由淀粉样蛋白生成性载脂蛋白A-II基因诱导的加速性老年淀粉样变性缩短了小鼠的寿命，但并未加速衰老进程。
Accelerated senile amyloidosis induced by amyloidogenic Apoa-II gene shortens the life span of mice but does not accelerate the rate of senescence.
作者信息
Higuchi K, Wang J, Kitagawa K, Matsushita T, Kogishi K, Naiki H, Kitado H, Hosokawa M
机构信息
Department of Senescence Biology, Kyoto University, Japan.
出版信息
J Gerontol A Biol Sci Med Sci. 1996 Jul;51(4):B295-302. doi: 10.1093/gerona/51a.4.b295.
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.
SAMP1品系是一种用于加速衰老和严重老年淀粉样变性的小鼠模型。我们研究了淀粉样前体载脂蛋白A-II基因（Apoa2c）对老年淀粉样变性的影响，以及具有SAMP1品系Apoa2c基因的同基因小鼠（R1.P1-Apoa2c）在正常衰老的SAMR1品系基因组上的寿命和衰老进程。在R1.P1-Apoa2c中检测到与年龄相关且严重的淀粉样沉积物，其寿命比SAMR1短20%。R1.P1-Apoa2c的衰老评分随年龄增长比SAMR1更快，并且Gompertz函数显示出更大的Y轴截距，但回归线斜率相同。这些结果表明，Apoa2c基因诱导的严重老年淀粉样变性会缩短小鼠寿命，但不会加速衰老速率。
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