TREM2 and Alzheimer disease: In microglia where TREM2 function is compromised, they fail to switch from homeostatic OXPHOS to activated glycolysis39 necessary to drive phagocytic function15,23 including of myelin debris.24 It would be therefore possible that individuals without TREM2 risk variants wouldn’t develop AD; however, the impact of common SNP variants on downstream TREM2 function (and hence links to AD pathology) is not fully established.