The increase of CRP at the microvasculature of the brain may act in synergy to promote arteriolosclerotic progression by different mechanisms like activation of classic complement system, mediation of low density lipoprotein uptake by macrophages, promotion of foam-cell formation, endothelial dysfunction, low nitric-oxide production, stimulation monotype recruitment, and vascular smooth muscle proliferation and migration [2]. This evidence concerns the gene CRP and endothelial dysfunction.