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Prolonged exposure to high glucocorticoid levels during life has been linked to hippocampal pathology and cognitive impairment.1 For example, excessive levels of endogenous or exogenous corticosteroids have been associated with impaired attention, concentration, and memory.1,2⇓ Longitudinal studies have correlated increased plasma cortisol with cognitive decline and hippocampal atrophy.3 In rats, adrenalectomy at midlife attenuates subsequent hippocampal degeneration and cognitive decline.4
AD is associated with hippocampal atrophy and increased hypothalamo–pituitary–adrenal (HPA) axis activity, both of which may correlate with cognitive deficits.3 If prolonged exposure to glucocorticoids also plays a role in AD, we hypothesized that countering such effects might have therapeutic potential. We evaluated mifepristone (RU 486, Roussel UCLAF, Romainville, Seine-St.-Davideins, France), a long-acting antagonist of progesterone and glucocorticoid receptors,5 for the treatment of AD.
This was a pilot, single-site, randomized, placebo-controlled, double blind, 6-week trial in patients with mild to moderate AD. The study was reviewed by the Institutional Review Board of New York University School of Medicine, and participants were enrolled after providing written informed consent. Key inclusion criteria were diagnosis of probable AD (National Institute …
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