Aβ1-42 treatment also increased the intracellular Ca2+ concentration, membrane permeabilization, and release of ATP and IL-1β, all of which were dependent on the P2X7 receptor.378 Blocking or deleting the P2X7 receptor in multiple AD mouse models reduced neuroinflammation, diminished leakiness of the BBB, and attenuated memory impairment and cognitive deficiency.381,382. This evidence concerns the gene IL1B and Alzheimer disease.