Su et al. (2019) found that even transient elevation of brain Aβ levels can allow T2DM to slightly disrupt the neural milieu in a way that encourages pathologies associated with the onset of memory deficits and AD. Martinez-Valbuena et al. (2019) argue that a potential common pathogenetic mechanism underlying both DM and AD is evidenced by the co-occurrence of amyloid brain lesions and deposits containing both tau and Aβ in pancreatic β cells. This evidence concerns the gene MAPT and diabetes mellitus.