We show that the activated microglia, validated by Iba-1 and CD86 co-staining, reveal short processes in the brain with extensive aggregated Aβ and Tau pathologies in Thy1-C/EBPβ transgenic mice after AD-FMT, Bacteroides fragilis or PUFA metabolites treatment (Figs. 3, 5 and 7). The gene discussed is CD86; the disease is Alzheimer disease.