Future studies could build on these results by testing in more severe models, such as the Cln3Δex7/8, Δex7/8:hAPP model, which exacerbated the CLN3 phenotype by introducing one copy of a human amyloid precursor protein (hAPP) with familial Alzheimer’s disease (FAD) causing mutations, resulting in increased lysosomal burden and a severely reduced lifespan (Centa et al., 2020). This evidence concerns the gene CLN3 and familial Alzheimer disease.