CLDN1 and Alzheimer disease: Shin et al. demonstrated the dysfunction of barrier function in AD disease models by showing Aβ buildup on the abluminal side of the endothelium, indicating an increase in BBB permeability via downregulation of tight junction expression (claudin-1, claudin-5, and VE-cadherin) and upregulation of MMP2 and reactive oxygen species (ROS) production [138].