In view of these considerations, we investigated whether the antibody-mediated neutralization of pathogenic NH2-truncated tau following i.v. 12A12mAb infusion could mitigate in vivo the occurrence of neurochemical derivatives from the abnormal APP and tau metabolisms which are largely recognized to compromise the Alzheimer’s disease nerve terminals at prodromal disease stages (Braak and Del Tredici, 2015). The gene discussed is APP; the disease is early-onset autosomal dominant Alzheimer disease.