of microglia between AD cases and controls. However, we found significantly decreased microglia in brains exhibiting PA (Additional file 1: Table S7; Additional file 1: Figure S6), proving that these studies are sufficiently powered to identify significant differences. In any case, we cannot rule out the possibility of a change in the activation stage of microglia in these individuals. Overall, these results suggest that TREM2 affects AD risk through a slightly different mechanism to that of ADAD or LOAD in general. Therefore, other pathogenic mechanisms should contribute to disease. We believe that a detailed modeling of immune response cells, reflecting the alternative microglia activation states, will generate more accurate profiles to elucidate the immune cell distribution in AD.
