{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,10]],"date-time":"2026-09-10T17:17:16Z","timestamp":1789060636262,"version":"build-2803163510"},"reference-count":39,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2025,2,5]],"date-time":"2025-02-05T00:00:00Z","timestamp":1738713600000},"content-version":"vor","delay-in-days":4,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100020950","name":"National Science and Technology Council","doi-asserted-by":"publisher","award":["112\u20102923\u2010B\u2010002\u2010001\u2010MY3"],"award-info":[{"award-number":["112\u20102923\u2010B\u2010002\u2010001\u2010MY3"]}],"id":[{"id":"10.13039\/501100020950","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100020950","name":"National Science and Technology Council","doi-asserted-by":"publisher","award":["113\u20102628\u2010B\u2010002\u2010013\u2010MY3"],"award-info":[{"award-number":["113\u20102628\u2010B\u2010002\u2010013\u2010MY3"]}],"id":[{"id":"10.13039\/501100020950","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005762","name":"National Taiwan University Hospital","doi-asserted-by":"publisher","award":["113\u2010N0075"],"award-info":[{"award-number":["113\u2010N0075"]}],"id":[{"id":"10.13039\/501100005762","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100005762","name":"National Taiwan University Hospital","doi-asserted-by":"publisher","award":["113\u2010X0018"],"award-info":[{"award-number":["113\u2010X0018"]}],"id":[{"id":"10.13039\/501100005762","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":[[2025,2]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Blood\u2010based biomarkers may offer a non\u2010invasive approach to diagnose cerebral amyloid angiopathy (CAA), especially in early\u2010stage. We evaluated the ability of plasma phosphorylated tau\u2010217 (p\u2010tau 217) to differentiate CAA from Alzheimer's disease (AD) and deep perforator arteriopathy (DPA).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Patients with AD (age 73.7\u2009\u00b1\u20098.1\u2009years), probable CAA (74.8\u2009\u00b1\u20096.9\u2009years), or DPA (66.1\u2009\u00b1\u200910.4\u2009years) were enrolled from memory and stroke clinics at a medical center in Taiwan. All participants received amyloid and tau PET scans. Plasma biomarkers were measured via a SIMOA immunoassay platform. The diagnostic utility of p\u2010tau 217 was assessed using ROC analyses and the Youden cutoff. Associations between plasma p\u2010tau 217 and neuroimaging variables in CAA were explored.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Patients with CAA had lower plasma p\u2010tau 217 (0.69\u2009\u00b1\u20090.76 vs. 1.28\u2009\u00b1\u20090.97\u2009pg\/mL,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) and a lower p\u2010tau 217\/A\u03b240 ratio (0.003\u2009\u00b1\u20090.002 vs. 0.006\u2009\u00b1\u20090.003,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001) than the AD group but higher levels than the DPA group (p\u2010tau 217, 0.27\u2009\u00b1\u20090.13\u2009pg\/mL,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009=\u20090.001; p\u2010tau 217\/A\u03b240, 0.001\u2009\u00b1\u20090.0005,\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001), although adjustment attenuated the difference in p\u2010tau 217 between CAA and DPA. Plasma A\u03b240, A\u03b242, and A\u03b240\/A\u03b242 were not significantly different between groups. Plasma p\u2010tau 217 had moderate to good diagnostic utility to differentiate CAA vs. AD (sensitivity, 64.4%; specificity, 89.5%; AUC, 0.809) and CAA vs. DPA (sensitivity, 67.8%; specificity, 100%; AUC, 0.855). In CAA, p\u2010tau 217 significantly correlated with the severity of CAA, amyloid PET signal intensity, and lobar microbleed count (\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Plasma p\u2010tau 217 may represent a non\u2010invasive biomarker for distinguishing cerebral amyloid angiopathy (CAA) from other conditions, including AD and DPA.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/ene.70066","type":"journal-article","created":{"date-parts":[[2025,2,5]],"date-time":"2025-02-05T07:18:15Z","timestamp":1738739895000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":15,"title":["Plasma Phosphorylated Tau 217 as a Discriminative Biomarker for Cerebral Amyloid 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