Additional studies are required to identify the cell types that express fractalkine/CX3CL1 and its CX3CR1 receptor that are involved in the rarefaction, and to identify the pathway activated by CX3CR1, as well as other mechanisms, that lead to the impaired eNOS/NO known to occur in AD [6, 36–38, 70, 83] and that when countered in our 2xTg; eNOS transgenic mice prevented rarefaction. This evidence concerns the gene CX3CR1 and Alzheimer disease.