PSEN1 and Alzheimer disease: Instead of utilizing familial AD mutations in APP or PS1 to drive Aβ pathology, we modeled chronic Aβ exposure by supplementing hiNS media with high concentrations (compared to endogenous Aβ levels in the CSF [63] of oligomeric Aβ ~ 0.24 μg/mL) for 3 to 5 weeks to induce progressive neurotoxicity (Fig. 3 and Fig. S6).