Bevan-Jones 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
Department of Psychiatry University of Cambridge Cambridge United Kingdom.
Department of Clinical Neurosciences University of Cambridge Cambridge United Kingdom.
Ann Clin Transl Neurol. 2018 Sep 14;5(10):1292-1296. doi: 10.1002/acn3.631. eCollection 2018 Oct.
The PET ligand [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 [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.
正电子发射断层扫描（PET）配体[F]AV-1451被开发用于结合阿尔茨海默病中的tau病理，但在遗传性tau蛋白病和语义性痴呆（一种与TDP-43病理密切相关的疾病）中均显示出结合增加。在此，我们评估了因C9orf72六核苷酸重复扩增所致的行为变异型额颞叶痴呆中的[F]AV-1451结合情况，该疾病以TDP-43病理为特征。我们发现，C9orf72突变增加了额颞叶皮质中的结合，与健康对照相比，其结合分布具有独特性。
