Some early suggestions for microglial metabolic alterations in AD were based on genome-wide association studies that identified an increased risk for AD in individuals carrying mutations or polymorphisms in genes involved in microglial metabolism, such as TREM2, progranulin, and APOE. The genetic overlap between factors regulating metabolic signalling, microglial immune functions, and AD raises the intriguing possibility that cascades controlling microglial metabolism may modify AD risk and disease progression [87, 88]. Here, GRN is linked to Alzheimer disease.