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[ 18 F]AV‐1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation
Author(s) -
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.
Publication year - 2016
Publication title -
annals of clinical and translational neurology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.824
H-Index - 42
ISSN - 2328-9503
DOI - 10.1002/acn3.366
Subject(s) - frontotemporal dementia , neuropathology , frontotemporal lobar degeneration , medicine , biomarker , dementia , tau protein , mutation , pick's disease , radioligand , tau pathology , tauopathy , pathology , alzheimer's disease , disease , neuroscience , genetics , gene , neurodegeneration , psychology , biology , receptor
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.

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