In order to understand the changes in Aβ and phosphorylated tau aggregation with and without pre-existing Alzheimer’s disease-like pathology, we treated hiPSC-derived PSEN1IN4 mutant cortical neurons and their isogenic controls (ICs) with TNF-ɑ for 18 days. The gene discussed is TNF; the disease is early-onset autosomal dominant Alzheimer disease.