At present, no long-term effective drug can delay cognitive declines in AD progressions, and the unmet needs on medicines or functional foods are currently developing in AD treatments, which the targets are mainly focused on the pathological theories of AD, including amyloid-β (Aβ) peptide aggregations to generate amyloid-like fibrils, hyper-phosphorylated Tau protein aggregations to form neurofibrillary tangles, and low levels of acetylcholine and neuron deaths (Querfurth and LaFerla 2010; Craig et al. 2011; Selkoe and Hardy 2016). Here, MAPT is linked to Alzheimer disease.