This was achieved by transgenic expression of mutant genes responsible for early-onset familiar AD [e.g., mutated Aβ precursor protein (APP) and/or presenilin (PSEN)-1 or -2] or frontotemporal dementia (mutated microtubule-associated protein tau), respectively (Ameen-Ali et al., 2017). This evidence concerns the gene PSEN1 and Alzheimer disease.