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Vol. 8, No. 6, pp. 301-308, November/December 2001
Departments of Neurology and Neuroscience, University of Minnesota,
Minneapolis, Minnesota 55455, USA
Recent advances in behavioral analyses of transgenic mouse models of
Alzheimer's disease (AD) are discussed, and their impact on our
understanding of the molecular basis of cognitive impairment in AD is
considered. Studies of the relationship between memory and Aß in
transgenic mice expressing the amyloid precursor protein (APP) and its
variants suggest that aging promotes the formation of soluble Aß
assemblies mediating negative effects on memory. A significant
component of memory loss in APP transgenic mice is apparently caused by
soluble Aß assemblies, but whether and how much of the dementia within
individuals afflicted with AD is caused by these Aß species is
unclear. Future studies in composite transgenic mice developing amyloid
plaques, neurofibrillary tangles, and other AD pathology may allow for
the determination of the relative contribution of Aß and non-Aß
components to dementia.
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