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We\u00a0assessed binding of the PET tracer [<jats:sup>18<\/jats:sup>F]AV\u20101451 in a range of dementias.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Phosphorimaging was used to quantify binding to postmortem brain tissue from 33 patients with different, histopathologically characterized, neurodegenerative dementias.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>[<jats:sup>18<\/jats:sup>F]AV\u20101451 showed high specific binding in cases with Alzheimer's disease (AD), moderate binding in Pick's disease and frontotemporal dementia with parkinsonism\u201017, and low but displaceable binding in corticobasal degeneration, progressive supranuclear palsy, non\u2013tau proteinopathies, and in controls without pathology. Tracer binding did not correlate with tau load within disease groups.<\/jats:p><\/jats:sec><jats:sec><jats:title>Discussion<\/jats:title><jats:p>[<jats:sup>18<\/jats:sup>F]AV\u20101451 binds to tau in AD, and some other tauopathies. However, evidence for a non\u2013tau binding site and lack of correlation between tracer binding and antibody staining suggest that reliable quantification of tau load with this tracer is problematic.<\/jats:p><\/jats:sec>","DOI":"10.1016\/j.jalz.2016.01.003","type":"journal-article","created":{"date-parts":[[2016,2,16]],"date-time":"2016-02-16T06:37:17Z","timestamp":1455604637000},"page":"1116-1124","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":188,"title":["Characterization of tau positron emission tomography tracer [<sup>18<\/sup>F]AV\u20101451 binding to postmortem tissue in Alzheimer's disease,\u00a0primary tauopathies, and other dementias"],"prefix":"10.1002","volume":"12","author":[{"given":"Kerstin","family":"Sander","sequence":"first","affiliation":[{"name":"Institute of Nuclear Medicine and Department of Chemistry University College London  London 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