Consistent with these findings, Clinton et al. reported that co-expression of Aβ, tau, and α-Syn in triple-pathology mice (mutant human SNCAA53T transgene in 3xTg-AD mice) amplifies each lesion and accelerates cognitive decline, supporting a feed-forward crosstalk in mixed AD–DLB phenotypes [127]. This evidence concerns the gene MAPT and Alzheimer disease.