Nakagawa Yasushi, Yuzuriha Takefumi, Iwaki Toru
Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Neuropathology. 2004 Sep;24(3):194-200. doi: 10.1111/j.1440-1789.2004.00549.x.
A major constituent of SP in the brains of Alzheimer's disease is 39-43 amino acid peptide called beta-amyloid peptide (Abeta). Recent data have demonstrated that Abeta has a strong tendency to form insoluble aggregates and that toxic effects of Abeta is based on its aggregation. In the current study, 100 microg of human synthetic Abeta 1-42 (sAbeta 1-42) was infused into the lateral ventricle of rat brain using a short-term infusion model. At 2 or 7 days following the infusion, sAbeta 1-42 was found to form insoluble aggregates, scattering throughout the entire ventricular systems. The sAbeta 1-42 aggregates were partially engulfed by phagocytic cells and deposited at the meningeal vessels or the choroid plexuses. However, these deposits mostly disappeared from the ventricles by 28 days post-infusion. Here, it is reported for the first time that considerable amounts of sAbeta 1-42 are almost cleared from the rat ventricular system by the mononuclear phagocytic system.
在阿尔茨海默病患者大脑中，淀粉样前体蛋白（SP）的一个主要成分是一种由39至43个氨基酸组成的肽，称为β-淀粉样肽（Aβ）。最近的数据表明，Aβ具有强烈的形成不溶性聚集体的倾向，并且Aβ的毒性作用基于其聚集。在当前的研究中，使用短期输注模型将100微克人合成Aβ1-42（sAβ1-42）注入大鼠脑侧脑室。在输注后2天或7天，发现sAβ1-42形成不溶性聚集体，散布于整个脑室系统。sAβ1-42聚集体部分被吞噬细胞吞噬，并沉积在脑膜血管或脉络丛处。然而，这些沉积物在输注后28天时大多从脑室中消失。在此首次报道，相当数量的sAβ1-42几乎被单核吞噬细胞系统从大鼠脑室系统中清除。
