| 研究概要 |
We have shown that amyloid beta (Aβ) interacts with membranes in a species-dependent and membrane composition manner. They cause membrane transformation, breach and viscosity (Morita et al. 2012; Vestergaard et al. 2013; Morita et al. 2014)). These may contribute towards understanding the peptide’s toxicity mechanisms. Towards studying the influence of oxidized membranes on Alzheimer’s Aβ-induced toxicity, we studied how oxidation of cholesterol influences membrane dynamics (Vestergaard et al. 2011), demonstrating that temperature increase renders oxidized membranes more fluid. Similar findings have been found using biological cells (Phan et al., 2013; Phan et al., In Preparation). The findings are useful for clarifying the impact of cholesterol in Aβ-induced toxicity. Our preliminary studies on the role of oxidized cholesterol in Aβ-induced membrane dynamics show that oxidized membranes associate with and are destabilized more readily by A. Potential neuro-protective agents interact with membranes in a structure-dependent manner as does their ability to inhibit Aβ aggregation (Phan et al., Submitted; Samarat et al., In Preparation) . 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 Aβ. We have developed a gold nano-particle immunosensor chip for detecting amyloid beta. T(Lien et al., In Preparation). This system was presented at an Electrochemistry International conference (Vestergaard et al., Electrochem 2013, UK, 2013).
|
