However, heparin and similar cofactors may not accurately mimic the physiological processes driving tau aggregation in the brain, as comparative studies have found differences in the conformations, properties, and activities of recombinant tau aggregates compared to AD‐derived aggregates.[5, 85] To address this limitation, more physiologically relevant cofactors, such as RNA[86] and arachidonic acid,[87, 88] have been explored as triggers for tau aggregation in vitro. Here, MAPT is linked to Alzheimer disease.