[ 18 F]AV‐1451 binding is increased in frontotemporal dementia due to C9orf72 expansion

Abstract The PET ligand [ 18 F] AV ‐1451 was developed to bind tau pathology in Alzheimer's disease, but increased binding has been shown in both genetic tauopathies and in semantic dementia, a disease strongly associated with TDP ‐43 pathology. Here we assessed [ 18 F] AV ‐1451 binding in behavioral variant frontotemporal dementia due to a hexanucleotide repeat expansion in C9orf72, characterized by TDP ‐43 pathology. We show that the C9orf72 mutation increases binding in frontotemporal cortex, with a distinctive distribution of binding compared with healthy controls.