Role of ros in ab42-mediated activation of cerebral endothelial cells

Abstract

There is evidence that the deposition of amyloid-beta peptide (Aβ) in brain parenchyma and brain vessels is the main cause of neuronal dysfunction in Alzheimer's disease (AD). Aβ exhibits multiple cytotoxic effects to neurons and causes dysfunction of the blood brain barrier (BBB). In the AD brains an increased deposition of Aβ in the cerebral vasculature is correlated with increased transmigration of blood-born inflammatory cells and neurovascular inflammation. However, regulatory mediators of these processes remain to be elucidated. In this study, we examined a role of ROS in actin polymerization and expression of adhesion molecules on the surface of the cerebral endothelial cells (CECs) that are activated by Aβ42.