While the poor bioavailability of thiamine has been suggested to limit its clinical benefits in Alzheimer’s disease patients (Blass et al., 1988; Nolan et al., 1991; Rodríguez et al., 2001), its analog benfotiamine has been shown to improve cognitive impairment and reduce amyloid deposition and hyperphosphorylated tau in rodent models of Alzheimer’s disease (Pan et al., 2010; Zhang et al., 2011). Here, MAPT is linked to Cognitive impairment.