Wild type ApoA-II gene does not rescue senescence-accelerated mouse (SAMP1) from short life span and accelerated mortality

J. Wang, T. Matsushita, K. Kogishi, C. Xia, A. Ohta, T. Chiba, A. Nakamura, H. Kondo, M. Mori, M. Hosokawa, K. Higuchi

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

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 ofApoa2c 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.

Original languageEnglish
Pages (from-to)B432-B439
JournalJournals of Gerontology - Series A Biological Sciences and Medical Sciences
Volume55
Issue number9
DOIs
Publication statusPublished - 2000 Jan 1
Externally publishedYes

ASJC Scopus subject areas

  • Ageing
  • Geriatrics and Gerontology

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