Journals of Gerontology Series A: Biological Sciences and Medical Sciences Large Type Edition
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The Journals of Gerontology Series A: Biological Sciences and Medical Sciences 55:B432-B439 (2000)
© 2000 The Gerontological Society of America

Wild Type ApoA-II Gene Does Not Rescue Senescence-Accelerated Mouse (SAMP1) From Short Life Span and Accelerated Mortality

Jing Wanga,b,c, Takatoshi Matsushitab, Kumiko Kogishib, Chen Xiab, Akira Ohtab, Takuya Chibab,c, Akihiro Nakamurac, Hisatoshi Kondod, Masayuki Moric, Masanori Hosokawab and Keiichi Higuchic

a Department of Pathology and Laboratory Medicine, University of British Columbia, Vancouver, Canada
b Field of Regeneration Control, Institute for Frontier Medical Science, Kyoto University, Kyoto, Japan
c Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, Matsumoto, Japan
d Atomic Bomb Disease Institute, Nagasaki University School of Medicine, Nagasaki, Japan

Keiichi Higuchi, Department of Aging Angiology, Research Center on Aging and Adaptation, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan E-mail: khiguchi{at}sch.md.shinshu-u.ac.jp.

Decision Editor: Jay Roberts, PhD

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.







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