The effect of partial endothelial NO synthase (eNOS) deficiency on cognitive deficit and amyloid pathology was investigated in a mouse model, where partial eNOS deficiency was found to increase behavioral dysfunction, Aβ accumulation, and microglial pathology in APP/PS1 mice, leading to the pathogenesis of AD [277] (Fig. 3A). The gene discussed is NOS3; the disease is amyloidosis.