Normal aging in experimental animals and humans has been demonstrated to affect various aspects of central cholinergic functions. Although deficits at the levels of the number of cholinergic neurons, the acetylcholine synthesis, and the number of muscarinic cholinergic receptors are probably less relevant, deficits at the levels of acetylcholine release, muscarinic cholinergic receptor plasticity, as well as muscarinic cholinergic receptor function are fairly pronounced and seem to justify the assumption that the functioning of the central cholinergic system is impaired by aging. However, whether these cholinergic deficits of normal aging are the sole neurochemical basis to explain age-associated memory impairment or whether other transmitter systems also play a role is still a matter of controversy.