Supporting these findings, transgenic mice overexpressing Dyrk1A (TG) exhibit defects in neurogenesis, reduced dendritic length and branching, and impaired long-term potentiation (LTP) and long-term depression (LTD), and normalization of its expression levels corrects the cognitive impairments seen in trisomic DS mouse models and in DS individuals (De la Torre et al., 2014). The gene discussed is DYRK1A; the disease is Dravet syndrome.