According to this hypothesis, it has been proposed that accumulation of Aβ peptide is the upstream event in AD pathogenesis, in both early-onset and late-onset forms, leading to the formation of amyloid plaques, which trigger tau hyperphosphorylations and the formation of NFT, ultimately leading to synaptic dysfunction, neuronal loss, degeneration, and dementia.[7, 8] However, there is growing evidence for the role of additional factors such as oxidative stress, neuroinflammation, and mitochondrial dysfunction in the pathogenesis of AD.[9]. This evidence concerns the gene MAPT and Alzheimer disease.