Monji A, Tashiro K, Yoshida I, Hayashi Y, Tashiro N
Department of Neuropsychiatry, Faculty of Medicine, Kyushu University, Fukuoka, Japan.
Brain Res. 1998 Jun 15;796(1-2):171-5. doi: 10.1016/s0006-8993(98)00342-4.
The aggregation of soluble A beta into insoluble amyloid fibrils is believed to be an important step in the pathogenesis of Alzheimer's disease (AD) and the prevention of this process therefore seems to be a promising strategy for the treatment of AD. Both apolipoprotein E(apoE) and laminin are known to play important roles in the regeneration of the central nervous system and both are known to accumulate in the senile plaques of the AD brains. In the present study, we therefore investigated whether or not laminin has any effect on A beta 40 fibril formation promoted by apoE4 in vitro. A thioflavine-T fluorometric assay and electron microscopic observations using negative staining together demonstrated that laminin inhibits A beta 40 fibril formation in vitro while it also inhibits A beta 40 fibril formation promoted by apoE4. These results suggested that either laminin or its derivatives may thus be effective as therapeutic agents for AD.
可溶性Aβ聚集成不溶性淀粉样纤维被认为是阿尔茨海默病（AD）发病机制中的一个重要步骤，因此预防这一过程似乎是治疗AD的一种有前景的策略。已知载脂蛋白E（apoE）和层粘连蛋白在中枢神经系统再生中都发挥重要作用，并且两者都已知会在AD大脑的老年斑中积累。因此，在本研究中，我们调查了层粘连蛋白在体外是否对apoE4促进的Aβ40纤维形成有任何影响。硫黄素-T荧光测定法和使用负染色的电子显微镜观察共同表明，层粘连蛋白在体外抑制Aβ40纤维形成，同时也抑制apoE4促进的Aβ40纤维形成。这些结果表明，层粘连蛋白或其衍生物可能因此作为AD的治疗剂是有效的。
