Abstract: Alzheimer’s disease (AD) is a progressive and irreversible neurodegenerative disorder that is characterized by memory loss and a decline in activities of daily life. More than 50 million people worldwide are affected by AD, and this number will continue to rise over 100 million within next three decades. Its major pathological features are the extracellular plaque deposits of the β-amyloid peptide and the intracellular flame-shaped neurofibrillary tangle-aggregation of hyperphosphorylated tau-proteins (pTau). A number of descriptive hypotheses including amyloid hypothesis and tau propagation hypothesis have been proposed to understand the causes of AD (Liu et al., 2019). According to the tau propagation hypothesis, the balance of kinase and phosphatase activity is changed in AD, generating various hyperphosphorylated species of tau. These pTau can bind with each other to produce oligomers, then contributing to the formation of paired helical filaments, the primary content of neurofibrillary tangle (Gendron and Petrucelli, 2009). Based on postmortem findings in AD patients, tau pathobiology was propagated to distinct brain regions in a stereotypical manner, starting from the entorhinal cortex then distributing to the hippocampus and neocortex. However, the mechanisms underlying this spread of pathological tau are still poorly understood.