MAPT and Alzheimer disease: In contrast with mouse datasets [27, 28], we found that human AD microglia can transition from homeostatic to a state associated with low AD pathology and characterized by upregulation of ribosomal genes (ribosomal response or RR), or to other states associated with increased AD pathology (early Aβ, late tau or EALT, and late Aβ response or LAR).