Together with the increased brain cortical and hippocampal Aβ levels observed in sucrose-treated mice, these reports suggested that metabolic alterations usually associated with T2D could contribute for the development of AD features (20, 21), in agreement with the previously reported profound mitochondrial anomalies and increased Aβ and phosphorylated tau protein levels in brain cortex and hippocampus upon CNS-induced insulin resistance (22), as well as with the higher predisposition of T2D patients for cognitive decline and eventually AD (23). The gene discussed is MAPT; the disease is type 2 diabetes mellitus.