Although clear evidence exists suggesting that thiamin homeostasis is altered in patients with AD, that thiamin deficiency aggravates plaque formation, and that many thiamin-dependent processes are diminished in the brains of AD patients (Gibson et al., 2013; Karuppagounder et al., 2009), little is known about possible alteration in the level of expression of THTR-1 and -2 in brain tissue of these patients. Here, SLC19A2 is linked to Alzheimer disease.