Moreover, overexpression of CCL2 driven by GFAP promoter in APP/CCL2 mice enhanced amyloidosis, increased microglial Iba-1immunoreactivity, and decreased cognition (16, 17) while APP/PS1/CCL2 null mice also displayed increased levels of Aβ oligomers and worsening of cognitive dysfunction (18). The gene discussed is CCL2; the disease is amyloidosis.