Accordingly, in the APP-SL70 mouse, a transgenic model of AD generated on a C57BL/6J genetic background that coexpresses KM670/671NL mutated amyloid precursor protein (APP) and L166P mutated presenilin (PS) one under the control of a neuron-specific Thy1 promoter, and with congophylic Aβ plaques starting from 5 to 6 months of age, phagocytic activity of microglia inversely correlates with Aβ plaque deposition and aging (Blume et al., 2018). Here, PRB2 is linked to Alzheimer disease.