The function of CXCL8 in the pathogenesis of AD remains unclear, but IL-6, IL-1b, TNF-α, and COX-2 levels increase when culturing human microglia with Aβ in the presence of CXCL8, suggesting that CXCL8 may be responsible for bringing the activated microglia to AD-injured brain regions as an alternative recruitment mechanism, which is important for the increase of Aβ pro-inflammatory responses (144, 145). This evidence concerns the gene IL1B and Alzheimer disease.