{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1360021393784364160.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.15252/emmm.202217123"}},{"identifier":{"@type":"URI","@value":"https://onlinelibrary.wiley.com/doi/pdf/10.15252/emmm.202217123"}},{"identifier":{"@type":"URI","@value":"https://onlinelibrary.wiley.com/doi/full-xml/10.15252/emmm.202217123"}},{"identifier":{"@type":"URI","@value":"https://www.embopress.org/doi/pdf/10.15252/emmm.202217123"}}],"dc:title":[{"@value":"Specific associations between plasma biomarkers and postmortem amyloid plaque and tau tangle loads"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:title>Abstract</jats:title>\n                  <jats:p>\n                    Several promising plasma biomarkers for Alzheimer's disease have been recently developed, but their neuropathological correlates have not yet been fully determined. To investigate and compare independent associations between multiple plasma biomarkers (p‐tau181, p‐tau217, p‐tau231, Aβ42/40, GFAP, and NfL) and neuropathologic measures of amyloid and tau, we included 105 participants from the Arizona Study of Aging and Neurodegenerative Disorders (AZSAND) with antemortem plasma samples and a postmortem neuropathological exam, 48 of whom had longitudinal p‐tau217 and p‐tau181. When simultaneously including plaque and tangle loads, the Aβ42/40 ratio and p‐tau231 were only associated with plaques (ρ\n                    <jats:sub>Aβ42/40</jats:sub>\n                    [95%CI] = −0.53[−0.65, −0.35], ρ\n                    <jats:sub>p‐tau231</jats:sub>\n                    [95%CI] = 0.28[0.10, 0.43]), GFAP was only associated with tangles (ρ\n                    <jats:sub>GFAP</jats:sub>\n                    [95%CI] = 0.39[0.17, 0.57]), and p‐tau217 and p‐tau181 were associated with both plaques (ρ\n                    <jats:sub>p‐tau217</jats:sub>\n                    [95%CI] = 0.40[0.21, 0.56], ρ\n                    <jats:sub>p‐tau181</jats:sub>\n                    [95%CI] = 0.36[0.15, 0.50]) and tangles (ρ\n                    <jats:sub>p‐tau217</jats:sub>\n                    [95%CI] = 0.52[0.34, 0.66]; ρ\n                    <jats:sub>p‐tau181</jats:sub>\n                    [95%CI] = 0.36[0.17, 0.52]). A model combining p‐tau217 and the Aβ42/40 ratio showed the highest accuracy for predicting the presence of Alzheimer's disease neuropathological change (ADNC, AUC[95%CI] = 0.89[0.82, 0.96]) and plaque load (\n                    <jats:italic>R</jats:italic>\n                    <jats:sup>2</jats:sup>\n                     = 0.55), while p‐tau217 alone was optimal for predicting tangle load (\n                    <jats:italic>R</jats:italic>\n                    <jats:sup>2</jats:sup>\n                     = 0.45). Our results suggest that high‐performing assays of plasma p‐tau217 and Aβ42/40 might be an optimal combination to assess Alzheimer's‐related pathology\n                    <jats:italic>in vivo</jats:italic>\n                    .\n                  </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1380021393784364166","@type":"Researcher","foaf:name":[{"@value":"Gemma Salvadó"}],"jpcoar:affiliationName":[{"@value":"Clinical Memory Research Unit, Department of Clinical Sciences, Malmö Lund University  Lund Sweden"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364164","@type":"Researcher","foaf:name":[{"@value":"Rik Ossenkoppele"}],"jpcoar:affiliationName":[{"@value":"Clinical Memory Research Unit, Department of Clinical Sciences, Malmö Lund University  Lund Sweden"},{"@value":"Alzheimer Center Amsterdam, Neurology Vrije Universiteit Amsterdam, Amsterdam UMC location VUmc  Amsterdam The Netherlands"},{"@value":"Amsterdam Neuroscience, Neurodegeneration  Amsterdam The Netherlands"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364160","@type":"Researcher","foaf:name":[{"@value":"Nicholas J Ashton"}],"jpcoar:affiliationName":[{"@value":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy University of Gothenburg  Gothenburg Sweden"},{"@value":"Institute of Psychiatry, Psychology and Neuroscience, Maurice Wohl Institute Clinical Neuroscience Institute King's College London  London UK"},{"@value":"NIHR Biomedical Research Centre for Mental Health and Biomedical Research Unit for Dementia at South London and Maudsley, NHS Foundation  London UK"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364165","@type":"Researcher","foaf:name":[{"@value":"Thomas G Beach"}],"jpcoar:affiliationName":[{"@value":"Banner Sun Health Research Institute  Sun City AZ USA"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364162","@type":"Researcher","foaf:name":[{"@value":"Geidy E Serrano"}],"jpcoar:affiliationName":[{"@value":"Banner Sun Health Research Institute  Sun City AZ USA"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364169","@type":"Researcher","foaf:name":[{"@value":"Eric M Reiman"}],"jpcoar:affiliationName":[{"@value":"Banner Alzheimer's Institute Arizona State University and University of Arizona  Phoenix AZ USA"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364163","@type":"Researcher","foaf:name":[{"@value":"Henrik Zetterberg"}],"jpcoar:affiliationName":[{"@value":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy University of Gothenburg  Gothenburg Sweden"},{"@value":"Clinical Neurochemistry Laboratory Sahlgrenska University Hospital  Mölndal Sweden"},{"@value":"Department of Neurodegenerative Disease UCL Institute of Neurology, Queen Square  London UK"},{"@value":"UK Dementia Research Institute at UCL  London UK"},{"@value":"Hong Kong Center for Neurodegenerative Diseases  Hong Kong China"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364161","@type":"Researcher","foaf:name":[{"@value":"Niklas Mattsson‐Carlgren"}],"jpcoar:affiliationName":[{"@value":"Clinical Memory Research Unit, Department of Clinical Sciences, Malmö Lund University  Lund Sweden"},{"@value":"Department of Neurology Skåne University Hospital  Lund Sweden"},{"@value":"Wallenberg Center for Molecular Medicine Lund University  Lund Sweden"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364167","@type":"Researcher","foaf:name":[{"@value":"Shorena Janelidze"}],"jpcoar:affiliationName":[{"@value":"Clinical Memory Research Unit, Department of Clinical Sciences, Malmö Lund University  Lund Sweden"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364170","@type":"Researcher","foaf:name":[{"@value":"Kaj Blennow"}],"jpcoar:affiliationName":[{"@value":"Department of Psychiatry and Neurochemistry, Institute of Neuroscience and Physiology, The Sahlgrenska Academy University of Gothenburg  Gothenburg Sweden"},{"@value":"Clinical Neurochemistry Laboratory Sahlgrenska University Hospital  Mölndal Sweden"}]},{"@id":"https://cir.nii.ac.jp/crid/1380021393784364168","@type":"Researcher","foaf:name":[{"@value":"Oskar Hansson"}],"jpcoar:affiliationName":[{"@value":"Clinical Memory Research Unit, Department of Clinical Sciences, Malmö Lund University  Lund Sweden"},{"@value":"Memory Clinic, Skåne University Hospital  Malmö Sweden"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"17574676"},{"@type":"EISSN","@value":"17574684"}],"prism:publicationName":[{"@value":"EMBO Molecular Medicine"}],"dc:publisher":[{"@value":"Springer Science and Business Media LLC"}],"prism:publicationDate":"2023-03-13","prism:volume":"15","prism:number":"5","prism:startingPage":"e17123"},"reviewed":"false","dc:rights":["http://creativecommons.org/licenses/by/4.0/"],"url":[{"@id":"https://onlinelibrary.wiley.com/doi/pdf/10.15252/emmm.202217123"},{"@id":"https://onlinelibrary.wiley.com/doi/full-xml/10.15252/emmm.202217123"},{"@id":"https://www.embopress.org/doi/pdf/10.15252/emmm.202217123"}],"createdAt":"2023-03-13","modifiedAt":"2025-12-06","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360021389818795008","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Novel aspects of the phosphorylation and structure of pathological tau: implications for tauopathy biomarkers"}]},{"@id":"https://cir.nii.ac.jp/crid/1360025430639868160","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Combining plasma Aβ and 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