Drugs indicated for use in Alzheimer's disease (AD) must clinically im
prove the cognitive symptomatology of the disorder, although nonexclus
ively. From a neurochemical standpoint, these drugs must oppose the mu
ltiple processes recognized as stigmata of AD. In these two ways, so-c
alled AD drugs may be considered substances modifying cerebral plastic
ity. Long-term evaluation of anticholinesterases and of tacrine, in pa
rticular, provides arguments in support of this initially purely biolo
gic, theoretical approach. This concept of neuroplasticity applied to
dementia may modify the traditional pharmaceutical drug development pr
ograms.