Abstract
Working memory is disrupted an Alzheimer's disease and stroke; therefore, any therapeutic drug should deficits in working memory. The win-shift foraging paradigm has been demostrated to be a model of working memory in rats. In the present study, this paradigm was adapted to mice because of the greater ease and economy of testing potential drugs in mice and the wider availability of strains of aged mice with naturally occuring working memory deficits. This study has demostrated strain differences in the working memory trace and that age induces a deficit that can be dete4cted at 11 months af age in mice. Tacrine and physostigmine enhance the memory trace in normal mice and physostigmine can reverse age-induced working memory deficits in subjects with mild and moderate deficits but not in subjects with severe deficits.
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