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

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...

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Detalles Bibliográficos
Autores principales: 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.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2018
Materias:
Brief Communication
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6186940/
https://www.ncbi.nlm.nih.gov/pubmed/30349864
http://dx.doi.org/10.1002/acn3.631
Descripción
Sumario: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.

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