| First Author | Wang J | Year | 2000 |
| Journal | J Gerontol A Biol Sci Med Sci | Volume | 55 |
| Issue | 9 | Pages | B432-9 |
| PubMed ID | 10995040 | Mgi Jnum | J:64194 |
| Mgi Id | MGI:1888846 | Doi | 10.1093/gerona/55.9.b432 |
| Citation | Wang J, et al. (2000) Wild type ApoA-II gene does not rescue senescence-accelerated mouse (SAMP1) from short life span and accelerated mortality. J Gerontol A Biol Sci Med Sci 55(9):B432-9 |
| abstractText | Biochemical and genetic data suggest that the Apoa2c allele of the apolipoprotein A-II gene causes severe senile amyloidosis (AApoAII) in SAMP1, a mouse model for accelerated senescence. We analyzed the effects of replacement of Apoa2c in SAMP1 mice with non-amyloidogenic Apoa2b on amyloidosis, lipoprotein metabolism, and progression of senescence using a congenic strain, P1.R1-Apoa2b, which has the Apoa2b chromosome region of SAMR1 in the genome of SAMP1. Age-associated amyloid deposition was not observed, but plasma concentrations of apoA-II protein and HDL-cholesterol decreased with age in P1.R1-Apoa2b. P1.R1-Apoa2b showed lower scores of senescence than did SAMP1. However, the life span and mortality rate doubling time were similar in P1.R1-Apoa2b and SAMP1. These results suggest that replacement of Apoa2c with non-amyloidogenic Apoa2b does not rescue SAMP1 mice from a short life span and accelerated mortality. |
