Notably, we found that disrupting the CX3CL1-CX3CR1 signaling axis reduces Aβ burden with concomitant increases in pro-inflammatory IL-1 and heightened microglial activation in both APPPS1/Cx3cr1−/− and APPPS1/Cx3cl1−/− transgenic mouse models of AD [18]. This evidence concerns the gene CX3CR1 and Alzheimer disease.