[18F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation

W. Richard Bevan Jones; Thomas E. Cope; Luca Passamonti; Tim D. Fryer; Young T. Hong; Franklin Aigbirhio; Jillian J. Kril; Shelley L. Forrest; Kieren Allinson; Jonathan P. Coles; P. Simon Jones; Maria G. Spillantini; John R. Hodges; John T. O'Brien; James B. Rowe

doi:10.1002/acn3.366

[¹⁸F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation

W. Richard Bevan Jones, Thomas E. Cope, Luca Passamonti, Tim D. Fryer, Young T. Hong, Franklin Aigbirhio, Jillian J. Kril, Shelley L. Forrest, Kieren Allinson, Jonathan P. Coles, P. Simon Jones, Maria G. Spillantini, John R. Hodges, John T. O'Brien, James B. Rowe

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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 [¹⁸F]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 [¹⁸F]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.

Original language	English
Pages (from-to)	940-947
Number of pages	8
Journal	Annals of Clinical and Translational Neurology
Volume	3
Issue number	12
DOIs	https://doi.org/10.1002/acn3.366
Publication status	Published - Dec 2016
Externally published	Yes

Bibliographical note

Copyright the Author(s) 2016. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

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Bevan Jones, W. R., Cope, T. E., Passamonti, L., Fryer, T. D., Hong, Y. T., Aigbirhio, F., Kril, J. J., Forrest, S. L., Allinson, K., Coles, J. P., Jones, P. S., Spillantini, M. G., Hodges, J. R., O'Brien, J. T., & Rowe, J. B. (2016). [¹⁸F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation. Annals of Clinical and Translational Neurology, 3(12), 940-947. https://doi.org/10.1002/acn3.366

@article{055d23d0520041cc93c5ede84b3805c2,

title = "[18F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation",

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 [18F]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 [18F]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.",

author = "\{Bevan Jones\}, \{W. Richard\} and Cope, \{Thomas E.\} and Luca Passamonti and Fryer, \{Tim D.\} and Hong, \{Young T.\} and Franklin Aigbirhio and Kril, \{Jillian J.\} and Forrest, \{Shelley L.\} and Kieren Allinson and Coles, \{Jonathan P.\} and Jones, \{P. Simon\} and Spillantini, \{Maria G.\} and Hodges, \{John R.\} and O'Brien, \{John T.\} and Rowe, \{James B.\}",

note = "Copyright the Author(s) 2016. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.",

year = "2016",

month = dec,

doi = "10.1002/acn3.366",

language = "English",

volume = "3",

pages = "940--947",

journal = "Annals of Clinical and Translational Neurology",

issn = "2328-9503",

publisher = "John Wiley \& Sons",

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}

Bevan Jones, WR, Cope, TE, Passamonti, L, Fryer, TD, Hong, YT, Aigbirhio, F, Kril, JJ, Forrest, SL, Allinson, K, Coles, JP, Jones, PS, Spillantini, MG, Hodges, JR, O'Brien, JT & Rowe, JB 2016, '[¹⁸F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation', Annals of Clinical and Translational Neurology, vol. 3, no. 12, pp. 940-947. https://doi.org/10.1002/acn3.366

TY - JOUR

T1 - [18F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation

AU - Bevan Jones, W. Richard

AU - Cope, Thomas E.

AU - Passamonti, Luca

AU - Fryer, Tim D.

AU - Hong, Young T.

AU - Aigbirhio, Franklin

AU - Kril, Jillian J.

AU - Forrest, Shelley L.

AU - Allinson, Kieren

AU - Coles, Jonathan P.

AU - Jones, P. Simon

AU - Spillantini, Maria G.

AU - Hodges, John R.

AU - O'Brien, John T.

AU - Rowe, James B.

N1 - Copyright the Author(s) 2016. Version archived for private and non-commercial use with the permission of the author/s and according to publisher conditions. For further rights please contact the publisher.

PY - 2016/12

Y1 - 2016/12

N2 - 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 [18F]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 [18F]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.

AB - 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 [18F]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 [18F]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.

UR - https://www.scopus.com/pages/publications/85013406275

UR - http://purl.org/au-research/grants/nhmrc/1037746

U2 - 10.1002/acn3.366

DO - 10.1002/acn3.366

M3 - Article

C2 - 28097206

SN - 2328-9503

VL - 3

SP - 940

EP - 947

JO - Annals of Clinical and Translational Neurology

JF - Annals of Clinical and Translational Neurology

IS - 12

ER -

[¹⁸F]AV-1451 PET in behavioral variant frontotemporal dementia due to MAPT mutation

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