However, in contrast to results described above, we see a significant increase in neurotoxicity in the subiculum (Fig. 7), and increased accumulation of pTau+ neurons and dystrophic neurites in the subiculum, cortex and hippocampus (Fig. 6) in the absence of Cx3cr1. Thus, while CX3CL1 signaling to neurons and TGFβ3-mediated neurogenesis may potentially be upregulated in 5xFAD;Cx3cr1−/− mice, our data suggest that this is not sufficient to reverse/reduce neuronal loss and ameliorate long-term cognitive decline. The gene discussed is CX3CL1; the disease is Mental deterioration.