{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T21:09:32Z","timestamp":1790111372103,"version":"4.0.1"},"reference-count":32,"publisher":"SAGE Publications","issue":"3","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2023,1,31]]},"abstract":"<jats:p>Background: Cerebrospinal fluid (CSF) biomarkers in patients with cerebral amyloid angiopathy-related inflammation (CAA-ri) have demonstrated inconsistent results. Objective: We investigated the relationship between CSF amyloid-\u03b2 protein (A\u03b2) and vascular pathological findings to elucidate the mechanisms of A\u03b2 elimination from the brain in CAA-ri. Methods: We examined A\u03b240 and A\u03b242 levels in CSF samples in 15 patients with CAA-ri and 15 patients with Alzheimer\u2019s disease and cerebral amyloid angiopathy (AD-CAA) using ELISA as a cross-sectional study. Furthermore, we pathologically examined A\u03b240 and A\u03b242 depositions on the leptomeningeal blood vessels (arteries, arterioles, and veins) using brain biopsy samples from six patients with acute CAA-ri and brain tissues of two autopsied patients with CAA-ri. Results: The median A\u03b240 and A\u03b242 levels in the CSF showed no significant difference between pre-treatment CAA-ri (A\u03b240, 6837 pg\/ml; A\u03b242, 324 pg\/ml) and AD-CAA (A\u03b240, 7669 pg\/ml, p\u200a=\u200a0.345; A\u03b242, 355 pg\/ml, p\u200a=\u200a0.760). A\u03b240 and A\u03b242 levels in patients with post-treatment CAA-ri (A\u03b240, 1770 pg\/ml, p\u200a=\u200a0.056; A\u03b242, 167 pg\/ml, p\u200a=\u200a0.006) were lower than those in patients with pre-treatment CAA-ri. Regarding A\u03b240 and A\u03b242 positive arteries, acute CAA-ri cases showed a higher frequency of partially A\u03b2-deposited blood vessels than postmortem CAA-ri cases (A\u03b240, 20.8% versus 3.9%, p\u200a=\u200a0.0714; A\u03b242, 27.4% versus 2.0%, p\u200a=\u200a0.0714, respectively). Conclusion: Lower levels of CSF A\u03b240 and A\u03b242 could be biomarkers for the cessation of inflammation in CAA-ri reflecting the recovery of the intramural periarterial drainage pathway and vascular function.<\/jats:p>","DOI":"10.3233\/jad-220838","type":"journal-article","created":{"date-parts":[[2022,12,20]],"date-time":"2022-12-20T12:56:10Z","timestamp":1671540970000},"page":"1173-1183","source":"Crossref","is-referenced-by-count":5,"title":["Cerebrospinal Fluid Biomarkers and Amyloid-\u03b2 Elimination from the Brain in Cerebral Amyloid Angiopathy-Related Inflammation"],"prefix":"10.1177","volume":"91","author":[{"given":"Kenji","family":"Sakai","sequence":"first","affiliation":[{"name":"Department of Neurology, Joetsu General Hospital, Joetsu, Japan"},{"name":"Department of Neurology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, 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Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tsuyoshi","family":"Hamaguchi","sequence":"additional","affiliation":[{"name":"Department of Neurology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan"},{"name":"Department of Neurology, Kanazawa Medical University, Uchinada, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Akiyoshi","family":"Kakita","sequence":"additional","affiliation":[{"name":"Department of Pathology, Brain Research Institute, Niigata University, Niigata, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Masahito","family":"Yamada","sequence":"additional","affiliation":[{"name":"Department of Neurology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan"},{"name":"Department of Internal Medicine, Kudanzaka Hospital, Tokyo, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kenjiro","family":"Ono","sequence":"additional","affiliation":[{"name":"Department of Neurology, Kanazawa University Graduate School of Medical Sciences, Kanazawa, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-220838_ref1","doi-asserted-by":"crossref","first-page":"17","DOI":"10.5853\/jos.2015.17.1.17","article-title":"Cerebral amyloid angiopathy: Emerging concepts","volume":"17","author":"Yamada","year":"2015","journal-title":"J Stroke"},{"key":"10.3233\/JAD-220838_ref2","doi-asserted-by":"crossref","first-page":"139","DOI":"10.1007\/s00401-018-1862-7","article-title":"Convective influx\/glymphatic system: Tracers injected into the CSF enter and leave the brain along separate periarterial basement membrane pathways","volume":"136","author":"Albargothy","year":"2018","journal-title":"Acta 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