Abstract

AbstractThe senescence-accelerated mouse (SAM) strains, consisting of nine SAM-prone (SAMP) mice strains and three SAM-resistant (SAMR) strains, have been used extensively as models for various age-related disorders. SAMP mice undergo accelerated aging while SAMR mice undergo normal aging processes. One of the most employed SAM strains is SAMP8, which has deficits in learning and memory. Coupled to age-dependent deposition of amyloid β-peptide, such deficits allow it to serve as a good model of dementia-related disorders such as Alzheimer’s disease (AD). Many studies have characterized the behavioral, pathological, genetic, and protein abnormalities of SAMP8 mice. Interestingly, genes and proteins that undergo significant alterations in SAMP8 brains are related to the following functional categories: neuroprotection, signal transduction, immune response, energy metabolism, mitochondrion, protein folding and degradation, reactive oxygen species production, cytoskeleton and transport, lipid abnormalities, and cholinergic dysfunction. This chapter provides a summary of these findings with regard to better understanding of AD pathogenesis.Key wordsSenescence-accelerated mouse strain (SAM)DementiaAlzheimer’s diseaseMurine modelsSAMP8

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