{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,6]],"date-time":"2026-10-06T20:55:57Z","timestamp":1791320157885,"version":"4.3.1"},"reference-count":72,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2018,11,21]],"date-time":"2018-11-21T00:00:00Z","timestamp":1542758400000},"content-version":"vor","delay-in-days":20,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100000024","name":"Canadian Institutes of Health Research","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100000024","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2018,11]]},"abstract":"<jats:sec><jats:title>Objective<\/jats:title><jats:p>To estimate the prevalence of amyloid positivity, defined by positron emission tomography (PET)\/cerebrospinal fluid (CSF) biomarkers and\/or neuropathological examination, in primary progressive aphasia (PPA) variants.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>We conducted a meta\u2010analysis with individual participant data from 1,251 patients diagnosed with PPA (including logopenic [lvPPA, n\u2009=\u2009443], nonfluent [nfvPPA, n\u2009=\u2009333], semantic [svPPA, n\u2009=\u2009401], and mixed\/unclassifiable [n\u2009=\u200974] variants of PPA) from 36 centers, with a measure of amyloid\u2010\u03b2 pathology (CSF [n\u2009=\u2009600], PET [n\u2009=\u2009366], and\/or autopsy [n\u2009=\u2009378]) available. The estimated prevalence of amyloid positivity according to PPA variant, age, and apolipoprotein E (ApoE) \u03b54 status was determined using generalized estimating equation models.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Amyloid\u2010\u03b2 positivity was more prevalent in lvPPA (86%) than in nfvPPA (20%) or svPPA (16%; <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001). Prevalence of amyloid\u2010\u03b2 positivity increased with age in nfvPPA (from 10% at age 50 years to 27% at age 80 years, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01) and svPPA (from 6% at age 50 years to 32% at age 80 years, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001), but not in lvPPA (<jats:italic>p<\/jats:italic>\u2009=\u20090.94). Across PPA variants, ApoE \u03b54 carriers were more often amyloid\u2010\u03b2 positive (58.0%) than noncarriers (35.0%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.001). Autopsy data revealed Alzheimer disease pathology as the most common pathologic diagnosis in lvPPA (76%), frontotemporal lobar degeneration\u2013TDP\u201043 in svPPA (80%), and frontotemporal lobar degeneration\u2013TDP\u201043\/tau in nfvPPA (64%).<\/jats:p><\/jats:sec><jats:sec><jats:title>Interpretation<\/jats:title><jats:p>This study shows that the current PPA classification system helps to predict underlying pathology across different cohorts and clinical settings, and suggests that age and ApoE genotype should be considered when interpreting amyloid\u2010\u03b2 biomarkers in PPA patients. Ann Neurol 2018;84:737\u2013748<\/jats:p><\/jats:sec>","DOI":"10.1002\/ana.25333","type":"journal-article","created":{"date-parts":[[2018,9,26]],"date-time":"2018-09-26T10:34:01Z","timestamp":1537958041000},"page":"729-740","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":199,"title":["Prevalence of amyloid\u2010\u03b2 pathology in distinct variants of primary progressive aphasia"],"prefix":"10.1002","volume":"84","author":[{"given":"David","family":"Bergeron","sequence":"first","affiliation":[{"name":"Interdisciplinary Clinic of Memory of the Child Jesus Laval University  Quebec City Quebec Canada"},{"name":"Alzheimer center Amsterdam Amsterdam UMC, Amsterdam Neuroscience, VU University  Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maria L.","family":"Gorno\u2010Tempini","sequence":"additional","affiliation":[{"name":"Memory and Aging Center, Department of Neurology University of California  San Francisco, San Francisco CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gil D.","family":"Rabinovici","sequence":"additional","affiliation":[{"name":"Memory and Aging Center, Department of Neurology University of California  San Francisco, San Francisco CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Miguel A.","family":"Santos\u2010Santos","sequence":"additional","affiliation":[{"name":"Memory and Aging Center, Department of Neurology University of California  San Francisco, San Francisco CA"},{"name":"Cognition and Brain Plasticity Group, Bellvitge Biomedical Research Institute, Llobregat Hospital  Barcelona Spain"},{"name":"Llobregat Hospital, ACE Foundation, Catalan Institute of Applied Neurosciences, UIC Barcelona  Barcelona Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"William","family":"Seeley","sequence":"additional","affiliation":[{"name":"Memory and Aging Center, Department of Neurology University of California  San Francisco, San Francisco CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Bruce L.","family":"Miller","sequence":"additional","affiliation":[{"name":"Memory and Aging Center, Department of Neurology University of California  San Francisco, San Francisco CA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yolande","family":"Pijnenburg","sequence":"additional","affiliation":[{"name":"Alzheimer center Amsterdam Amsterdam UMC, Amsterdam Neuroscience, VU University  Amsterdam the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"M. 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