Although CX3CR1 deficiency exacerbates AD-related neuronal and behavioral pathologies in mice overexpressing human Aβ, these effects are likely to be associated with the level of cytokine production and not Aβ plaque load, suggesting that alteration of proinflammatory factors, including TNF-α and IL-6 may modulate CX3CL1 signaling [43]. This evidence concerns the gene CX3CL1 and Alzheimer disease.