Subsequently, as microglial LD accumulation was mainly pronounced in plaque-bound xMGs, we further determined whether iPSC-derived TREM2-R47H xMGs exhibit an overall reduction in their reactivity to amyloid pathology by quantifying the proximity of human microglia to plaques, expression of the DAM-specific marker CD9, and secretion of APOE by human microglia. This evidence concerns the gene CD9 and amyloidosis.