Tau aggregation and cell-to-cell propagation are central features of Alzheimer’s disease (AD) pathology. Experimental modelling of tau seeding has traditionally relied on post-mortem human- and mouse-derived brain material, limiting scalability and reproducibility. There remains a need for non-recombinant human-relevant pathogenic tau seeds that do not have a finite supply. We address this gap by establishing a non-finite source of seed-competent tau and apply the assay to investigate the effects of overexpressing AD genetic risk factors on tau aggregation.