Despite the challenges inherent to imaging tau pathology, which include its intracellular location; the presence of multiple human tau isoforms (three repeat [3R], four repeat [4R]) and morphologies (paired helical filament [PHF], straight filament [SF]); numerous post‐translational modifications (e.g., phosphorylation, truncation, nitration); and, in the case of Alzheimer's disease (AD), lower concentrations than amyloid beta (Αβ) in colocalizing tau and Aβ deposits (for review see Villemagne et al.2 This evidence concerns the gene MAPT and Alzheimer disease.