期刊
MITOCHONDRIA AND OXIDATIVE STRESS IN NEURODEGENERATIVE DISORDERS
卷 1147, 期 -, 页码 112-121出版社
WILEY-BLACKWELL
DOI: 10.1196/annals.1427.013
关键词
Parkinson's disease; amyotrophic lateral sclerosis; reactive oxygen species; antioxidants; mitochondrial permeability transition; apoptosis; MPTP
资金
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R21NS048295] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON DRUG ABUSE [P01DA008924] Funding Source: NIH RePORTER
- NIDA NIH HHS [P01 DA08924] Funding Source: Medline
- NINDS NIH HHS [R21 NS48295] Funding Source: Medline
Mitochondrial impairment and oxidative damage are intimately involved in the pathogenesis of neurodegenerative diseases. Which is the initiating event is probably irrelevant because each can set into motion a self-sustaining and amplifying feed-forward cycle between reactive oxygen species (ROS) generation and mitochondrial impairment. Recent approaches to the development of neuroprotective agents have therefore targeted mitochondria protection and/or reduction of oxidative stress. There are several hurdles in the quest for neuroprotective drugs. The difficulties include penetration of the blood-brain barrier and delivery of drugs to mitochondria. Here we describe a novel class of mitochondria-targeted peptides that can promote mitochondrial function, reduce mitochondrial ROS generation, inhibit mitochondrial permeability transition, and prevent apoptosis and necrosis. These peptides can readily penetrate the blood-brain barrier and have demonstrated efficacy in animal models of Parkinson's disease and amyotrophic lateral sclerosis.
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