MAPT and Alzheimer disease: Glutamatergic & cholinergic neurons and astrocytes. iPSC-neurons show AD phenotypic traits consistent with the Aβ tau hypotheses after limited time in culture (e.g., elevated Aβ production, increased levels of p-tau) and responsiveness to β and γ secretase inhibitors.Genome-editing technologies (e.g., ZFN, TALENs, and CRISPR/Cas9) can be used to add, disrupt or modify the sequence of specific genes related to AD, measure their impact on human iPSC-derived neurons and, ideally, design patient tailored treatments.To identify disease pathways & drug targets, & assess therapeutic compounds.