The misfolding of amyloid beta (Aβ) is one of the predominant hallmarks in the pathology of Alzheimer's disease (AD). In this study, we showed that the formation of the Aβ ion channel on the membrane depended on the cholesterol concentration. From a mechanical aspect, we found that cholesterol levels affected the stability and assembly of lipid bilayers. Measurements on planar lipid bilayers indicated that a small amount of cholesterol interacted with Aβ proteins and promoted the insertion process. Conversely, high cholesterol integrated the lipid bilayer and exerted an opposite effect on Aβ insertion. The Aβ ion channel was then detected by graphene-based field-effect transistors. Results demonstrated that the Aβ ion channel promoted a Ca2+ flux in the presence of 15% cholesterol but prevented a Ca2+ flux in high cholesterol. Thus, cholesterol had a complex impact on the Aβ ion channel that can be described as two different effects. First, a small amount of cholesterol interacted with Aβ and facilitated the Aβ ion channel formation in the membrane. Second, a large amount of cholesterol did not induce the ion flux in the membrane, which can be explained by the cholesterol damage to the regular distribution of the lipid bilayer. Overall, this study suggested a possible approach to consider cholesterol levels for the treatment of AD patients.

中文翻译：

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胆固醇调节脂质双层中Aβ离子通道的形成。

淀粉样蛋白β（Aβ）的错误折叠是阿尔茨海默氏病（AD）病理学的主要标志之一。在这项研究中，我们表明膜上Aβ离子通道的形成取决于胆固醇的浓度。从机械方面，我们发现胆固醇水平影响脂质双层的稳定性和组装。对平面脂质双层的测量表明，少量胆固醇与Aβ蛋白相互作用并促进了插入过程。相反，高胆固醇整合了脂质双层，并对Aβ插入产生相反的作用。然后通过基于石墨烯的场效应晶体管检测Aβ离子通道。结果表明，在15％的胆固醇存在下，Aβ离子通道促进了Ca2 +通量，但在高胆固醇中阻止了Ca2 +通量。从而，胆固醇对Aβ离子通道有复杂的影响，可以描述为两种不同的影响。首先，少量胆固醇与Aβ相互作用并促进膜中Aβ离子通道的形成。其次，大量的胆固醇没有引起膜中的离子通量，这可以由胆固醇对脂质双层规则分布的破坏来解释。总的来说，这项研究提出了一种可能的方法来考虑胆固醇水平来治疗AD患者。这可以通过胆固醇对脂质双层规则分布的破坏来解释。总的来说，这项研究提出了一种可能的方法来考虑胆固醇水平来治疗AD患者。这可以通过胆固醇对脂质双层规则分布的破坏来解释。总的来说，这项研究提出了一种可能的方法来考虑胆固醇水平来治疗AD患者。