Inhibition of these motifs by DC8E8 and subsequent prevention of PHF core formation is a good explanation for the mechanism underlying how DC8E8 is capable of interfering with the multiple tau-mediated activities contributing to AD pathology, including (1) transition from physiological tau to pathological tau; (2) formation of tau dimers, trimers and other tau oligomers; and (3) formation of insoluble tau aggregates. This evidence concerns the gene MAPT and Alzheimer disease.