It has been known for decades that abnormally aggregated Tau proteins (PHFs) or so-called neurofibrillary tangles codeposit with several transition metals (Good et al., 1992), and compromised metal homeostasis has been demonstrated to be closely linked with the pathogenesis of AD and tauopathy in vivo (Atwood et al., 2000; Bush, 2003; Lang et al., 2012; Lovell et al., 1998). This evidence concerns the gene MAPT and tauopathy.