{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,25]],"date-time":"2026-08-25T13:16:31Z","timestamp":1787663791108,"version":"build-2736575974"},"reference-count":47,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2025,9,19]],"date-time":"2025-09-19T00:00:00Z","timestamp":1758240000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2025,9,19]],"date-time":"2025-09-19T00:00:00Z","timestamp":1758240000000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Annals of Neurology"],"published-print":{"date-parts":[[2026,1]]},"abstract":"<jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>To identify clinical and radiological features of cerebral amyloid angiopathy\u2010related inflammation (CAA\u2010ri), and compare these features with those of sporadic CAA, to improve the understanding, diagnosis, and clinical care of CAA\u2010ri.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>We retrospectively reviewed routine clinical data from 37 patients with CAA\u2010ri and 158 patients with sporadic CAA, including conventional vascular risk factors and comorbidities. We assessed brain magnetic resonance imaging for: radiological markers of CAA; features of amyloid\u2010related imaging abnormalities with edema\/effusion (ARIA\u2010E) including parenchymal white matter hyperintensities, sulcal hyperintensities, and gyral swelling; and evidence of neurodegeneration (medial temporal atrophy and global cortical atrophy).<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Compared with patients with sporadic CAA, patients with CAA\u2010ri had more numerous lobar cerebral microbleeds (median 207[IQR 33\u2010811] vs 19[IQR 7\u201058],\n                      <jats:italic>p<\/jats:italic>\n                      \u2009&lt;\u20090.001), and higher rates of medial temporal and global cortical atrophy. In comparison with sporadic CAA, all ARIA\u2010E features were much more common in patients with CAA\u2010ri (parenchymal hyperintensities 89% vs 3%, sulcal hyperintensities 78% vs 9%, and gyral swelling 86% vs 0.6%), as were conventional vascular risk factors (hypertension, dyslipidemia) and long\u2010term comorbidities (inflammatory and infectious disorders, autoimmune or connective tissue disorders, or malignancies).\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Interpretation<\/jats:title>\n                    <jats:p>Features of ARIA\u2010E (parenchymal white matter hyperintensities, sulcal hyperintensities, and gyral swelling) are more common in CAA\u2010ri in comparison with \u201cnon\u2010inflammatory\u201d sporadic CAA, suggesting shared mechanisms with Alzheimer's disease immunotherapy and a potential role in improving diagnostic accuracy for CAA\u2010ri. The high prevalence of atrophy and lobar cerebral microbleeds suggests a potential mechanistic role for capillary CAA, Alzheimer's disease, or both, in CAA\u2010ri. Cardiovascular risk factors and other long\u2010term comorbidities may also be relevant to the underlying mechanisms of CAA\u2010ri. ANN NEUROL 2026;99:148\u2013158<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/ana.78029","type":"journal-article","created":{"date-parts":[[2025,9,19]],"date-time":"2025-09-19T10:42:30Z","timestamp":1758278550000},"page":"148-158","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["Clinical\u2013Radiological Spectrum of Cerebral Amyloid Angiopathy\u2010Related Inflammation"],"prefix":"10.1002","volume":"99","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-7342-2488","authenticated-orcid":false,"given":"Larysa","family":"Panteleienko","sequence":"first","affiliation":[{"name":"Stroke Research Center, Department of Translational Neuroscience and Stroke UCL Queen Square Institute of Neurology  London UK"},{"name":"Deptartment of Neurology Bogomolets National Medical University  Kyiv 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