Senescence-accelerated mouse - Neurochemical studies on aging
Senescence-accelerated mouse - Neurochemical studies on aging
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DOI：
10.1111/j.1749-6632.1996.tb39080.x
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发表时间：
1996-01-01
期刊：
影响因子：
--
通讯作者：
Ihara, Y
中科院分区：
文献类型：
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作者：
Nomura, Y;Yamanaka, Y;Ihara, Y
加速衰老小鼠（SAMP8）被称为加速衰老和记忆功能障碍的小鼠模型。 [3H]1-(2-氯苯基)-N-甲基-N-(1-甲基丙基)-3-异喹啉甲酰胺 (PK-11195) 作为神经胶质细胞增生的神经化学标记物的结合活性随着 SAMP8 大脑皮层和海马的衰老而显着增加。胶质纤维酸性蛋白（GFAP）的免疫反应性也增强。 SAMP8 大脑中 β-淀粉样前体蛋白 (APP) 样免疫反应性和 APP 的 27-kDa-羧基末端片段增加。此外，抗APP抗体对SAMP8脑干中海绵状变性周围的反应性星形胶质细胞进行染色。这些结果表明，星形细胞增多和 APP 衍生片段的产生在 SAMP8 大脑中显着发生。
Senescence-accelerated mouse (SAMP8) is known as a murine model of accelerated aging and memory dysfunction. The binding activity of [3H] 1-(2-chlorophenyl)-N-methyl-N-(1-methylpropyl)-3-isoquinolinecarboxam ide (PK-11195) as a neurochemical marker of gliosis markedly increased with aging in the cerebral cortex and hippocampus of SAMP8. Immunoreactivity for glial fibrillary acidic protein (GFAP) was also enhanced. A beta-amyloid precursor protein (APP)-like immunoreactivity and 27-kDa-carboxyl terminal fragments of APP increased in SAMP8 brain. In addition, anti-APP antibody stained reactive astrocytes surrounding spongy degeneration in brain stern of SAMP8. These results suggest that astrocytosis and production of APP-derived fragments occur markedly in SAMP8 brains.