For instance, in an Alzheimer’s disease mouse model, microglia significantly overexpressed complement components (C3, C4B, and CFB), chemokines (CCL12, CCL3, CCL4, and CXCL16), and immune-related genes (H2-D1, AXL, APOE, and LGALS3B; Mathys et al., 2017); APOE, SPP1, and LPL are specifically upregulated in microglia surrounding amyloid plaques (Keren-Shaul et al., 2017). Here, APOE is linked to early-onset autosomal dominant Alzheimer disease.