In the early stage of AD, astrocytes are activated in response to the accumulation of Aβ plaques, which in turn release chemokines and cytokines, such as transforming growth factor-β and monocyte chemoattractant protein-1, and respond to pro-inflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α, simultaneously increasing Aβ production and resulting in the inability of the BBB to maintain normal function [37,38,39,40,41]. The gene discussed is CCL2; the disease is Alzheimer disease.