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

Autor: Bevan-Jones RW; Department of Psychiatry University of Cambridge Cambridge United Kingdom., Cope TE; Department of Clinical Neurosciences University of Cambridge Cambridge United Kingdom., Jones SP; Department of Clinical Neurosciences University of Cambridge Cambridge United Kingdom., Passamonti L; Department of Clinical Neurosciences University of Cambridge Cambridge United Kingdom., Hong YT; Wolfson Brain Imaging Centre University of Cambridge Cambridge United Kingdom., Fryer T; Wolfson Brain Imaging Centre University of Cambridge Cambridge United Kingdom., Arnold R; Department of Psychiatry University of Cambridge Cambridge United Kingdom., Coles JP; Division of Anaesthesia University of Cambridge Cambridge United Kingdom., Aigbirhio FA; Wolfson Brain Imaging Centre University of Cambridge Cambridge United Kingdom., Patterson K; Department of Clinical Neurosciences University of Cambridge Cambridge United Kingdom.; Medical Research Council Cognition and Brain Sciences Unit Cambridge United Kingdom., O'Brien JT; Department of Psychiatry University of Cambridge Cambridge United Kingdom., Rowe JB; Department of Clinical Neurosciences University of Cambridge Cambridge United Kingdom.; Medical Research Council Cognition and Brain Sciences Unit Cambridge United Kingdom.
Jazyk: angličtina
Zdroj: Annals of clinical and translational neurology [Ann Clin Transl Neurol] 2018 Sep 14; Vol. 5 (10), pp. 1292-1296. Date of Electronic Publication: 2018 Sep 14 (Print Publication: 2018).
DOI: 10.1002/acn3.631
Abstrakt: 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.
Databáze: MEDLINE
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