Recently, an interesting novel transgenic mouse associated with DLB and PDD (CaMKIIα‐tTA/A53T α‐syn dTg mice) has been generated using the Tet‐off system and the CaMKIIα promoter.31, 32 CaMKIIα‐tTA/A53T α‐syn dTg mice express A53T human α‐synuclein in the neurons of the forebrain, the region involved in cognitive function, and exhibit cognitive deficits accompanied by α‐synuclein pathology.31, 32 To determine whether the CaMKIIα‐tTA/A53T α‐syn dTg mice are a valid animal model of DLB and PDD, we further characterized their behavioral, molecular, and pharmacological phenotypes. This evidence concerns the gene CAMK2A and Cognitive impairment.