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. Here, TNF is linked to Alzheimer disease.