For interpretation of the results obtained with the APP/PS1 model used in this study, similarly to other AD pathology and symptomatic animal models (e.g., APP overexpression, APP knock-in, and tau aggregation, cholinergic), the nature of the pathology, as well as the stage of pathology progression, should be considered a crucial driver for obtaining functional/symptomatic effects and hence add to the complexity of adequate back-translation of clinical findings. The gene discussed is PSEN1; the disease is Alzheimer disease.