TREM2 and Alzheimer disease: These phenotype changes led to the loss of the homeostatic receptor P2RY12 and upregulation of genes such as APOE, TREM2, or CD11c, with specific gene alterations that are unique to the human microglia in contrast to murine microglia, suggesting that this system is best for modeling AD and other neurodegenerative diseases that murine microglia [170].