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当代阿耳茨海默病研究

Editor-in-Chief

ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

Research Article

外源性丁酰胆碱酯酶与 5XFAD/丁酰胆碱酯酶敲除小鼠脑中 β-淀粉样蛋白斑块的相互作用

卷 18, 期 6, 2021

发表于: 27 August, 2021

页: [470 - 481] 页: 12

弟呕挨: 10.2174/1567205018666210827122704

价格: $65

摘要

背景:在阿尔茨海默病 (AD) 和淀粉样蛋白模型(如 5XFAD 小鼠)中,丁酰胆碱酯酶 (BChE) 与 β-淀粉样蛋白 (Aβ) 斑块相关,并具有独特的生化特征,使其与神经元中发现的不同。有人提出与 Aβ 斑块相关的 BChE 可能参与该结构的成熟,从而参与疾病进展。 目的:目前尚不清楚与 Aβ 斑块结合的 BChE 是否由于不同的一级结构或由于该酶与 Aβ 斑块的关联而改变了生化特性。此外,这种 BChE 的来源和结合机制仍然未知。 方法:将来自 5XFAD/BChE-KO 小鼠的脑组织切片与外源 BChE 一起孵育,并对该酶的活性进行染色。已努力确定 BChE 或 Aβ 的哪个区域可能参与这种关联。 结果:我们发现 5XFAD/BChE-KO 脑组织与外源性 BChE 的孵育导致这种酶与 Aβ 斑块和神经元相关。与神经元 BChE 相比,与 Aβ 斑块结合的 BChE 具有与 AD 中所见相似的生化特性。 BChE 的突变和阻断 Aβ 表型的努力未能阻止这种关联。结论:BChE 与 Aβ 斑块的关联以及由此产生的生化变化表明,当 BChE 与 Aβ 斑块而非神经元结合时,可能会发生构象变化。 5XFAD/BChE-KO 模型非常适合探索 BChE 与 Aβ 斑块的结合机制以及 BChE 参与 AD 发病机制。

关键词: 丁酰胆碱酯酶,β淀粉样蛋白斑块,5XFAD,神经变性,阿尔茨海默病,卡尔诺夫斯基根组织化学。

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