Open Access[ 18 F]AV‐1451 binding is increased in frontotemporal dementia due to C9orf72 expansion
Author(s) -
BevanJones Richard W.,
Cope Thomas E.,
Jones Simon P.,
Passamonti Luca,
Hong Young T.,
Fryer Tim,
Arnold Robert,
Coles Jonathan P.,
Aigbirhio Franklin A.,
Patterson Karalyn,
O'Brien John T.,
Rowe James B.
Publication year - 2018
Publication title -
annals of clinical and translational neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.824
H-Index - 42
ISSN - 2328-9503
DOI - 10.1002/acn3.631
Subject(s) - c9orf72 , frontotemporal dementia , medicine , dementia , frontotemporal lobar degeneration , tau pathology , semantic dementia , trinucleotide repeat expansion , neuroscience , pathology , alzheimer's disease , disease , genetics , psychology , biology , gene , allele
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.