Thus genes such as RUNX1 (which may contribute to childhood leukaemia in people with DS), APP (a key Alzheimer disease gene) and SYNJ1, RCAN1 and ITSN1, which have been linked to endosomal/synaptic abnormalities [23], [24], [25] are unlikely to contribute to the phenotype of this mouse model of DS. This evidence concerns the gene ITSN1 and early-onset autosomal dominant Alzheimer disease.