摘要
背景：淀粉样β蛋白（Aβ）的积累在阿尔茨海默病（AD）病变的发病机制中起着关键作用。最近血清素信号传导的缺乏与转基因小鼠和人类中Aβ水平的增加有关。此外，色氨酸羟化酶-2（Tph2），第二种色氨酸羟化酶同种型，控制脑血清素合成。然而，仍有待确定Tph2缺陷型APP / PS1小鼠是否影响体内Aβ斑块的形成。 方法：采用定量和定性免疫化学方法，以及刚果红染色法评价这些动物的Aβ负荷和星形胶质细胞增生。 结果：我们研究了6-10个月龄的Tph2条件性敲除（Tph2 CKO）AD小鼠对星形胶质细胞和老年斑中皮层和海马的改变。使用刚果红染色并用Aβ抗体免疫染色，我们显示，与野生型（WT）组相比，在8至10个月时Tph2 CKO实验组中斑块负荷或斑块数量显着增加。使用GFAP +星形胶质细胞免疫荧光法，我们发现在10个月时Tph2 CKO中GFAP +星形胶质细胞的密度显着增强。我们显示Aβ斑块共定位的自噬标记物LC3和p62。然而，我们没有观察到GFAP +星形胶质细胞和自噬标记物之间的任何共定位，但检测到βIII-微管蛋白+神经元和自噬标记物之间的共定位。 结论：总的来说，我们的工作在体内提供了Tph2在淀粉样蛋白斑生成中发挥作用的初步证据。
关键词: Tph2，Aβ斑块，APP / PS1，自噬，星形胶质细胞，阿尔茨海默病。
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