AGTR1 and Alzheimer disease: Studies performed on animal models of AD and postmortem examinations of human brains has led investigators to suggest that the excessive activation of the brain AT1R and insufficient activation of AT2R may induce excessive generation of reactive oxygen species (ROS), and this may account for the prevalence of neurodegenerative processes over the neuroprotective processes in the brains of AD patients [109,110,111,112,113].