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Mitochondrial complex I deficiency in Parkinson's disease.

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This article is published in The Lancet.The article was published on 1989-06-03. It has received 1548 citations till now. The article focuses on the topics: NAD(P)H Dehydrogenase (Quinone) & Substantia nigra.

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PGC-1α at the intersection of bioenergetics regulation and neuron function: from Huntington's disease to Parkinson's disease and beyond

TL;DR: The role of PGC-1α in normal nervous system function and potentially neurological disease has been investigated in this article, where the role of PPARγ co-activator was shown to contribute to the development of Parkinson's disease.
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The Role of the Antioxidant Response in Mitochondrial Dysfunction in Degenerative Diseases: Cross-Talk between Antioxidant Defense, Autophagy, and Apoptosis.

TL;DR: The pathological involvement of mitochondrial dysfunction in relation to oxidative stress, energy metabolism, mitochondrial dynamics, and cell death will be explored and offers potential therapeutic targets in the development of future treatments for these degenerative diseases.
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Therapeutic potential of N-acetylcysteine in age-related mitochondrial neurodegenerative diseases.

TL;DR: The mechanisms of N-acetylcysteine action at the cellular level, and the possible usefulness of this antioxidant for the treatment of age-associated neurodegenerative diseases are reviewed.
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Partial Mitochondrial Inhibition Causes Striatal Dopamine Release Suppression and Medium Spiny Neuron Depolarization via H2O2 Elevation, Not ATP Depletion

TL;DR: It is shown that acute exposure to the mitochondrial complex I inhibitor rotenone causes concentration-dependent suppression of single-pulse evoked dopamine release monitored in real time with carbon-fiber microelectrodes in guinea pig striatal slices, with no effect on DA content.
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