{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,18]],"date-time":"2026-08-18T00:49:28Z","timestamp":1787014168458,"version":"build-2736575974"},"reference-count":36,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T00:00:00Z","timestamp":1779235200000},"content-version":"vor","delay-in-days":19,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,5,1]],"date-time":"2026-05-01T00:00:00Z","timestamp":1777593600000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"funder":[{"DOI":"10.13039\/501100004587","name":"Instituto de Salud Carlos III","doi-asserted-by":"publisher","id":[{"id":"10.13039\/501100004587","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100020407","name":"European Research Area Network on Cardiovascular Diseases","doi-asserted-by":"publisher","award":["ERA\u2010CVD_JTC2020\u2010015"],"award-info":[{"award-number":["ERA\u2010CVD_JTC2020\u2010015"]}],"id":[{"id":"10.13039\/501100020407","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Euro J of Neurology"],"published-print":{"date-parts":[[2026,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Cerebral amyloid angiopathy (CAA) frequently co\u2010occurs with Alzheimer's disease (AD), complicating diagnosis in patients with cognitive impairment. The CSF biomarker profile of CAA remains poorly understood, particularly with AD co\u2010pathology. We aimed to characterize CSF biomarkers in CAA, assess diagnostic accuracy, and examine associations with neuroimaging markers.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We included 261 participants from a hospital\u2010based cohort, recruited from memory clinic outpatients and neurology inpatients. Groups comprised healthy controls (HC,\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200935), CAA without AD co\u2010pathology (CAA\u2010nonAD,\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200927), CAA with AD co\u2010pathology (CAA\u2010AD,\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u200930), and AD (\n                      <jats:italic>n<\/jats:italic>\n                      \u2009=\u2009169). CSF A\u03b240, A\u03b242, p\u2010tau181, and t\u2010tau were quantified using automated immunoassays. Group differences were tested using ANCOVA adjusted for age and sex. ROC analyses with 10\u2010fold cross\u2010validation and bootstrapping assessed diagnostic performance. Associations between CSF biomarkers and CAA\u2010related MRI markers were examined using ANCOVA.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      A\u03b240 concentrations were lower in CAA\u2010nonAD and CAA\u2010AD compared to AD and HC (\n                      <jats:italic>p<\/jats:italic>\n                      \u2010value\n                      <jats:sub>bf<\/jats:sub>\n                      \u2009&lt;\u20090.05). A\u03b242 was reduced in CAA\u2010AD and AD versus HC, with no difference between CAA\u2010nonAD and AD. p\u2010tau181 and t\u2010tau were elevated in AD and CAA\u2010AD compared with CAA\u2010nonAD and HC (\n                      <jats:italic>p<\/jats:italic>\n                      \u2010value\n                      <jats:sub>bf<\/jats:sub>\n                      \u2009&lt;\u20090.05). A\u03b240 showed the highest diagnostic accuracy for CAA (AUC\u2009=\u20090.73; 95% CI: 0.66\u20130.80), followed by A\u03b242 (AUC\u2009=\u20090.71; 95% CI: 0.64\u20130.78). In AD patients, A\u03b242 best discriminated coexisting CAA (AUC\u2009=\u20090.77). Higher CAA\u2010SVD burden scores were associated with lower A\u03b240 (\n                      <jats:italic>p<\/jats:italic>\n                      \u2010value\n                      <jats:sub>bf<\/jats:sub>\n                      \u2009&lt;\u20090.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>CSF A\u03b240 and A\u03b242 provide complementary diagnostic value for identifying CAA, both in isolation and with AD co\u2010pathology. Reduced A\u03b240 is associated with greater CAA\u2010related vascular burden, supporting its role as a marker of vascular amyloid pathology.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/ene.70613","type":"journal-article","created":{"date-parts":[[2026,5,20]],"date-time":"2026-05-20T13:45:07Z","timestamp":1779284707000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":1,"title":["<scp>CSF<\/scp>\n                    Biomarker Profile of Cerebral Amyloid Angiopathy: Diagnostic Performance and Imaging Correlates in a Hospital\u2010Based Neurology Cohort"],"prefix":"10.1111","volume":"33","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-2097-4430","authenticated-orcid":false,"given":"Aida","family":"Fern\u00e1ndez\u2010Lebrero","sequence":"first","affiliation":[{"name":"Hospital del Mar Research Institute  Barcelona Spain"},{"name":"Servei de Neurologia, Hospital del Mar  Barcelona Spain"},{"name":"Department of 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