Abstract
There is increasing evidence for a mitochondrial disturbance in Parkinson's disease (PD). We present data which favor a defect of complex I of the respiratory chain only in substantia nigra pars compacta. Evidence from literature supports the view that this complex I defect is specific for Parkinson's disease. Questions like feasibility of postmortem biochemical analyses, impairment of the mitochondrial genome, and evidence for the complex I defect as a causative event for PD are discussed in detail. We consider complex I defect to play a most important role in the cell death of dopaminergic neurons.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine / pharmacology
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Adult
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Aged
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Aged, 80 and over
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DNA, Mitochondrial / analysis
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Electron Transport
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Humans
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Iron / metabolism*
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Middle Aged
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Mitochondria / drug effects*
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Mitochondria / enzymology
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NAD(P)H Dehydrogenase (Quinone) / metabolism*
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Parkinson Disease / enzymology*
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Parkinson Disease / etiology
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Reproducibility of Results
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Substantia Nigra / drug effects*
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Substantia Nigra / enzymology
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Substantia Nigra / ultrastructure
Substances
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DNA, Mitochondrial
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1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
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Iron
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NAD(P)H Dehydrogenase (Quinone)