Similarly in a mouse model of DLB-AD, that simultaneously expresses PS1(M146 V), APP(Swe), tau(P301L) and aSyn(A53T), a substantial increase in deposition of Aβ, tau and aSyn was observed, accompanied by accelerated cognitive decline, suggestive of a synergistic effect of these proteins in driving both pathology and phenotype [80]. This evidence concerns the gene APP and Alzheimer disease.