In a PS19 mice model of neurodegenerative tauopathy and AD, microglia-specific transcription factors Irf8, Spi1, and Runx1 are observed to be significantly upregulated, whereas complement C3aR deletion, the complement factor C3 complement receptor that mediates neuroimmune crosstalk, decreases Irf8, Spi1, and Runx1 expression and rescues tau pathology and attenuates neuroinflammation, synaptic deficits, and the deleterious effect (Lian et al., 2015; Hong et al., 2016; Litvinchuk et al., 2018). This evidence concerns the gene SPI1 and Alzheimer disease.