Molecular sensing using model membranes

我们已经(i)表明淀粉样蛋白（Ab）以一种依赖于物种和膜组成的方式与膜相互作用。它们引起膜转化、破裂和粘滞。这些可能有助于理解毒性机制；（二）研究胆固醇氧化如何影响膜动力学，证明温度升高使氧化膜更具流动性。我们使用生物细胞也有类似的发现。这些发现有助于阐明胆固醇在抗体诱导毒性中的作用；（iv）氧化膜增强Ab与膜的结合；(v)潜在的神经保护剂以结构依赖的方式与膜相互作用，其抑制Ab聚集的能力也是如此。在功能基团水平上揭示这些化合物的重要性，为量身定制潜在的生物活性候选药物打开了关键。我们为Ab研制了一种免疫传感器芯片。

We have (i) shown that amyloid beta (Ab) interacts with membranes in a species-dependent and membrane composition manner. They cause membrane transformation, breach and viscosity. These may contribute towards understanding toxicity mechanisms; (ii) studied how oxidation of cholesterol influences membrane dynamics, demonstrating that temperature increase renders oxidized membranes more fluid. We have similar findings using biological cells. The findings are useful for clarifying the impact of cholesterol in Ab-induced toxicity; (iv) oxidized membranes enhance Ab's association with membranes; (v) potential neuro-protective agents interact with membranes in a structure-dependent manner as does their ability to inhibit Ab aggregation. Unraveling the importance of these compounds, at a functional group level opens the key to tailored design of potential bioactive drug candidates. We have developed an immunosensor chip for Ab.