IL1B and Alzheimer disease: When treated withinflammatory cytokines, such as tumor necrosis factor α (TNF-α), interleukin-1beta (IL-1β), and IL-8, through the vascular or parenchymal channel,neuroinflammation was seen to increase BBB permeability by altering expressionof ZO-1 and increasing dextran permeability.91 This also showed neuroinflammation on the brain side of the chip,demonstrating the effectiveness of this model to resemble AD pathology.