Historically, AD disease-modifying strategies beyond symptomatic medications have relied on (a) anti-Aβ production and aggregation agents, decreasing the synthesis of Aβ, such as β- and γ-secretase; (b) neutralizing or removing the toxic aggregate or misfolded forms of Aβ by immunotherapy; (c) anti-tau protein drugs [33,34]. This evidence concerns the gene MAPT and Alzheimer disease.