The utility of such a model is many-fold: (1) less expensive than modeling in aldh5a1-/- mice, whose lifespan is truncated; (2) the capacity for high-throughput analysis; (3) bypass of peripheral metabolic processes with focus on neuropharmacology; (4) potential to “prioritize” therapeutics applicable to SSADHD to move forward to preclinical animal studies; and (5) in vitro modeling of the developing brain, with ability to study the impact of candidate drugs on neurogenesis. This evidence concerns the gene ALDH5A1 and succinic semialdehyde dehydrogenase deficiency.