Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
9015887 | Pharmacology & Therapeutics | 2005 | 11 Pages |
Abstract
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 Q10, 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 Q10 can affect certain of these processes. Levels of coenzyme Q10 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 Q10 can protect the nigrostriatal dopaminergic system. A phase II trial of coenzyme Q10 in patients with early, untreated PD demonstrated a positive trend for coenzyme Q10 to slow progressive disability that occurs in PD.
Keywords
FADH2TH-irIAPUPDRSSOD21-methyl-4-phenylpyridiniumΔΨmMPTPCOAPTPC. elegansflavin adenine dinucleotideUCP1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridineMPP+mitochondrial outer membrane permeabilizationROSadenosine 5′ triphosphateATPAIFPermeability transition poreParkinson's diseasetyrosine hydroxylase immunoreactiveUncoupling proteinsApoptosiselectron transport chainapoptosis-inducing factorMOMPNeuroprotectionunified Parkinson disease rating scaleinhibitors of apoptosis proteinsMitochondriaNADHnicotinamide adenine dinucleotideETcTransmembrane potentialCaenorhabditis eleganscoenzyme ACoenzyme Q10Reactive oxygen species
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Authors
Clifford W. Shults,