Microglia are the resident macrophages and primary immune effectors in the brain that are central to neuroinflammatory mechanisms of Alzheimer’s disease (AD) pathogenesis.The causal role of microglia in AD is evidenced by data from recent unbiased genome-wide association studies (GWAS) that have identified several single-nucleotide polymorphisms (SNPs) in immune related genes as independent risk factors for late-onset AD . Approximately two thirds of the 29 susceptibility genes are exclusively or most highly expressed in microglia . In human AD and mouse models of AD pathology brains, microglia with activated morphology are frequently found surrounding amyloid-beta (Aβ) plaques . Microglial depletion in mouse models of AD pathology also results in decreased neuropathological features of AD. Overall, these convergent findings implicate microglia in the pathogenesis of AD, but whether microglia are protective or detrimental ] remains elusive.