ergoline and Alzheimer-Disease

Up to date 6 patients with initial presenile idiopathic cognitive decline (PICD) and 5 suffering from a presenile Alzheimer-type dementia (PAD) with a mean age of 59.5 were admitted to the trial. The 6 PICD patients were assigned to a double-blind nicergoline/placebo 6-month course with an oral dose of 30 mg twice a day. PAD patients were treated in an open design (nicergoline oral dose 30 mg twice a day) for at least 6 months. Until now only 4 PICD and 3 PAD patients have been treated regularly for 6 months. Two of 4 PICD patients showed a progressive enhancement of contingent negative variation (CNV), shorter reaction time (RT) and an improvement of clinical status. The other 2 PICD patients, on the contrary, showed a progressive mild worsening of CNV-RT and clinical patterns. The double-blind trial is not yet completed. CNV activity, RTs and clinical patterns progressively improved also in 2 PAD patients while in the 3rd they remained nearly unchanged or minimally worse during the 6-month treatment. The positive nicergoline effect on CNV-RT and clinical status noted in our patients appeared similar to that observed by other authors with DHEMT in patients with senile dementia of Alzheimer type. No adverse drug-related reactions were seen.

Topics: Alzheimer Disease; Cognition Disorders; Contingent Negative Variation; Double-Blind Method; Electroencephalography; Electrophysiology; Ergolines; Female; Humans; Male; Middle Aged; Nicergoline; Reaction Time

Oxidant stress secondary to dopamine metabolism has been proposed as a pathogenic factor in the development of Parkinson's disease. Biochemical abnormalities extending beyond the central nervous system have been identified in patients with this condition. Previous investigators have found abnormally elevated concentrations of the lipid peroxidation product, malondialdehyde, in the plasma and serum of patients with Parkinson's disease. We attempted to replicate these findings but controlled for other factors that could influence malondialdehyde levels. We detected no significant elevations in mean serum malondialdehyde concentrations in either levodopa-treated or untreated patients with Parkinson's disease, compared to normal controls; similarly, no elevation was 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 neurodegenerative disease had significantly elevated mean serum malondialdehyde levels, consistent with previous studies of diabetic patients. Autoxidation is one of the two major routes by which dopamine and dopa metabolism may generate oxygen free radicals. We analyzed the autoxidation 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 two other antioxidant substances, alpha-tocopherol and uric acid, were also statistically similar in these groups. In conclusion, analysis of several blood products relevant to oxidant stress, including malondialdehyde, 5-S-cysteinyl-dopa, alpha-tocopherol, and uric acid, failed to distinguish patients with Parkinson's disease or dementia of Alzheimer's type from controls.

Topics: Aged; Alzheimer Disease; Antiparkinson Agents; Brain; Cabergoline; Carbidopa; Diabetes Mellitus; Ergolines; Female; Free Radicals; Humans; Levodopa; Lipid Peroxidation; Male; Malondialdehyde; Oxidative Stress; Parkinson Disease; Selegiline; Vitamin E