Bradykinin, lysine-bradykinin, and bradykinin degradation products act through the activation of two G protein-coupled bradykinin receptors (BRs): B1R and B2R. Pharmacological antagonism or genetic deletion of B1R (Prediger et al., 2008; Lacoste et al., 2013; Passos et al., 2013; Asraf et al., 2016) and B2R (Bicca et al., 2015; Caetano et al., 2015) have been shown to alleviate the cognitive deficits in Aβ-injected or transgenic AD animal models. This evidence concerns the gene BDKRB1 and Alzheimer disease.