Potential animal models for senile dementia of Alzheimer's type, with emphasis on AF64A-induced cholinotoxicity.

In this review we have described and critiqued several commonly used proposed animal models for SDAT. In particular, we have focussed on the AF64A-treated animal. Major pertinent neurochemical and behavioral data obtained so far with AF64A have been presented, and these effects have been compared with neurochemical and behavioral changes in the SDAT patient. We have commented on the possible mechanism(s) of action of AF64A in vivo, and have also presented some observations and speculations concerning the selectivity of action of AF64A as a specific presynaptic cholinotoxin. Much work has yet to be done with all the available animal models, including the AF64A-treated animal, before one could definitively state which one is the ideal model for SDAT. Data obtained to date with the AF64A-treated animal are nevertheless most encouraging. Despite some caveats, AF64A is a valuable neurochemical tool with which one can induce a persistent cholinergic deficiency of presynaptic origin. As with all new tools, however, one must always exercise due care to use it properly, and interpret the results obtained following its administration with caution.