Abstract

Late-onset Alzheimer's disease (AD) is the most common form of AD appearing after 65 years of age. To date, however, there are no non-genetically manipulated rodent models that develop a similar sporadic onset of AD with age-related amyloid-beta (A beta) deposition. Although the senescence accelerated mouse prone 8 (SAMP8) mice have been proposed as a model of AD, the presence of A beta deposits remains controversial. In this study, we describe the time course of A beta deposition in SAMP8 mice as well as in control SAMR1 and ICR-CD1 strains of mice. From as early as 6 months onward, SAMP8 mice show A beta deposition in the hippocampus that increase in number and extent with age. These deposits are comprised of clustered granules that contain A beta(42), A beta(40), and other A beta protein precursor fragments. By marked contrast, control mice show only low numbers of A beta clusters that do not develop until 15 months of age. The demonstration that SAMP8 mice present with amyloid deposits in their hippocampus makes this animal model a useful tool to understand the mechanisms involved in A beta deposition in AD.