In particular, a role for oxidative and nitrosative stress in mediating BVR-A dysfunction was proposed, whereby the observed increase of oxidative and nitrosative stress in the hippocampus of 3xTg-AD mice were responsible for the oxidative damage observed at the expense of BVR-A, named the increase of 3-nitrotyrosine (3-NT) [81] (Table 2). This evidence concerns the gene BLVRA and Alzheimer disease.