IFNAR2 and Alzheimer disease: Consistently, single-cell transcriptomic analysis of microglia revealed that ABCs accelerate the transition from HMs to DAMs, inflammation, and IFN-R subclusters, and enhance neurodegeneration-associated microglial activity.7,9,47 Further cellular experiments demonstrated that AD mouse-derived ABCs promoted inflammatory factor expression in microglia and impaired their phagocytosis of Aβ (supplementary Fig. 7a–d).