The same model was previously characterized also by the buildup of Aβ protein 1–42 in the hippocampus and the cerebral cortex and an increased expression of inflammatory proteins such as inducible nitric oxide synthase (iNOS) and COX-2 in mice brains [17, 39], thus mimicking several pathophysiological aspects of AD with a prominent contribution of oxidative stress and inflammation. This evidence concerns the gene PTGS2 and Alzheimer disease.