Deutsch_1984_Life.Sci_34_2279

A deficiency of central neural transmission mediated by acetylcholine (ACh) is implicated in the etiopathology of Alzheimer's disease. The appreciation of this neurochemical deficit has led to treatment strategies designed to facilitate central cholinergic transmission (1). A major limitation of current clinical studies is the availability of centrally-effective, long-acting cholinomimetic agents. This situation has led to the search for such agents.