Chips with the AD cells had reduced BBB permeability, as seen in AD patients, as well as other AD-specific features, such as decreased expression of both claudin-1 and claudin-5, decreased VE-cadherin expression, increased expression of matrix-metalloproteinase-2, increased expression of reactive oxygen species, and the deposition of Aβ peptides at the endothelium [151]. This evidence concerns the gene CLDN1 and Alzheimer disease.