No association between Glu298Asp endothelial nitric oxide synthase polymorphism and Italian sporadic Alzheimer's disease

Neurosci Lett. 2003 May 8;341(3):229-32. doi: 10.1016/s0304-3940(03)00210-6.


A great amount of evidence suggests that neuroinflammation may be a major pathogenetic mechanism in the pathophysiology of sporadic Alzheimer's Disease (sAD). Recently, polymorphisms in the endothelial nitric oxide synthase (NOS3) gene have been associated to late onset Alzheimer's Disease in a British population. However, other groups failed to replicate this finding in Asiatic and Caucasian populations. We conducted a case-control study including a clinically well-defined group of 149 sAD patients and 149 age and sex matched controls to test the association between NOS3 Glu298Asp polymorphism and sAD in an ethnically homogenous Italian population. All subjects were genotyped at NOS3 and apolipoprotein E. No significant difference was found in either allele or genotype frequencies between cases and controls, even after stratification for Apolipoprotein E4 carrier status. The NOS3 Glu298Asp polymorphism does not appear to influence the risk of developing sAD in an Italian population.

Publication types

  • Comparative Study

MeSH terms

  • Aged
  • Aged, 80 and over
  • Alzheimer Disease / enzymology
  • Alzheimer Disease / epidemiology
  • Alzheimer Disease / genetics*
  • Case-Control Studies
  • Chi-Square Distribution
  • Dipeptides / genetics*
  • Female
  • Humans
  • Italy / epidemiology
  • Male
  • Middle Aged
  • Nitric Oxide Synthase / genetics*
  • Nitric Oxide Synthase Type III
  • Polymorphism, Genetic / physiology*


  • Dipeptides
  • gamma-glutamylaspartic acid
  • NOS3 protein, human
  • Nitric Oxide Synthase
  • Nitric Oxide Synthase Type III