Accelerated senile amyloidosis induced by amyloidogenic ApoA-II gene shortens the life span of mice but does not accelerate the rate of senescence

The SAMP1 strain is a mouse model for accelerated senescence and severe senile amyloidosis. We studied the effects of the amyloidogenic apolipoprotein A-II gene (Apoa2(c)) on senile amyloidosis and the life span and progress of senescence of congenic mice (R1.P1-Apoa2(c)) which have Apoa2(c) of the SAMP1 strain on the genome of the normally aging SAMR1 strain. Age-associated and severe amyloid deposits were detected in R1.P1-Apoa2(c), as well as a 20% shorter life span than that of SAMR1. The scores of senescence increased more rapidly with age in R1.P1-Apoa2(c) than that of SAMR1, and the Gompertz function showed a bigger Y intercept but the same slope of regression line. These results suggest that severe senile amyloidosis induced by the Apoa2(c) gene shortens the life span of mice but does not accelerate the rate of senescence.