Several hypotheses have been proposed to explain the pathogenesis of AD, including the amyloid cascade hypothesis [64], tau hypothesis [65], hypothesis of mitochondrial dysfunction [66], the inflammation hypothesis [67], the glutamate hypothesis [68], etc. Contemporary approaches to the therapy of AD focus on the development of multifunctional compositions that can bind to several targets [45,69,70]. This evidence concerns the gene MAPT and Alzheimer disease.