ABSTRACT
The "glucocorticoid cascade hypothesis" for pathological ageing of the brain is supported by strong experimental data, but the clinical correlates are far less clear. The basal ACTH and cortisol secretion have been studied before and after the dexamethasone suppression test in patients in the early stages of clinically probable Alzheimer's disease and in controls, and the results were all normal. These findings do not support the hypothesis that the pathological brain ageing of Alzheimer's type is caused by hyperactivity of the pituitary-adrenal axis.
Subject(s)
Adrenocorticotropic Hormone/blood , Alzheimer Disease/blood , Dexamethasone , Aged , Alzheimer Disease/diagnosis , Alzheimer Disease/physiopathology , Circadian Rhythm/physiology , Female , Humans , Hydrocortisone/blood , Male , Middle Aged , Neuropsychological Tests , Pituitary-Adrenal System/physiopathologyABSTRACT
The response of plasma beta-endorphin (beta-EP) to dexamethasone suppression was studied in 14 patients with Alzheimer's disease (AD), 14 patients with Parkinson's disease (PD), and 13 age-matched controls in order to evaluate whether an impairment of the opiate system is present in these neurodegenerative disorders. Basal circulating beta-EP was in normal range in all subjects, although the mean concentration was slightly reduced in the patients compared to controls. After 1 mg dexamethasone given at 11:00 p.m. the night before, plasma beta-EP concentration measured at 08:00 a.m. and 04:00 p.m. was not inhibited in AD and PD patients while it was significantly reduced in controls. Circulating ACTH and cortisol were similar in patients and controls and a normal inhibition of plasma cortisol after dexamethasone was observed in 13/14 AD and 12/14 PD patients. The resistance of beta-EP to dexamethasone inhibition is consistent with previous clinical and experimental data indicating a disorder of the opiate system in brain degenerative diseases.
