The protein fragments of beta-amyloid accumulates outside the neurons, whereas tau protein accumulates inside them [1, 2]. Based on the recent clinical evidence, it is known that the progression of Alzheimer’s disease is due to the formation of beta-amyloid plaques, which are formed by the cleavage of amyloid precursor protein (APP) by β-secretase and γ-secretase protease enzymes [3]. This evidence concerns the gene APP and early-onset autosomal dominant Alzheimer disease.