To further characterize potential mechanisms of BBB dysfunction that are relevant to neurodegenerative diseases like AD, we evaluated how STZ treatment affected the total numbers of iBECs, expression levels and localization of the TJPs claudin-5 and ZO-1, as well as the BBB glucose transporter GLUT-1 11 days post-treatment. The gene discussed is CLDN5; the disease is Alzheimer disease.