Nitric oxide (NO) production by microglial cells, astrocytes, and brain microvessels is enhanced in patients with Alzheimer's disease, and there is a growing evidence that NO is involved in neuronal death in Alzheimer's disease.1 The oxidative stress caused by NO in the brain could be genetically regulated, and NO synthase (NOS) genes could modulate the susceptibility of developing the disease. Two isoforms of NOS, inducible (NOS2) and endothelial (NOS3), have been examined in Alzheimer's disease. A pentanucleotide repeat polymorphism within the promoter region of the NOS2 gene is not associated with Alzheimer's disease but may be a predisposing factor in the development of dementia with Lewy bodies.2 Similarly, a rare polymorphism in a 27 base pair repeat in intron 4 of NOS3 is not linked to an increased risk of developing Alzheimer's disease.3 On the other hand, Dahiyat et al 4 analyzed a missense Glu298Asp variant in exon 7 of the NOS3 gene in a British population sample and found an increased frequency of the Glu/Glu genotype among patients with Alzheimer's disease compared with controls, and interaction with the APOE gene was also …