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-β (Aβ) deposition. Although the senescence accelerated mouse prone 8 (SAMP8) mice have been proposed as a model of AD, the presence of Aβ deposits remains controversial. In this study, we describe the time course of Aβ 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 Aβ deposition in the hippocampus that increase in number and extent with age. These deposits are comprised of by clustered granules that contain Aβ42, Aβ40, and other Aβ protein precursor fragments. By marked contrast, control mice show only low numbers of Aβ 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 Aβ deposition in AD.
|Original language||American English|
|Number of pages||13|
|Journal||Journal of Alzheimer's Disease|
|Publication status||Published - 2010|
- Alzheimer's disease