Dysfunction in IR and its downstream PI3K/AKT/GSK3 signalling pathway seems to be a key pathology shared by the models (Table 1), occurring either as a primary toxic event, and, thus, expressed to a larger extent with consequently severe cognitive deficits in non-transgenic AD models, or as a collateral damage, expressed to a lesser extent and leading to less dominant cognitive impairment in non-transgenic PD models (Fig. 1). The gene discussed is AKT1; the disease is Parkinson disease.