We have used DS fetal brain samples in search for initial evidence and employed engineered mice with MMU16 partial trisomy (Ts65Dn) or direct excess of the splicing-associated nuclear kinase Dyrk1A, overdosed in DS for further analyses.
These alterations are comparable with those found in the partial trisomy chromosome 16 murine models of DS and suggest a causative role of DYRK1A in mental retardation and in motor anomalies of DS.