An intense reaction of microglia following CNS insult, characterized by active proliferation and retracted cellular processes. In AD, accumulation of Abeta can be a possible cause of such physiological phenomenon, as microglia is seen surrounding senile plaques. Abeta interaction with microglial pattern recognition receptors (PRRs) leads to NLRP3 inflammasome activation, production of toxic NOS and ROS and release of proinflammatory cytokines.