{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T12:18:06Z","timestamp":1790511486350,"version":"4.1.0"},"reference-count":29,"publisher":"SAGE Publications","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JAD"],"published-print":{"date-parts":[[2015,11,3]]},"abstract":"<jats:p>Background: Capillary amyloid-\u03b2 (capA\u03b2) deposition in the cerebral cortex is the neuropathological feature providing the basis for categorizing cerebral amyloid angiopathy (CAA) into two distinct types, CAA-Type1 with capA\u03b2 and CAA-Type2 without capA\u03b2. Objective: We investigated the neuropathological and clinical characteristics of capA\u03b2 deposition in a prospective population-based study. Methods: Vantaa 85+ includes 601 individuals aged \u226585 years, of which 300 were studied clinically and neuropathologically. 278 subjects were analyzed for the apolipoprotein E (APOE) genotype. The diagnosis of capA\u03b2 was determined using immunohistochemistry against A\u03b2, and of CAA using Congo red confirmed by A\u03b2 immunohistochemistry, both analyzed in six brain areas. The severity of capA\u03b2 was graded semi-quantitatively, and the severity of CAA was based on the percentage of affected vessels. Alzheimer\u2019s disease (AD)-type neuropathology (CERAD score and Braak stage) was analyzed using standard methods. Results: CAA-Type1 was present in 86\/300, CAA-Type2 in 135\/300, and 79\/300 had no CAA. CapA\u03b2 was most frequent in the occipital lobe (79\/86). CAA-Type1 was associated with the severity of CAA (p\u200a&lt; \u200a0.001), dementia (p\u200a&lt; \u200a0.001), severe AD-type neuropathology (p-value 0.09 for CERAD C and 0.017 for Braak stages V-VI), and APOE \u025b4 allele carrier status (p\u200a&lt; \u200a0.001). Conclusions: This population-based study confirmed the presence of distinct CAA-Type1 and its association with the severity of CAA, severe AD-type neuropathology, and the APOE \u025b4 carrier status. Both the severity and localization of the deposition seemed to determine the clinical significance of capA\u03b2.<\/jats:p>","DOI":"10.3233\/jad-150241","type":"journal-article","created":{"date-parts":[[2015,11,3]],"date-time":"2015-11-03T11:24:36Z","timestamp":1446549876000},"page":"149-157","source":"Crossref","is-referenced-by-count":33,"title":["Capillary Amyloid-\u03b2 Protein Deposition in a Population-Based Study (Vantaa 85+)"],"prefix":"10.1177","volume":"49","author":[{"given":"Mira","family":"M\u00e4kel\u00e4","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anders","family":"Paetau","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tuomo","family":"Polvikoski","sequence":"additional","affiliation":[{"name":"Institute for Ageing and Health, Newcastle University, Campus for Ageing and Vitality, Newcastle upon Tyne, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Liisa","family":"Myllykangas","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Maarit","family":"Tanskanen","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Helsinki and Helsinki University Central Hospital, Helsinki, Finland"},{"name":"Department of Pathology, Kanta-H\u00e4me Central Hospital, H\u00e4meenlinna, Finland"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","reference":[{"key":"10.3233\/JAD-150241_ref1","doi-asserted-by":"crossref","first-page":"2757","DOI":"10.1002\/j.1460-2075.1985.tb04000.x","article-title":"Neuronal origin of a cerebral amyloid: Neurofibrillary tangles of Alzheimer\u2019s disease contain the same protein as the amyloid of plaque cores and blood vessels","volume":"4","author":"Masters","year":"1985","journal-title":"EMBO J"},{"key":"10.3233\/JAD-150241_ref2","doi-asserted-by":"crossref","first-page":"924","DOI":"10.1161\/01.STR.14.6.924","article-title":"Cerebral amyloid angiopathy: Incidence and complications in the aging brain. 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