Accordingly, another study showed that Aβ, acting via ALX/FPR2 receptors, induces chemotaxis and superoxide production in mouse neutrophils and stimulates cultured murine microglial cells, which strongly suggested its pivotal role in recruitment of microglial cells to senile plaques, induction of oxidative stress, and consequent neuroinflammation in AD [31]. Here, FPR2 is linked to Alzheimer disease.