{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,12]],"date-time":"2026-10-12T22:32:52Z","timestamp":1791844372272,"version":"4.3.4"},"reference-count":40,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"5","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2025,3,4]]},"abstract":"<jats:sec xml:lang=\"en\">\n                    <jats:title>Background<\/jats:title>\n                    <jats:p xml:lang=\"en\">Cerebral amyloid angiopathy (CAA) is driven by vascular A\u03b2 (amyloid\u2010beta) deposition, which can be detected as reduced A\u03b2 species in cerebrospinal fluid (CSF). We sought to identify relationships between CSF A\u03b2 and tau concentrations and various manifestations of CAA.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p xml:lang=\"en\">This is a retrospective cross\u2010sectional single\u2010center study of patients diagnosed with CAA per Boston Criteria version 2.0, had magnetic resonance imaging brain scans, and underwent CSF testing for A\u03b2 and tau concentrations between 2008 and 2022. Associations between clinical\/magnetic resonance imaging features and CSF biomarker concentrations were investigated with univariate and multivariate models.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p xml:lang=\"en\">\n                      We identified 31 patients aged 69.6\u00b18.4\u2009years, of whom 20 presented with cognitive complaints, 9 with CAA\u2010related macrohemorrhage (lobar intraparenchymal or convexity subarachnoid hemorrhage), and 2 with transient focal neurological episodes. Presence of macrohemorrhage (301.8\u00b1112\u2009pg\/mL versus 400.9\u00b1123\u2009pg\/mL,\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.029), cortical superficial siderosis (309.6\u00b1131\u2009mg\/dL versus 412.3\u00b1100\u2009pg\/mL,\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.021), and severe enlarged perivascular spaces in centrum semiovale (285.8\u00b191\u2009pg\/mL versus 428.3\u00b1117\u2009pg\/mL,\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      &lt;0.001) were associated with lower A\u03b242 concentrations. A\u03b242 concentrations inversely correlated with the number of these manifestations, being lowest in patients having all three. Patients with cognitive complaints had higher t\u2010tau (total tau; 551\u00b1320\u2009pg\/mL versus 317.2\u00b1141\u2009pg\/mL,\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.03) and trended toward having higher p\u2010tau (phosphorylated tau at threonine 181) concentrations (75.69\u00b139\u2009pg\/mL versus 49.24\u00b122\u2009pg\/mL,\n                      <jats:italic toggle=\"no\">P<\/jats:italic>\n                      =0.05).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec xml:lang=\"en\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p xml:lang=\"en\">Lower CSF A\u03b242, suggesting higher amyloid burden, is associated with CAA\u2010related macrohemorrhages and severe enlarged perivascular spaces in centrum semiovale, suggesting potential mechanistic links and CSF A\u03b242 as a potential biomarker for progression of CAA. CSF tau concentrations are linked to cognitive complaints, likely representing comorbid Alzheimer disease pathology.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1161\/jaha.124.040025","type":"journal-article","created":{"date-parts":[[2025,3,3]],"date-time":"2025-03-03T07:21:56Z","timestamp":1740986516000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":16,"title":["Cerebrospinal Fluid Beta\u2010Amyloid Concentration and Clinical and Radiographic Manifestations of Cerebral Amyloid Angiopathy"],"prefix":"10.1161","volume":"14","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-1842-7099","authenticated-orcid":false,"given":"Baris","family":"Alten","sequence":"first","affiliation":[{"name":"Mass General Brigham Neurology Residency Program","place":["Boston, USA"]},{"name":"Massachusetts General Hospital","place":["Boston, USA"]},{"name":"Brigham and Women\u2019s Hospital","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0009-0009-2264-1603","authenticated-orcid":false,"given":"Elif","family":"Gokcal","sequence":"additional","affiliation":[{"name":"Massachusetts General Hospital","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-5832-8178","authenticated-orcid":false,"given":"Andrew","family":"Warren","sequence":"additional","affiliation":[{"name":"Massachusetts General Hospital","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7957-8643","authenticated-orcid":false,"given":"Susanne J.","family":"van Veluw","sequence":"additional","affiliation":[{"name":"Massachusetts General Hospital","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9358-3262","authenticated-orcid":false,"given":"Mariel","family":"Kozberg","sequence":"additional","affiliation":[{"name":"Massachusetts General Hospital","place":["Boston, USA"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2169-4457","authenticated-orcid":false,"given":"M. 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