Over the past three decades, many experimental studies have documented that Aβ is the culprit of neurodegeneration in AD [26, 29], thereby confirming the deposition of Aβ and the accumulation of hyperphosphorylated Tau protein in neurons as the major pathogenesis of AD to lead to impaired synaptic plasticity and cognitive dysfunction, as well as the occurrence of dementia. This evidence concerns the gene MAPT and Alzheimer disease.