Allain_1997_Clin.Ther_19_4

Drugs indicated for use in Alzheimer's disease (AD) must clinically improve the cognitive symptomatology of the disorder, although nonexclusively. From a neurochemical standpoint, these drugs must oppose the multiple processes recognized as stigmata of AD. In these two ways, so-called AD drugs may be considered substances modifying cerebral plasticity. Long-term evaluation of anticholinesterases and of tacrine, in particular, provides arguments in support of this initially purely biologic, theoretical approach. This concept of neuroplasticity applied to dementia may modify the traditional pharmaceutical drug development programs.