BDKRB1 and Alzheimer disease: 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).