The 22q11 mouse model available at Sylics shows robust Schizophrenia-relevant deficits

Sylics characterized an accepted model in the field of schizophrenia research based on a microdeletion in the orthologous human 22q11.2 locus. In humans, a microdeletion of the 22q11.2 locus leads to a 20-fold increased risk for schizophrenia. Mouse models of this 22q11.2 deletion syndrome are perceived as highly translational relevant due to the genetic and phenotypic similarities between the mouse model and patients. At Sylics, using our own tests and protocols, we have validated the presence of relevant behavioral changes that were reported by the creators of this model (link). For instance, we found deficits in sensorimotor gating measured as the percentage of prepulse inhibition (PPI) of a startle response in this model (see Figure above). Furthermore, we detected significant deficits in working memory performance in terms of re-entry errors in the 8-arm radial maze. These and other phenotypes make this mouse line a good model for schizophrenia related drug screening studies. If you would like to receive more information about the model or discuss a study design using this model please reach out to reach out to us.