{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,9]],"date-time":"2026-10-09T19:21:54Z","timestamp":1791573714081,"version":"4.3.4"},"reference-count":57,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2023,3,31]],"date-time":"2023-03-31T00:00:00Z","timestamp":1680220800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000957","name":"Alzheimer's Association","doi-asserted-by":"publisher","award":["AARF\u2010D\u2010619473"],"award-info":[{"award-number":["AARF\u2010D\u2010619473"]}],"id":[{"id":"10.13039\/100000957","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000957","name":"Alzheimer's Association","doi-asserted-by":"publisher","award":["AARF\u2010D\u2010619473\u2010RAPID"],"award-info":[{"award-number":["AARF\u2010D\u2010619473\u2010RAPID"]}],"id":[{"id":"10.13039\/100000957","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000065","name":"National Institute of Neurological Disorders and Stroke","doi-asserted-by":"publisher","award":["K23\u2010NS114167"],"award-info":[{"award-number":["K23\u2010NS114167"]}],"id":[{"id":"10.13039\/100000065","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["P01\u2010AG066597"],"award-info":[{"award-number":["P01\u2010AG066597"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["P30\u2010AG072979"],"award-info":[{"award-number":["P30\u2010AG072979"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["R01\u2010AG054519"],"award-info":[{"award-number":["R01\u2010AG054519"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000049","name":"National Institute on Aging","doi-asserted-by":"publisher","award":["U19\u2010AG062418"],"award-info":[{"award-number":["U19\u2010AG062418"]}],"id":[{"id":"10.13039\/100000049","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Ann Clin Transl Neurol"],"published-print":{"date-parts":[[2023,5]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>\n                      Within Lewy body spectrum disorders (LBSD) with \u03b1\u2010synuclein pathology (\u03b1Syn), concomitant Alzheimer's disease (AD) pathology is common and is predictive of clinical outcomes, including cognitive impairment and decline. Plasma phosphorylated tau 181 (p\u2010tau\n                      <jats:sub>181<\/jats:sub>\n                      ) is sensitive to AD neuropathologic change (ADNC) in clinical AD, and plasma glial fibrillary acidic protein (GFAP) is associated with the presence of \u03b2\u2010amyloid plaques. While these plasma biomarkers are well tested in clinical and pathological AD, their diagnostic and prognostic performance for concomitant AD in LBSD is unknown.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      In autopsy\u2010confirmed \u03b1Syn\u2010positive LBSD, we tested how plasma p\u2010tau\n                      <jats:sub>181<\/jats:sub>\n                      and GFAP differed across \u03b1Syn with concomitant ADNC (\u03b1Syn+AD;\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200919) and \u03b1Syn without AD (\u03b1Syn;\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200930). Severity of burden was scored on a semiquantitative scale for several pathologies (e.g., \u03b2\u2010amyloid and tau), and scores were averaged across sampled brainstem, limbic, and neocortical regions.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Linear models showed that plasma GFAP was significantly higher in \u03b1Syn+AD compared to \u03b1Syn (\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u2009=\u20090.31, 95% CI\u2009=\u20090.065\u20130.56, and\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.015), after covarying for age at plasma, plasma\u2010to\u2010death interval, and sex; plasma p\u2010tau\n                      <jats:sub>181<\/jats:sub>\n                      was not (\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.37). Next, linear models tested associations of AD pathological features with both plasma analytes, covarying for plasma\u2010to\u2010death, age at plasma, and sex. GFAP was significantly associated with brain\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u2010amyloid (\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u2009=\u200915, 95% CI\u2009=\u20096.1\u201325, and\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.0018) and tau burden (\n                      <jats:italic>\u03b2<\/jats:italic>\n                      \u2009=\u200912, 95% CI\u2009=\u20092.5\u201322, and\n                      <jats:italic>P<\/jats:italic>\n                      \u2009=\u20090.015); plasma p\u2010tau\n                      <jats:sub>181<\/jats:sub>\n                      was not associated with either (both\n                      <jats:italic>P<\/jats:italic>\n                      \u2009&gt;\u20090.34).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>Findings indicate that plasma GFAP may be sensitive to concomitant AD pathology in LBSD, especially accumulation of \u03b2\u2010amyloid plaques.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/acn3.51768","type":"journal-article","created":{"date-parts":[[2023,3,31]],"date-time":"2023-03-31T14:11:50Z","timestamp":1680271910000},"page":"802-813","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":36,"title":["Plasma GFAP associates with secondary Alzheimer's pathology in Lewy body disease"],"prefix":"10.1002","volume":"10","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1879-2766","authenticated-orcid":false,"given":"Katheryn A. 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