The pattern of changes in [18F]THK5317 retention was heterogeneous across all patients, with qualitative differences both between the two AD groups (prodromal and dementia) and among individual patients, highlighting that heterogeneous Tau tracer uptake among patients with symptomatic AD, in contrast to the homogeneous changes seen in glucose metabolism, better tracked clinical progression [117]. The gene discussed is MAPT; the disease is dementia.