[18F]AV‐1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation. Issue 12 (18th October 2016)

• Record Type: Journal Article
• Authors: Bevan Jones, W. Richard; Cope, Thomas E.; Passamonti, Luca; Fryer, Tim D.; Hong, Young T.; Aigbirhio, Franklin; Kril, Jillian J.; Forrest, Shelley L.; Allinson, Kieren; Coles, Jonathan P.; Simon Jones, P.; Spillantini, Maria G.; Hodges, John R.; O'Brien, John T.; Rowe, James B.
• Is Part Of: Annals of clinical and translational neurology. Volume 3:Issue 12(2016)
• Page Start: 940
• Page End: 947
• Publication Date: 2016-10-18
• Subjects: Nervous system -- Diseases -- Periodicals; Neurology -- Periodicals; 616.8005
• DOI: 10.1002/acn3.366
• Languages: English
• ISSNs: 2328-9503

Abstract

Abstract: The validation of tau radioligands could improve the diagnosis of frontotemporal lobar degeneration and the assessment of disease‐modifying therapies. Here, we demonstrate that binding of the tau radioligand [ 18 F]AV‐1451 was significantly abnormal in both magnitude and distribution in a patient with familial frontotemporal dementia due to a MAPT 10 + 16C>T gene mutation, recapitulating the pattern of neuropathology seen in her father. Given the genetic diagnosis and the non‐Alzheimer's pathology, these findings suggest that [ 18 F]AV‐1451 might be a useful biomarker in primary tauopathies. Largerscale in vivo and post‐mortem studies will be needed to assess the technique's specificity.