The consistency of findings, despite differences in methodologies (i.e., in vivo [18 F]-Flortaucipir PET versus post-mortem NFT burden) and neurodegenerative disease groups (i.e., DLBs versus AD), reinforced the robustness of our findings and collectively implicated tau-related white matter damage as a significant driver of disease course in people with DLBs. The gene discussed is MAPT; the disease is Alzheimer disease.