The investigators plan to study 16 patients with early PD, 16 controls who are spouses, and 16 unrelated age and sex-matched controls. Patients and controls will undergo platelepheresis in order to collect mitochondria for study. The patients will be studied prior to drug therapy, after 1 month of treatment with carbidopa/L-dopa, after two years of drug treatment. Mitochondria studied in a blind fashion will undergo extensive evaluation of the electron transport chain and western blotting studies. This work will confirm or refute earlier published work suggesting platelet mitochondrial complex I deficiency in PD, study the effects of the 2 most commonly used therapies on mitochondrial function and longitudinally evaluate effects of two years of disease progression on platelet mitochondrial electron transport activities and immunologically active complex III. As effective therapies to slow the course of the disease are now available, it is important to establish the significance of electron transport deficiencies in PD. Such studies might confirm a biological marker which will provide insight into the etiology of PD and might be used to confirm early PD and possibly identify at-risk patients.
| Naviaux, R K; Markusic, D; Barshop, B A et al. (1999) Sensitive assay for mitochondrial DNA polymerase gamma. Clin Chem 45:1725-33 |
| Shults, C W; Haas, R H; Passov, D et al. (1997) Coenzyme Q10 levels correlate with the activities of complexes I and II/III in mitochondria from parkinsonian and nonparkinsonian subjects. Ann Neurol 42:261-4 |
| Shults, C W; Nasirian, F; Ward, D M et al. (1995) Carbidopa/levodopa and selegiline do not affect platelet mitochondrial function in early parkinsonism. Neurology 45:344-8 |
| Haas, R H; Nasirian, F; Nakano, K et al. (1995) Low platelet mitochondrial complex I and complex II/III activity in early untreated Parkinson's disease. Ann Neurol 37:714-22 |
