Using these methods, we have been able to study the effects of a chronic inflammatory challenge on human cortical neurons with familial Alzheimer’s disease-related mutations and ICs, on both intracellular Aβ and tau aggregation, and the clearance of these aggregates into the media, providing novel insights into how neurons maintain protein homeostasis and how this is disrupted by inflammation. This evidence concerns the gene MAPT and familial Alzheimer disease.