Characterization of tau positron emission tomography tracer [18F]AV-1451 binding to postmortem tissue in Alzheimer's disease, primary tauopathies, and other dementias

被引:145
作者
Sander, Kerstin [1 ,2 ]
Lashley, Tammaryn [3 ]
Gami, Priya [3 ]
Gendron, Thibault [1 ]
Lythgoe, Mark F. [4 ]
Rohrer, Jonathan D. [5 ]
Schott, Jonathan M. [5 ]
Revesz, Tamas [3 ]
Fox, Nick C. [5 ]
Arstad, Erik [1 ,2 ]
机构
[1] UCL, Inst Nucl Med, London, England
[2] UCL, Dept Chem, London, England
[3] UCL, Inst Neurol, Dept Mol Neurosci, Queen Sq Brain Bank, London, England
[4] UCL, Ctr Adv Biomed Imaging, Div Med, London, England
[5] UCL, Dementia Res Ctr, Inst Neurol, Dept Neurodegenerat Dis, London, England
关键词
Dementia; Tau; Neurodegeneration; PET; F-18]AV-1451; Phosphorimaging; Immunohistochemistry; NEUROPATHOLOGIC ASSESSMENT; PATHOLOGY; PHOSPHORYLATION; DEGENERATION; CONSORTIUM; SEVERITY; BODIES;
D O I
10.1016/j.jalz.2016.01.003
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Introduction: Aggregation of tau is a hallmark of many neurodegenerative diseases, and tau imaging with positron emission tomography (PET) may allow early diagnosis and treatment monitoring. We assessed binding of the PET tracer [F-18]AV-1451 in a range of dementias. Methods: Phosphorimaging was used to quantify binding to postmortem brain tissue from 33 patients with different, histopathologically characterized, neurodegenerative dementias. Results: [F-18]AV-1451 showed high specific binding in cases with Alzheimer's disease (AD), moderate binding in Pick's disease and frontotemporal dementia with parkinsonism-17, and low but displaceable binding in corticobasal degeneration, progressive supranuclear palsy, non-tau proteino-pathies, and in controls without pathology. Tracer binding did not correlate with tau load within disease groups. Discussion: [F-18]AV-1451 binds to tau in AD, and some other tauopathies. However, evidence for a non tau binding site and lack of correlation between tracer binding and antibody staining suggest that reliable quantification of tau load with this tracer is problematic. (C) 2016 The Alzheimer's Association. Published by Elsevier Inc. All rights reserved.
引用
收藏
页码:1116 / 1124
页数:9
相关论文
共 29 条
[1]   "End-Stage" Neurofibrillary Tangle Pathology in Preclinical Alzheimer's Disease: Fact or Fiction? [J].
Abner, Erin L. ;
Kryscio, Richard J. ;
Schmitt, Frederick A. ;
SantaCruz, Karen S. ;
Jicha, Gregory A. ;
Lin, Yushun ;
Neltner, Janna M. ;
Smith, Charles D. ;
Van Eldik, Linda J. ;
Nelson, Peter T. .
JOURNAL OF ALZHEIMERS DISEASE, 2011, 25 (03) :445-453
[2]   NEUROFIBRILLARY TANGLES BUT NOT SENILE PLAQUES PARALLEL DURATION AND SEVERITY OF ALZHEIMERS-DISEASE [J].
ARRIAGADA, PV ;
GROWDON, JH ;
HEDLEYWHYTE, ET ;
HYMAN, BT .
NEUROLOGY, 1992, 42 (03) :631-639
[3]   Specific tau phosphorylation sites correlate with severity of neuronal cytopathology in Alzheimer's disease [J].
Augustinack, JC ;
Schneider, A ;
Mandelkow, EM ;
Hyman, BT .
ACTA NEUROPATHOLOGICA, 2002, 103 (01) :26-35
[4]   NEUROPATHOLOGICAL STAGING OF ALZHEIMER-RELATED CHANGES [J].
BRAAK, H ;
BRAAK, E .
ACTA NEUROPATHOLOGICA, 1991, 82 (04) :239-259
[5]   Neuropathologic diagnostic and nosologic criteria for frontotemporal lobar degeneration: consensus of the Consortium for Frontotemporal Lobar Degeneration [J].
Cairns, Nigel J. ;
Bigio, Eileen H. ;
Mackenzie, Ian R. A. ;
Neumann, Manuela ;
Lee, Virginia M. -Y. ;
Hatanpaa, Kimmo J. ;
White, Charles L., III ;
Schneider, Julie A. ;
Grinberg, Lea Tenenholz ;
Halliday, Glenda ;
Duyckaerts, Charles ;
Lowe, James S. ;
Holm, Ida E. ;
Tolnay, Markus ;
Okamoto, Koichi ;
Yokoo, Hideaki ;
Murayama, Shigeo ;
Woulfe, John ;
Munoz, David G. ;
Dickson, Dennis W. ;
Ince, Paul G. ;
Trojanowski, John Q. ;
Mann, David M. A. .
ACTA NEUROPATHOLOGICA, 2007, 114 (01) :5-22
[6]   Early Clinical PET Imaging Results with the Novel PHF-Tau Radioligand [F18]-T808 [J].
Chien, David T. ;
Szardenings, A. Katrin ;
Bahri, Shadfar ;
Walsh, Joseph C. ;
Mu, Fanrong ;
Xia, Chunfang ;
Shankle, William R. ;
Lerner, Alan J. ;
Su, Min-Ying ;
Elizarova, Arkadij ;
Kolb, Hartmuth C. .
JOURNAL OF ALZHEIMERS DISEASE, 2014, 38 (01) :171-184
[7]   Brain homogenates from human tauopathies induce tau inclusions in mouse brain [J].
Clavaguera, Florence ;
Akatsu, Hiroyasu ;
Fraser, Graham ;
Crowther, R. Anthony ;
Frank, Stephan ;
Hench, Juergen ;
Probst, Alphonse ;
Winkler, David T. ;
Reichwald, Julia ;
Staufenbiel, Matthias ;
Ghetti, Bernardino ;
Goedert, Michel ;
Tolnay, Markus .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2013, 110 (23) :9535-9540
[8]   Pathological inclusion bodies in tauopathies contain distinct complements of tau with three or four microtubule-binding repeat domains as demonstrated by new specific monoclonal antibodies [J].
de Silva, R ;
Lashley, T ;
Gibb, G ;
Hanger, D ;
Hope, A ;
Reid, A ;
Bandopadhyay, R ;
Utton, M ;
Strand, C ;
Jowett, T ;
Khan, N ;
Anderton, B ;
Wood, N ;
Holton, J ;
Revesz, T ;
Lees, A .
NEUROPATHOLOGY AND APPLIED NEUROBIOLOGY, 2003, 29 (03) :288-302
[9]  
Dickson D., 2011, Neurodegeneration ed, P135, DOI [10.1002/9781444341256.ch15, DOI 10.1002/9781444341256]
[10]   Cerebellar Involvement in Progressive Supranuclear Palsy: A Clinicopathological Study [J].
Kanazawa, Masato ;
Shimohata, Takayoshi ;
Toyoshima, Yasuko ;
Tada, Mari ;
Kakita, Akiyoshi ;
Morita, Takashi ;
Ozawa, Tetsutaro ;
Takahashi, Hitoshi ;
Nishizawa, Masatoyo .
MOVEMENT DISORDERS, 2009, 24 (09) :1312-1318