While the mechanisms explaining how P2X7R activation leads to an AD-like phenotype are still to be determined, several pathways have been proposed to be regulated via P2X7R during AD and tauopathies, including phosphorylation of the tau kinase glycogen synthase 3β (GSK-3β), leading thereby to the hyperphosphorylation of tau [183,186] and inflammatory pathways, including a pathogenic CD8+ T cell recruitment [184]. This evidence concerns the gene CD8A and Alzheimer disease.