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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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Mitochondrial Dysfunction in Parkinson's Disease-Cause or Consequence?

TL;DR: Whether the mitochondrial dysfunction the authors have detected in Parkinson’s disease is a pathogenic cause of neuronal loss or whether it is itself a consequence of dysfunction in other pathways is discussed.
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Mitochondrial localization of alpha-synuclein protein in alpha-synuclein overexpressing cells.

TL;DR: The results suggest that under overexpression conditions, alpha-syn may translocate to mitochondria and cause enhanced toxicity in response to sub toxic concentrations of mitochondrial toxins.
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Parkinson's disease and cancer: two wars, one front

TL;DR: How insights from one disease can inform us about, and possibly help us to treat, the other is discussed and areas of convergence are considered.
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The mitochondrial protein BNIP3L is the substrate of PARK2 and mediates mitophagy in PINK1/PARK2 pathway

TL;DR: It is demonstrated that BNIP3L, as a substrate of PARK2, promotes mitophagy in the PINK1/PARK2 pathway associated with PD pathogenesis.
Journal ArticleDOI

Use of Transmitochondrial Cybrids To Assign a Complex I Defect to the Mitochondrial DNA-Encoded NADH Dehydrogenase Subunit 6 Gene Mutation at Nucleotide Pair 14459 That Causes Leber Hereditary Optic Neuropathy and Dystonia

TL;DR: Observations suggest that the ND6 np 14459 mutation may alter the coenzyme Q-binding site of complex I, which is the cause of Leber hereditary optic neuropathy and/or pediatric-onset dystonia in three unrelated families.
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