{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,2]],"date-time":"2026-09-02T12:54:05Z","timestamp":1788353645530,"version":"build-2803163510"},"reference-count":39,"publisher":"Wiley","issue":"7","license":[{"start":{"date-parts":[[2024,2,16]],"date-time":"2024-02-16T00:00:00Z","timestamp":1708041600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100000002","name":"National Institutes of Health","doi-asserted-by":"publisher","award":["5R01NS104147\u201002"],"award-info":[{"award-number":["5R01NS104147\u201002"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100001826","name":"ZonMw","doi-asserted-by":"publisher","award":["733050822"],"award-info":[{"award-number":["733050822"]}],"id":[{"id":"10.13039\/501100001826","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal of Neurochemistry"],"published-print":{"date-parts":[[2024,7]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>\n                    Brain amyloid\u2010\u03b2 (A\u03b2) deposits are key pathological hallmarks of both cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD). Microvascular deposits in CAA mainly consist of the A\u03b2\n                    <jats:sub>40<\/jats:sub>\n                    peptide, whereas A\u03b2\n                    <jats:sub>42<\/jats:sub>\n                    is the predominant variant in parenchymal plaques in AD. The relevance in pathogenesis and diagnostic accuracy of various other A\u03b2 isoforms in CAA remain understudied. We aimed to investigate the biomarker potential of various A\u03b2 isoforms in cerebrospinal fluid (CSF) to differentiate CAA from AD pathology. We included 25 patients with probable CAA, 50 subjects with a CSF profile indicative of AD pathology (AD\u2010like), and 23 age\u2010 and sex\u2010matched controls. CSF levels of A\u03b2\n                    <jats:sub>1\u201034<\/jats:sub>\n                    , A\u03b2\n                    <jats:sub>1\u201037<\/jats:sub>\n                    , A\u03b2\n                    <jats:sub>1\u201038<\/jats:sub>\n                    , A\u03b2\n                    <jats:sub>1\u201039<\/jats:sub>\n                    , A\u03b2\n                    <jats:sub>1\u201040<\/jats:sub>\n                    , and A\u03b2\n                    <jats:sub>1\u201042<\/jats:sub>\n                    were quantified by liquid chromatography mass spectrometry. Lower CSF levels of all six A\u03b2 peptides were observed in CAA patients compared with controls (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.0005\u20130.03). Except for A\u03b2\n                    <jats:sub>1\u201042<\/jats:sub>\n                    (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20091.0), all peptides were decreased in CAA compared with AD\u2010like subjects (\n                    <jats:italic>p<\/jats:italic>\n                    \u2009=\u20090.007\u20130.03). Besides A\u03b2\n                    <jats:sub>1\u201042<\/jats:sub>\n                    , none of the A\u03b2 peptides were decreased in AD\u2010like subjects compared with controls. All A\u03b2 peptides combined differentiated CAA from AD\u2010like subjects better (area under the curve [AUC] 0.84) than individual peptide levels (AUC 0.51\u20130.75). Without A\u03b2\n                    <jats:sub>1\u201042<\/jats:sub>\n                    in the model (since decreased A\u03b2\n                    <jats:sub>1\u201042<\/jats:sub>\n                    served as AD\u2010like selection criterion), the AUC was 0.78 for distinguishing CAA from AD\u2010like subjects. CAA patients and AD\u2010like subjects showed distinct disease\u2010specific CSF A\u03b2 profiles. Peptides shorter than A\u03b2\n                    <jats:sub>1\u201042<\/jats:sub>\n                    were decreased in CAA patients, but not AD\u2010like subjects, which could suggest different pathological mechanisms between vascular and parenchymal A\u03b2 accumulation. This study supports the potential use of this panel of CSF A\u03b2 peptides to indicate presence of CAA pathology with high accuracy.\n                    <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                      <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc16074-fig-0004-m.png\">\n                        <jats:alt-text>image<\/jats:alt-text>\n                      <\/jats:graphic>\n                    <\/jats:boxed-text>\n                  <\/jats:p>","DOI":"10.1111\/jnc.16074","type":"journal-article","created":{"date-parts":[[2024,2,16]],"date-time":"2024-02-16T04:44:26Z","timestamp":1708058666000},"page":"1254-1264","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":13,"title":["Profiling amyloid\u2010\u03b2 peptides as biomarkers for cerebral amyloid angiopathy"],"prefix":"10.1111","volume":"168","author":[{"ORCID":"https:\/\/orcid.org\/0000-0001-9004-934X","authenticated-orcid":false,"given":"Emma","family":"van den Berg","sequence":"first","affiliation":[{"name":"Department of Neurology, Donders Institute for Brain, Cognition and Behaviour Radboud University Medical Center  Nijmegen The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0000-4964-8973","authenticated-orcid":false,"given":"Iris","family":"Kersten","sequence":"additional","affiliation":[{"name":"Department of Neurology, Donders Institute for Brain, Cognition and Behaviour Radboud University Medical Center  Nijmegen The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0001-6958-2393","authenticated-orcid":false,"given":"Gunnar","family":"Brinkmalm","sequence":"additional","affiliation":[{"name":"Institute of Neuroscience and Physiology The Sahlgrenska Academy at the University of Gothenburg  M\u00f6lndal Sweden"},{"name":"Clinical Neurochemistry Laboratory Sahlgrenska University Hospital  M\u00f6lndal Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0003-0451-4669","authenticated-orcid":false,"given":"Kjell","family":"Johansson","sequence":"additional","affiliation":[{"name":"Clinical Neurochemistry Laboratory Sahlgrenska University Hospital  M\u00f6lndal Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5679-516X","authenticated-orcid":false,"given":"Anna M.","family":"de Kort","sequence":"additional","affiliation":[{"name":"Department of Neurology, Donders Institute for Brain, Cognition and Behaviour Radboud University Medical Center  Nijmegen The Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-8495-4578","authenticated-orcid":false,"given":"Catharina J. 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