Frontotemporal dementia is a devastating degenerative brain disease that causes altered personality, behavior, cognition and often motor impairment. Mutations in the MAPT gene that encodes tau can underlie familial forms of FTD (FTD-tau). Brain organoids from patient-derived induced pluripotent stem cell (iPSC) lines patterned towards the most affected brain region, the cerebral cortex, are valuable human models for understanding disease progression and testing candidate therapeutics. Cerebral cortical organoid modeling is limited by low efficiency, high variability across hPSC donors and lines, and high activation of stress pathways. We developed a novel organoid method and quality control (QC) metrics that enable efficient, scalable production of well-patterned cortical organoids. We validated the protocol by testing on 64 hPSC lines. Well-patterned cortical organoids exhibited markedly lower stress signatures and higher cortical quality scores, similar to those of the developing brain. Applying this protocol across multiple patient donor lines revealed phenotypes associated with the V337M, R406W and IVS10+16 MAPT mutations causing FTD-tau. Notably, approximately a third of primary tauopathy-risk genes identified by GWAS were differentially expressed in progenitor cell populations and newly differentiated neurons. These observations indicate a potential neurodevelopmental contribution to FTD-tau and underscore the value of these models to elucidate disease mechanisms and how the disease evolves over time.