More studies are necessary in order to elucidate the pathways of the endothelial nitric oxide synthase (eNOS) in cerebrovascular diseases and in defining how different allelic combinations of the eNOS gene single-nucleotide polymorphism (SNP) could favor this pathological process.
Vasoreactivity induced by L-arginine, which is the substrate for endothelial nitric oxide synthase, is a parameter of endothelial function and has been shown to be altered in patients with cerebrovascular disease.
Both asymmetric dimethylarginine (ADMA), which is an inhibitor of endothelial nitric oxide synthase and the fatty acid-binding protein 2 (FABP2) A54T gene polymorphism have been associated with cerebrovascular disease.
Carriers of eNOS Asp298, particularly if exposed to adverse environmental infuences on endothelial function, may be at increased risk of developing atherosclerosis and cerebrovascular disease.
Since NOS-III is also expressed in vascular cells, and cerebrovascular disease (CVD) frequently complicates the pathology of AD, we investigated the role of NOS-III in relation to CVD in AD.