Our findings may have potential implications for AD clinical trials (e.g., anti-Aβ or anti-tau treatments): For Aβ+ individuals without abnormal temporal meta-ROI tau, reducing cortical Aβ plaques might be a promising therapeutic strategy to decelerate the further spreading of tau aggregates, and prevent subsequent tau-associated neurodegeneration and cognitive decline. This evidence concerns the gene MAPT and Alzheimer disease.