Neuroendocrine dysfunction in Alzheimer's disease: results following TRH stimulation

Several neuroendocrine abnormalities, including abnormal responses to thyrotropin-releasing hormone (TRH), have been reported in patients with Alzheimer's disease (AD). Some (e.g., Sunderland et al 1985; Thomas et al 1987.) but not all (e.g., El Sobky et al 1986; Molchan et al 1991; Peabody et al 1986) studies have found diminished thyroid-stimulating hormone (TSH) responses to TRH in AD patients. Prolactin (PgL) responses to TRH have been found to be elevated (El Sobky et al 1986; Peabody et al 1986), diminished (Newhouse et al 1986), or unchanged (Franceshi et al 1988; Thomas et al 1987) in AD. Growth hormone (GH) responses have been found to be increased (Thomas et al 1987) or unchanged (Peabody et al 1986). Cortisol responses to TRH have not been studied by elevations in basal corUsol (Davis et a11986), blunted cortisol circadian rhythms (Raskind et al 1982), and escape from dexamethasone suppression (Greenwald et al 1986) have been