Journal
PHARMACOLOGY & THERAPEUTICS
Volume 107, Issue 1, Pages 120-130Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.pharmthera.2005.02.002
Keywords
coenzyme Q(10); Parkinson's disease; mitochondria; neuroprotection; apoptosis
Categories
Funding
- NINDS NIH HHS [P01 NSO44233] Funding Source: Medline
Ask authors/readers for more resources
Mitochondrial dysfunction has been well established to occur in Parkinson's disease (PD) and appears to play a role in the pathogenesis of the disorder. A key component of the mitochondrial electron transport chain (ETC) is coenzyme Q(10), which not only serves as the electron acceptor for complexes I and II of the ETC but is also an antioxidant. In addition to being crucial to the bioenergetics of the cell, mitochondria play a central role in apoptotic cell death through a number of mechanisms, and coenzyme Q(10) can affect certain of these processes. Levels of coenzyme Q(10) have been reported to be decreased in blood and platelet mitochondria from PD patients. A number of preclinical studies in in vitro and in vivo models of PD have demonstrated that coenzyme Q(10) can protect the nigrostriatal dopaminergic system. A phase IIb trial or coenzyme Q(10) in patients with early, untreated PD demonstrated a positive trend for coenzyme Q(10) to slow progressive disability that occurs, in PD. (c) 2005 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available