Two isoforms of DMT1, DMT1-IRE and DMT1+IRE, have been shown to colocalize with Aβ in the plaques of the AD brain and the levels of both DMT1 isoforms are significantly increased in the frontal cortex and hippocampus in a APP/PS1 transgenic mouse model (Zheng et al., 2009), which was accompanied by a reduction in Fpn expression (Xian-hui et al., 2015), suggesting that the deregulation of iron metabolism-related protein DMT1 and Fpn plays a critical role in the iron-mediated neuropathogenesis of AD. Here, SLC11A2 is linked to Alzheimer disease.