<i>Background:</i> Neuropathological studies supported by experimental animal studies show that the constituents of the innate immunity are intimately involved in the early steps of the pathological cascade of Alzheimer’s disease (AD). <i>Objectives:</i> To show the evidence that constituents of the innate immunity contribute to the etiology of late-onset AD. <i>Methods:</i> Evaluation of the relationship between the constituents of the innate immunity and genetic risk factors for late-onset AD. <i>Results:</i> Complement activation and activated microglia are early neuropathogical events in AD brains. Genome-wide association studies have demonstrated gene loci that are linked to the complement system. The production capacity for inflammatory cytokines is under genetic control and the offspring with a parental history of late-onset AD have a higher production capacity for inflammatory cytokines. <i>Conclusion:</i> Epidemiological and genetic data suggest that the innate immunity is involved in the etiology of late-onset AD.