Based on our results and the above findings of others it is possible that, early in the course of AD, diffuse neuronally derived Aβ (and possibly Aβ released from ECs [70]), which is known to cause oxidative stress and release of inflammatory mediators including fractalkine from neurons, astrocytes, and activated ECs and SMCs [2, 5, 7, 9, 58, 59, 68, 69, 78] leads to peri-collateral recruitment of CD11b+ immune cells, lower eNOS-NO and VEGF signaling and other changes in collateral ECs and SMCs associated with vascular inflammation (Fig. 7). This evidence concerns the gene CX3CL1 and Alzheimer disease.