Abstract
The Senescence-Accelerated Mouse (SAM) strains are unique and appropriate models for genetic studies on aging because the SAMP strains have an "accelerated senescence" phenotype for which the SAMR strains are controls, and each SAMP strain has a strain-specific age-associated disorder. Furthermore, because they have gone through sufficient generations of sister-brother mating, they can be considered inbred strains, which can be analyzed genetically. There are now 11 SAMP strains and 3 SAMR strains descended from the progenitor litters. Analysis with the Gompertz function shows that the SAMP strains have the same initial mortality rate (IMR) as the SAMR strains but a shorter mortality rate doubling time (MRDT), presumably due to genes that accelerated the rate of senescence in the SAMP strains. This accelerated senescence may also occur in cultured fibroblast-like cells. We performed molecular genetic characterization of all the SAM strains to acquire a base of genetic information from which we could develop hypotheses on the mechanism of development of SAM strains and genetic factors that contribute to accelerated senescence.
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