Neuroendocrine dysfunction in early-onset Alzheimer’s disease
To explore hypothalamic-pituitary-somatotropic (HPS) and -adrenal (HPA) system integrity in early-onset Alzheimer’s disease (AD) 10 drug-naive patients and matched controls received 50 µg GHRH at 9:00 and 100 µg CRH at 18:00 as an i.v. bolus dose. Compared with controls, patients with AD showed attenuated GHRH-induced GH responses and decreased ACTH but normal cortisol secretion following CRH. GH responses to GHRH were negatively correlated with the plasma insulin-like growth factor (IGF-I) concentrations and the severity of dementia. A positive correlation was found between GHRH-evoked GH release and ACTH responses to CRH. The results suggest a pathologic process at the level of the pituitary and/or hypothalamus possibly involving a cholinergic, monoaminergic, and/or peptidergic imbalance in AD and support the view that altered HPS and HPA secretory dynamics in AD are related to the underlying brain dysfunction.
KeywordsACTH Response Basal Growth Hormone Neuroendocrine Dysfunction Blunt Growth Hormone Response Brain Electrical Activity Mapping
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