蛋白激酶与阿尔采末病

被引：8

作者：

魏小龙

张永祥

机构：

[1] 军事医学科学院毒物药物研究所!北京

来源：

生理科学进展 | 1999年 / 04期

基金：

国家攀登计划;

关键词：

蛋白激酶; 阿尔采末病;

D O I：

暂无

中图分类号：

R749.15 [];

学科分类号：

100205 ;

摘要：

阿尔采末病（Ａｌｚｈｅｉｍｅｒ＇ｓｄｉｓｅａｓｅ，ＡＤ）的典型病症之一是学习和记忆功能障碍。老年斑、淀粉样蛋白沉积及神经原纤维缠结（ＮＦＴ）是其大脑主要的病理学特征。动物在学习和记忆行为实验时记忆的获得与保持以及海马长时程增强效应（ＬＴＰ）的诱生均与蛋白激酶Ｃ（ＰＫＣ）的活性呈明显的正相关，蛋白激酶可能通过信号转导途径调节β 淀粉样蛋白（Ａβ）的前体蛋白（ＡＰＰ）剪切代谢成Ａβ，ｔａｕ蛋白的磷酸化是ＮＦＴ形成的主要原因，ｐｒｅｓｅｎｉｌｉｎ（ＰＳ）蛋白的磷酸化与ＡＰＰ的生成及剪切代谢密切相关。磷酸激酶对ｔａｕ蛋白及ＰＳ蛋白具有直接的磷酸化作用。因此蛋白激酶在学习和记忆及ＡＤ脑内病理学变化的形成过程中起重要作用。

引用

页码：359 / 362

页数：4

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