This AD platform simulates the cerebral–vascular interface, successfully mimicking several of the vascular phenotypes observed in AD patients, including the greater permeability of the BBB coincident with the downregulation of certain tight junction proteins (claudin-1 and claudin-5), adherens junction proteins and VE-cadherin, as well as the upregulation of matrix-metalloproteinase-2 (MMP-2), the accumulation of reactive oxygen species (ROS), and the aggregation of Aβ on the abluminal side of the BBB endothelium. This evidence concerns the gene CDH5 and Alzheimer disease.