In particular, they seem to be an appropriate model for mimicking disease mechanisms, as a higher susceptibility to amyloid beta oligomers (Aβ1-42 oligomers), typical of AD pathology [14], was found in neuronal precursors derived from iPSC of patients with a mutation in the PSEN1 gene (PSEN1-A246E mutation) [15], and in iPSCs-derived neurons of sporadic AD patients and of a patient carrying the pathogenic APP-E693Δ mutation [16]. Here, APP is linked to Alzheimer disease.