To summarize the findings from the studies on CX3CL1 axis in AD models, it can be stated that suppressing the CX3CL1 signal in hAPP mice and hTau mice causes increased tau phosphorylation and even exacerbates cognitive deficits, while in APP-PS1 and CRND8, it induces a reduction of Aβ deposition and microglial phagocytosis [15,70]. This evidence concerns the gene APP and Alzheimer disease.