This suggests that the very strong microglial response to plaque deposition that we have previously reported in transgenic mouse models of AD (43,44), particularly the up to 9-fold increase in Trem2 expression, preferentially involves engagement of anti-inflammatory pathways that may contribute to the resistance of mice with a heavy amyloid load from developing the full AD pathology of Tau tangles and neurodegeneration, discussed further in Refs 44 and 104. This evidence concerns the gene MAPT and amyloidosis.