The latter can be explained by Aβ-independent tau accumulation (for example, primary age-related tauopathy (PART)), off-target binding of tau PET tracers (for example, to monoamine oxidase B, neuromelanin, iron accumulation and/or microhemorrhages, which all become more pronounced with advancing age), increased false-negative Aβ status and/or false-positive tau PET scans, partial volume effects resulting from atrophy or an atypical neurobiological phenotype (for example, a tau-first subtype)34–39. This evidence concerns the gene MAOB and Atrophy.