Galantamine, a cholinesterase inhibitor that allosterically modulates nicotinic receptors: Effects on the course of Alzheimer's disease

Citation
J. Coyle et P. Kershaw, Galantamine, a cholinesterase inhibitor that allosterically modulates nicotinic receptors: Effects on the course of Alzheimer's disease, BIOL PSYCHI, 49(3), 2001, pp. 289-299
Citations number
69
Categorie Soggetti
Neurosciences & Behavoir
Journal title
BIOLOGICAL PSYCHIATRY
ISSN journal
00063223 → ACNP
Volume
49
Issue
3
Year of publication
2001
Pages
289 - 299
Database
ISI
SICI code
0006-3223(20010201)49:3<289:GACITA>2.0.ZU;2-5
Abstract
Despite the proven efficacy of acetylcholinesterase inhibitors in Alzheimer 's disease, there is a need for new and more effective treatments. Galantam ine is a novel treatment for Alzheimer's disease that inhibits acetylcholin esterase and modulates nicotinic receptors. In randomized, double-blind, pl acebo-controlled studies of up to 6 months duration, galantamine significan tly improved cognitive function. Galantamine also had beneficial effects on instrumental and basic activities of daily living, and postponed the progr ession of behavioral symptoms. Patients who completed one of the 6-month, p lacebo-controlled studies were eligible to enter a 6-month, open-extension study of 24-mg/day dose of galantamine. At the end of 12 months, cognitive function and activities of daily living were preserved in those patients wh o had been treated throughout the study with galantamine 24 mg/day. At 12 m onths, this group of patients had significantly better cognitive functions than patients who had been treated with a placebo for 6 months before recei ving galantamine. These studies indicate that galantamine postpones the pro gression of symptoms in Alzheimer's disease. Since galantamine shows the gr eatest benefits when treatment is started early, its long-term benefits may result from an effect on the underlying disease process; such an effect mi ght be mediated by galantamine's concomitant action on nicotinic receptors. (C) 2001 Society of Biological Psychiatry.