Brain lesions observedduring the course of AD involve two main aspects: extracellular amyloid-beta(Aβ)deposition as senile plaques and intracellular tau accumulation forming neurofibrillarytangles and promoting cytoskeletal disorganization.
在AD进展过程中脑内病理学改变主要涉及2个方面：细胞外淀粉样蛋白β(Aβ)沉积形成的老年斑和细胞内tau蛋白积聚形成的神经纤维缠绕并最终促进细胞骨架的破坏、分解。
参考来源 - APP/PS1阿尔茨海默病转基因小鼠白质异常特点及其与脑内淀粉样病变之间关系的研究·2,447,543篇论文数据，部分数据来源于NoteExpress
Research into new treatments for Alzheimer's, for example, has started to overturn what we thought we knew about the role of amyloid-beta proteins in the disease.
比如说，关于老年痴呆新疗法的研究已经开始颠覆我们之前淀粉状贝塔蛋白质的角色的认识。
One of the products, with the long-winded name amyloid beta-peptide 42, has the unfortunate property that its molecules like to stick to each other.
所形成的产物之一有一个冗长的名字——淀粉样贝塔-肽42，它具有一种不祥的特性，即它们分子彼此之间容易纠缠在一起。
Amyloid beta itself might be injuring nerve cells or the plaques, made of accumulations of amyloid beta, could be the culprits.
淀粉样β蛋白本身可能损伤神经细胞或者有它聚集形成的老年斑才是罪魁祸首。
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