Iron-dependent enzymes in Parkinson's disease.
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.
Reichmann
H
H
Department of Neurology, University of Würzburg, Federal Republic of Germany.
Janetzky
B
B
Riederer
P
P
D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine / Q000494:pharmacology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D004272:DNA, Mitochondrial / Q000032:analysis; D004579:Electron Transport; D006801:Humans; D007501:Iron / Q000378:metabolism*; D008875:Middle Aged; D008928:Mitochondria / Q000187:drug effects* / Q000201:enzymology; D016660:NAD(P)H Dehydrogenase (Quinone) / Q000378:metabolism*; D010300:Parkinson Disease / Q000201:enzymology* / Q000209:etiology; D015203:Reproducibility of Results; D013378:Substantia Nigra / Q000187:drug effects* / Q000201:enzymology / Q000648:ultrastructure
D004272:DNA, Mitochondrial; D015632:1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine; D007501:Iron; D016660:NAD(P)H Dehydrogenase (Quinone)