NO EVIDENCE FOR SYSTEMIC OXIDANT STRESS IN PARKINSONS OR ALZHEIMERS-DISEASE

Oxidant stress secondary to dopamine metabolism has been proposed as a pathogenic factor in the development of Parkinson's disease. Biochemi cal abnormalities extending beyond the central nervous system have bee n identified in patients with this condition. Previous investigators h ave found abnormally elevated concentrations of the lipid peroxidation product, malondialdehyde, in the plasma and serum of patients with Pa rkinson's disease, We attempted to replicate these findings but contro lled for other factors that could influence malondialdehyde levels, We detected no significant elevations in mean serum malondialdehyde conc entrations in either levodopa-treated or untreated patients with Parki nson's disease, compared to normal controls; similarly, no elevation w as found in a group of patients with dementia of Alzheimer's type. On the other hand, a group of subjects with diabetes mellitus but no neur odegenerative disease had significantly elevated mean serum malondiald ehyde levels, consistent with previous studies of diabetic patients. A utoxidation is one of the two major routes by which dopamine and dopa metabolism may generate oxygen free radicals. We analyzed the autoxida tion product of dopa, 5-S-cysteinyl-dopa, in the plasma of these same groups of patients with neurodegenerative disease and normal controls; no significant differences were identified. serum concentrations of t wo other antioxidant substances, cz-tocopherol and uric acid, were als o statistically similar in these groups. In conclusion, analysis of se veral blood products relevant to oxidant stress, including malondialde hyde, 5-S-cysteinyl-dopa, a-tocopherol, and uric acid, failed to disti nguish patients with Parkinson's disease or dementia of Alzheimer's ty pe from controls.