Summary
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.
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© 1990 Springer-Verlag Wien
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Lesch, K.P. et al. (1990). Neuroendocrine dysfunction in early-onset Alzheimer’s disease. In: Maurer, K., Riederer, P., Beckmann, H. (eds) Alzheimer’s Disease. Epidemiology, Neuropathology, Neurochemistry, and Clinics. Key Topics in Brain Research. Springer, Vienna. https://doi.org/10.1007/978-3-7091-3396-5_37
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DOI: https://doi.org/10.1007/978-3-7091-3396-5_37
Publisher Name: Springer, Vienna
Print ISBN: 978-3-211-82197-8
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