iNOS deficiency strongly reduced the nitrotyrosination of Aβ42, attenuated Aβ aggregation and cognitive deficit in AD mouse model.454 Using a similar model, Nathan et al. found that the deficiency of iNOS also reduced activation of glial cells, protected the AD-like mice against premature mortality.458 But some studies got a conflicting result. This evidence concerns the gene NOS2 and Alzheimer disease.