Others noted that decreasing CX3CL1/CX3CR1 signaling activity exacerbated plaque-independent cognitive deficits in APP-overexpressing AD mouse models (Cho et al., 2011); deficiency in CX3CR1 was found to increase tau hyperphosphorylation (Bhaskar et al., 2010; Cho et al., 2011; Lee et al., 2014) and to increase neurodegeneration (Cardona et al., 2006). This evidence concerns the gene CX3CL1 and Alzheimer disease.