Receptor for advanced glycation endproducts as a potential therapeutic target for Alzhemer’s disease

Abstract

Objective of the research is studying of the pathological effects of beta-amyloid on cerebral endothelial cells (CECs) and identifying of potential therapeutic target for Alzheimer’s disease. In this study, immortalized cerebral endothelial cells (bEnd3) were used. Methods of quantitative immunofluorescence microscopy (QIM) and confocal immunofluorescence microscopy of double immunofluorescence labeled proteins were applied. We demonstrated that Aβ binding to the receptor for advanced glycation endproducts (RAGE) on the CECs surfaces is resulted in NADPH oxidase complex assembling and subsequent ROS generation. We also found that RAGE inhibitor azelnidipin was capable of abrogating Aβ-induced ROS production.