Mitochondrial Complex I Deficiency in Parkinson's Disease

These results indicated a specific defect of Complex I activity in the substantia nigra of patients with Parkinson's disease

A. H. V. Schapira

2006

Scholarcy highlights

  • Address correspondence and reprint requests to Dr A
  • Total protein and mitochondrial mass were similar in the two groups
  • NADH-ubiquinone reductase and NADH cytochrome c reductase activities were significantly reduced, whereas succinate cytochrome c reductase activity was normal. These results indicated a specific defect of Complex I activity in the substantia nigra of patients with Parkinson's disease
  • This biochemical defect is the same as that produced in animal models of parkinsonism by 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine and adds further support to the proposition that Parkinson's disease may be due to an environmental toxin with action(s) similar to those of MPTP

Need more features? Save interactive summary cards to your Scholarcy Library.