阿尔茨海默病发病机制及其与三体 21 的联系的可能假 说

Endriyas Kelta Wabalo*, Chala Kenenisa Edae
吉马大学健康研究所

摘要

大脑中的“斑块”和“缠结”被认为是阿尔茨海默病的标志。斑块的主要成分是一种蛋白质（“a-β”），
它是从一种大得多的称为淀粉样前体蛋白（APP）的母蛋白中分离出来的，而缠结的主要成分则是 tau 蛋白，它通常
起到稳定神经元轴突内微管的作用。有几种可能阐述了淀粉样蛋白形成的变化及其对神经元死亡带来 AD 的影响；
第一种是淀粉样级联假说，它描述了早发性 AD 是如何由 APP、早老蛋白和 apoE4 的突变诱导的。第二种可能性是
阿尔茨海默病的钙假说，它论证了阿尔茨海默病中钙诱导的记忆丧失。将 AD 和 DS 中 Aβ 斑块中存在的 β- 淀粉样
蛋白（Aβ）前体蛋白（APP）编码基因定位到 21 号染色体，有力证明 21 号染色体基因产物是 AD 和 DS 的主要神
经源性罪魁祸首。本综述的主要目的是阐明阿尔茨海默病的可能假说，并确定 21 号染色体基因产物是 AD 和 DS 发
病机制中的主要神经源性罪魁祸首。总之，本综述中讨论的关于 AD 发病机制的不同假设很好地说明了 AD 的发病
机制、其与 DS 的联系以及某些治疗剂作用于 AD 和 DS 治疗的潜在靶点。

关键词

阿尔茨海默病；三体 21；Amloid 蛋白；Amloid-Protien 斑块；Amlooid 蛋白缠结

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