We next studied in vivo effect of TA-3 employing 6xTg mice that express a mutant form (P301L) of Tau in addition to a mutant APP [APPswe/Ind/fl (K670N/M671L/V717F/I716V)] and a mutant PS1 (M146L/L286V) because 6xTg mice develop both amyloid plaques and Tau NFTs at younger ages, coupled with accelerated neurological deficits compared to other AD animal models 19, ensuring study of the effect of TA on the clearance of both Tau and Aβ, together with impact of Tau clearance on the associated neurological deficits. The gene discussed is MAPT; the disease is Alzheimer disease.