In an AD animal model, exendin‐4 treatment activates GLP‐1R, decreases mitochondrial toxicity, improves recognition and memory impairment, reduces neuroinflammatory cytokines, decreases amyloid‐β‐induced oxidative stress, and increases levels of synaptic proteins [80, 81, 82, 83, 84]. Here, GLP1R is linked to Alzheimer disease.