To investigate the relationship between inflammation and protein aggregation in Alzheimer’s disease, we exposed iPSC-derived Alzheimer’s disease neurons, which produce higher proportions of aggregation-prone Aβ peptides, to the proinflammatory cytokine tumour necrosis factor (TNF), a key mediator common to both central and systemic inflammatory pathways, and measured changes in the production and composition of extracellular aggregates of disease-associated proteins. Here, TNF is linked to Alzheimer disease.