However, pharmacological blockade or genetic deletion of the B1R and B2R significantly reverses the cognitive impairments caused by a single intracerebroventricular (i.c.v) injection of Aβ1–40 in rodents, suggesting that B1R and B2R were potential drug targets for the treatment of AD (Prediger et al., 2008). This evidence concerns the gene BDKRB2 and Alzheimer disease.