Iron-dependent enzymes in Parkinson's disease

J Neural Transm Suppl. 1995:46:157-64.

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

  • Research Support, Non-U.S. Gov't

MeSH terms

  • 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine / pharmacology
  • Adult
  • Aged
  • Aged, 80 and over
  • DNA, Mitochondrial / analysis
  • Electron Transport
  • Humans
  • Iron / metabolism*
  • Middle Aged
  • Mitochondria / drug effects*
  • Mitochondria / enzymology
  • NAD(P)H Dehydrogenase (Quinone) / metabolism*
  • Parkinson Disease / enzymology*
  • Parkinson Disease / etiology
  • Reproducibility of Results
  • Substantia Nigra / drug effects*
  • Substantia Nigra / enzymology
  • Substantia Nigra / ultrastructure

Substances

  • DNA, Mitochondrial
  • 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine
  • Iron
  • NAD(P)H Dehydrogenase (Quinone)