For stroke-related events, we observed a significant interaction effect with Aβ load on longitudinal tau accumulation in CU participants in the opposite direction, such that longitudinal increases in tau accumulation were attenuated in CU participants with both high Aβ load and stroke-related events compared to CU participants with high Aβ load and without stroke-related events (β = −0.08, P < 0.001) (Table 2). The gene discussed is MAPT; the disease is Stroke.