[ 18 F]AV‐1451 binding is increased in frontotemporal dementia due to C9orf72 expansion
Annals of Clinical and Translational Neurology2018Vol. 5(10), pp. 1292–1296
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Richard W. Bevan‐Jones, Thomas Cope, Simon P Jones, Luca Passamonti, Young T. Hong, Tim D. Fryer, Robert Arnold, Jonathan Coles, Franklin A. Aigbirhio, Karalyn Patterson, John T. O’Brien, James B. Rowe
Abstract
The PET ligand [18F]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 [18F]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.
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