It has been suggested that neuroinflammation (referred here as the activation of microglia and the secretion of cytokines such as tumor necrosis factor-α) would be an upstream mediator of neuronal insulin resistance in the AD brain.46 It could be speculated that the associations we detected would be attributed to Aβ-related microglial reactivity, since we demonstrated associations in regions typical for Aβ accumulation, and the majority of our study participants were already Aβ positive. This evidence concerns the gene TNF and Alzheimer disease.