Accelerated Senile Amyloidosis Induced by Amyloidogenic ApoA-II Gene Shortens the Life Span of Mice But Does Not Accelerate the Rate of Senescence

Abstract

The SAMPI 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 (RI.PI-Apoa2^c) which have Apoa2^c of the SAMPI strain on the genome of the normally aging SAMRI strain. Age-associated and severe amyloid deposits were detected in RI.PI-Apoa2^c, as well as a 20% shorter life span than that of SAMRI. The scores of senescence increased more rapidly with age in RI.PI-Apoa2^c than that of SAMRI, 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.