Overall, given the lack of evidence for evolving pathology in Trp73+/- + TgCRND8 mice [19,22], or discernible pathology (as here), and the failure of genetic analyses to confirm an influence of Trp73 in human cohorts, the concept of a significant role for P73 in AD pathogenesis is not supported. This evidence concerns the gene TP73 and Alzheimer disease.