transcription factors of the differentially expressed genes found between AD-NPCs and N-NPCs during differentiation. Hence, disturbed Wnt signaling might be also associated with the premature neuronal differentiation in AD-NPCs. Although iPSCs-based research in the present study provides a new perspective on AD pathogensis and treatment, we should be aware the complexity of genetic factors involved in the neurodegeneration of AD and the limitation of FAD-iPSCs modeling the sporadic AD. Further investigations of sporadic AD and other genetic defects caused FAD will help unfold the mystery of AD initiation and facilitate the development of more effective AD therapies.
