Journals of Gerontology Series A: Biological Sciences and Medical Sciences, Vol 51, Issue 4 B295-B302, Copyright © 1996 by The Gerontological Society of America

JOURNAL ARTICLE

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

K Higuchi, J Wang, K Kitagawa, T Matsushita, K Kogishi, H Naiki, H Kitado and M Hosokawa
Department of Senescence Biology, Kyoto University, Japan.

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 (Apoa2c) on senile amyloidosis and the life span and progress of senescence of congenic mice (R1.P1-Apoa2c) which have Apoa2c of the SAMPI strain on the genome of the normally aging SAMR1 strain. Age-associated and severe amyloid deposits were detected in R1.P1-Apoa2c, as well as a 20% shorter life span than that of SAMR1. The scores of senescence increased more rapidly with age in R1.P1- Apoa2c 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 Apoa2c gene shortens the life span of mice but does not accelerate the rate of senescence.

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				J. Wang, T. Matsushita, K. Kogishi, C. Xia, A. Ohta, T. Chiba, A. Nakamura, H. Kondo, M. Mori, M. Hosokawa, and K. Higuchi 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., September 1, 2000; 55(9): 432B - 439. [Abstract] [Full Text]