These intraneuronal tangles contain fibrillary structures that are formed by the aggregation of hyperphosphorylated microtubular-associated tau protein.1 An increase in intracellular tau aggregates is highly linked to more severe disease states of AD and other tauopathies.2 These observations have encouraged efforts to develop treatment approaches that can slow down or prevent the formation of pathological tau.3,4 Diverse therapeutic strategies have been proposed to reduce tau expression or inhibit the formation of tau aggregates.5 This evidence concerns the gene MAPT and Alzheimer disease.