ABSTRACT
Nearly 30 years ago, the decline in learning and memory ability observed in Alzheimer’s disease (AD) was advanced to be derived from a deficiency in cholinergic neurotransmission, linked to the loss of cholinergic neurons in the Nucleus Basalis of Maynert and other nuclei projecting to the hippocampus and mesial temporal regions (Cummings et al., 1998; Geula, 1998). This speculation was logically termed ‘‘cholinergic hypothesis.’’ A consequent theory predicted that drugs able to potentiate central cholinergic function should be of therapeutic interest in cognition treatment and even behavioral problems experienced with AD.
