In aggregate, it has become obvious that by more accurately modeling human neurodevelopmental and neurodegenerative diseases in vitro, a number of insights into the cellular and molecular mechanisms underlying the disease state have already arisen. hiPSC-based platforms, combined with genome-scale analyses of sequence variations and transcripts, are increasingly facilitating studies of the temporal dynamics of human disease and allowing researchers to study human-specific elements of disease, asking when critical changes occur in the disease process. From insights into the mechanisms of tau changes in AD, to increased FOXG1 expression in two hiPSC cohorts of ASD, to the critical role of ASPN in microencephaly, cellular models are revealing convergent mechanisms underlying genetically heterogeneous neurological conditions.
