Mitochondrial oxidative phosphorylation defects in Parkinson's disease - PubMed (original) (raw)
Mitochondrial oxidative phosphorylation defects in Parkinson's disease
J M Shoffner et al. Ann Neurol. 1991 Sep.
Abstract
Parkinson's disease has been associated with defects in oxidative phosphorylation (Oxphos). We analyzed mitochondria isolated from muscle biopsies of 6 patients with Parkinson's disease for deficiencies in Oxphos enzymes and for mutations in the mitochondrial DNA. Oxphos enzyme assays were compared to the 5 to 95% confidence intervals from 16 control subjects. Four patients had complex I defects, whereas 1 patient had a complex IV defect. A genetic basis for Parkinson's disease was suggested by the presence of affected relatives of 2 patients with Parkinson's disease. Known pathological mitochondrial DNA mutations (insertion-deletions or point mutations) were not found. We conclude that Parkinson's disease is a systemic disorder of Oxphos, probably of a complex genetic etiology. Premature cell death in the nigrostriatal dopamine pathway could be due to energetic impairment and accentuated free radical generation caused by an Oxphos defect.
Comment in
- Mitochondrial function in Parkinson's disease.
Dagani F, Anderson JJ, Chase TN. Dagani F, et al. Ann Neurol. 1992 Aug;32(2):226-7. doi: 10.1002/ana.410320220. Ann Neurol. 1992. PMID: 1472244 No abstract available.
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