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Mitochondria: a therapeutic target in neurodegeneration Moreira PI; Zhu X; Wang X; Lee HG; Nunomura A; Petersen RB; Perry G; Smith MABiochim Biophys Acta 2010[Jan]; 1802 (1): 212-20Mitochondrial 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.|Alzheimer Disease/drug therapy/metabolism[MESH]|Animals[MESH]|Antioxidants/metabolism/therapeutic use[MESH]|Humans[MESH]|Mitochondria/*drug effects/*metabolism[MESH]|Mitochondrial Proteins/metabolism[MESH]|Models, Biological[MESH]|Neurodegenerative Diseases/*drug therapy/metabolism[MESH]|Oxidative Stress[MESH]|Parkinson Disease/drug therapy/metabolism[MESH] |