Journal ArticleDOI
Respiratory chain abnormalities in skeletal muscle from patients with Parkinson's disease
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In this article, the mitochondrial respiratory chain function in skeletal muscle from patients with Parkinson's disease was studied and the results showed low activity in all complexes studied (I, II and IV).About:
This article is published in Journal of the Neurological Sciences.The article was published on 1991-08-01. It has received 226 citations till now. The article focuses on the topics: Mitochondrial respiratory chain & Respiratory chain.read more
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Drosophila pink1 is required for mitochondrial function and interacts genetically with parkin.
Ira E. Clark,Mark W. Dodson,Changan Jiang,Joseph Cao,Jun R. Huh,Jae Hong Seol,Soon Ji Yoo,Bruce A. Hay,Ming Guo +8 more
TL;DR: Removal of Drosophila PINK1 homologue function results in male sterility, apoptotic muscle degeneration, defects in mitochondrial morphology and increased sensitivity to multiple stresses including oxidative stress, which underscores the importance of mitochondrial dysfunction as a central mechanism of Parkinson's disease pathogenesis.
Journal ArticleDOI
Mitochondrial genetics: a paradigm for aging and degenerative diseases?
TL;DR: Application of the hypothesis that a variety of degenerative processes may be associated with defects in oxidative phosphorylation has provided new insights into such diverse clinical problems as ischemic heart disease, late-onset diabetes, Parkinson's Disease, Alzheimer's disease, and aging.
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The Role of Oxidative Stress in Parkinson’s Disease
TL;DR: Animal models of PD have yielded some insights into the molecular pathways of neuronal degeneration and highlighted previously unknown mechanisms by which oxidative stress contributes to PD, but therapeutic attempts to target the general state of oxidative stress in clinical trials have failed to demonstrate an impact on disease progression.
Journal ArticleDOI
α-Synuclein Promotes Mitochondrial Deficit and Oxidative Stress
Leigh J. Hsu,Yutaka Sagara,Armando Arroyo,Edward Rockenstein,Abbyann Sisk,Margaret Mallory,Jeffrey J. Wong,Takato Takenouchi,Makoto Hashimoto,Eliezer Masliah +9 more
TL;DR: Results suggest that abnormal accumulation of α-synuclein could lead to mitochondrial alterations that may result in oxidative stress and, eventually, cell death.
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Origin and functional consequences of the complex I defect in Parkinson's disease
Russell H. Swerdlow,Janice K. Parks,Scott W. Miller,Jeremy B. Tuttle,Patricia A. Trimmer,Jason P. Sheehan,James P. Bennett,Robert E. Davis,Parker Wd +8 more
TL;DR: The complex I defect in PD appears to be genetic, arising from mitochondrial DNA, and may play an important role in the neurodegeneration of PD by fostering reactive oxygen species production and conferring increased neuronal susceptibility to mitochondrial toxins.
References
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Journal ArticleDOI
Cleavage of Structural Proteins during the Assembly of the Head of Bacteriophage T4
TL;DR: Using an improved method of gel electrophoresis, many hitherto unknown proteins have been found in bacteriophage T4 and some of these have been identified with specific gene products.
Journal Article
Cleavage of structural proteins during the assemble of the head of bacterio-phage T4
TL;DR: Using an improved method of gel electrophoresis, many hitherto unknown proteins have been found in bacteriophage T4 and some of these have been identified with specific gene products as mentioned in this paper.
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Electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets: procedure and some applications.
TL;DR: A method has been devised for the electrophoretic transfer of proteins from polyacrylamide gels to nitrocellulose sheets that results in quantitative transfer of ribosomal proteins from gels containing urea.
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A simplification of the protein assay method of Lowry et al. which is more generally applicable
TL;DR: A simple method based on a linear log-log protein standard curve is presented to permit rapid and totally objective protein analysis using small programmable calculators.
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Chronic Parkinsonism in humans due to a product of meperidine-analog synthesis
TL;DR: It is proposed that this chemical selectively damages cells in the substantia nigra in patients who developed marked parkinsonism after using an illicit drug intravenously.