Brain, Vol. 115, No. 2, 333-342, 1992
© 1992 Oxford University Press
research-article |
BRAIN, SKELETAL MUSCLE AND PLATELET HOMOGENATE MITOCHONDRIAL FUNCTION IN PARKINSON'S DISEASE
1Department of Neuroscience, Royal Free Hospital School of Medicine London, UK 2Parkinson Disease Society Brain Bank London, UK 3University Department of Clinical Neurology, Institute of Neurology London, UK
Correspondence to:
Correspondence to. Professor A. H. V Schapira, Department of Neurosoence, Royal Free Hospital School of Medicine, Rowland Hill Street, London NW3 2PF, UK.
The recent discovery of mitochondrial complex I deficiency in the substantia nigra of patients with idiopathic Parkinson's disease has provided new understanding into the possible mechanisms that may underlie this neurodegenerative disorder. The biochemical defect is identical to that induced in humans, primates and mice exposed to the neurotoxin 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine. We have studied mitochondrial respiratory chain function in various brain regions, in skeletal muscle and in blood platelets from patients with idiopathic Parkinson's disease and from matched controls We provided evidence suggesting that the complex I deficency in Parkinson's disease is limited to the brain and that this defect is specific for the substantia nigra. The tissue specificity of the complex I deficiency in Parkinson's disease and its localization to the substantia nigra support the proposition that complex I deficiency may be directly involved in the cause of dopaminergic cell death in Parkinson's disease. An understanding of the molecular basis of this biochemical defect will provide valuable insight into the cause of Parkinson's disease. Our finding of normal mitochondnal function in platelet homogenates suggests that this tissue cannot be used to develop a ‘diagnostic test’ for Parkinson's disease.
Received September 20, 1991. Revised December 16, 1991. Accepted January 14, 1992.
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