Recent studies have shown that deficits of endothelial NOS1 in AD play an important role in the phosphorylation of the AD-related lesion tau in murine APP/PS1 TgAD models (Austin and Katusic, 2016) while increased NOS-1 activity and NO transmission in the hippocampus was evidenced to modulate aggression (Miszczuk et al., 2016; Zhou et al., 2016). This evidence concerns the gene APP and Alzheimer disease.