{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,2]],"date-time":"2026-07-02T08:43:29Z","timestamp":1782981809251,"version":"3.54.5"},"reference-count":20,"publisher":"SAGE Publications","issue":"7","license":[{"start":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T00:00:00Z","timestamp":1771891200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by-nc\/4.0\/"},{"start":{"date-parts":[[2026,2,24]],"date-time":"2026-02-24T00:00:00Z","timestamp":1771891200000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.sagepub.com\/page\/policies\/text-and-data-mining-license"}],"funder":[{"DOI":"10.13039\/100000002","name":"national institutes of health","doi-asserted-by":"publisher","award":["K08NS131530; R00AG059893; R01NS128790; R56NS131387"],"award-info":[{"award-number":["K08NS131530; R00AG059893; R01NS128790; R56NS131387"]}],"id":[{"id":"10.13039\/100000002","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000968","name":"American Heart Association","doi-asserted-by":"crossref","award":["23SCEFIA1152994"],"award-info":[{"award-number":["23SCEFIA1152994"]}],"id":[{"id":"10.13039\/100000968","id-type":"DOI","asserted-by":"crossref"}]},{"name":"American Heart Association \/ Bugher Foundation","award":["814728; 812095"],"award-info":[{"award-number":["814728; 812095"]}]},{"DOI":"10.13039\/100012213","name":"rappaport foundation","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100012213","id-type":"DOI","asserted-by":"publisher"}]},{"name":"Fundatie van Renswoude"},{"name":"Bekker la Bastide Fonds"},{"name":"Schuurman Schimmel & van Outeren Stichting"},{"name":"Stichting Vreedefonds"},{"name":"Hendrik Muller Fonds"}],"content-domain":{"domain":["journals.sagepub.com"],"crossmark-restriction":true},"short-container-title":["J Cereb Blood Flow Metab"],"published-print":{"date-parts":[[2026,7]]},"abstract":"<jats:p>\n                    Cerebral amyloid angiopathy (CAA) is a small vessel disease associated with hemorrhagic lesions including microbleeds and intracerebral hemorrhage. Growing evidence suggests vascular remodeling may be a critical step leading to CAA-related vessel rupture. The APP23 mouse model is one of few models of cerebral amyloidosis that develop spontaneous microbleeds, visible on T2*-weighted MRI as hypointense lesions. However, it remains unknown whether this model recapitulates the microbleed-associated vascular remodeling observed in human tissue. In this study, we used in-vivo 9.4\u2009T MRI and histopathology to study the neuropathological correlates of MRI-observed hypointense lesions in 18- and 24-month-old APP23 transgenic (Tg) mice and wildtype (WT) littermates (12 Tg, 17 WT). Tg mice had more cortical and deep lesions (\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    \u2009&lt;\u20090.001,\n                    <jats:italic toggle=\"yes\">p<\/jats:italic>\n                    \u2009&lt;\u20090.001)). Brains were serially sectioned from a subset of these mice (11 Tg, five WT) and lesions retrieved. All cortical lesions were microbleeds (and in Tg mice). However, 96% of deep lesions (Tg and WT) were calcifications, suggesting caution is needed when interpreting deep hypointense lesions as microbleeds. A qualitative analysis of histopathologically-confirmed microbleeds revealed vascular remodeling including vessel wall thickening and decreased vascular amyloid-\u03b2 at most vessel rupture sites, resembling human findings, suggesting APP23 mice may be an appropriate model to study mechanisms of CAA-related hemorrhage.\n                  <\/jats:p>","DOI":"10.1177\/0271678x261424057","type":"journal-article","created":{"date-parts":[[2026,2,25]],"date-time":"2026-02-25T05:00:48Z","timestamp":1771995648000},"page":"1905-1914","update-policy":"https:\/\/doi.org\/10.1177\/sage-journals-update-policy","source":"Crossref","is-referenced-by-count":0,"title":["Neuropathological correlates of MRI-observed hypointense lesions in the APP23 mouse model of cerebral amyloid angiopathy"],"prefix":"10.1177","volume":"46","author":[{"given":"Maarten L","family":"van den Berg","sequence":"first","affiliation":[{"name":"MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA"},{"name":"J Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston, MA, USA"},{"name":"University of Amsterdam, Amsterdam, the Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Leon P","family":"Munting","sequence":"additional","affiliation":[{"name":"MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lee","family":"Hanlin","sequence":"additional","affiliation":[{"name":"MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Irvin","family":"Yi","sequence":"additional","affiliation":[{"name":"MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA"},{"name":"Harvard College, Cambridge, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Joshua","family":"Bailey","sequence":"additional","affiliation":[{"name":"MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Douglas S","family":"Richardson","sequence":"additional","affiliation":[{"name":"Department of Molecular and Cellular Biology, Harvard Center for Biological Imaging, Harvard University, Cambridge, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Theodore J","family":"Zwang","sequence":"additional","affiliation":[{"name":"MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, 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":"MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA"},{"name":"J Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston, MA, USA"},{"name":"BHF-UK DRI Centre for Vascular Dementia Research, University of Edinburgh, Edinburgh, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-9358-3262","authenticated-orcid":false,"given":"Mariel G","family":"Kozberg","sequence":"additional","affiliation":[{"name":"MassGeneral Institute for Neurodegenerative Disease, Massachusetts General Hospital, Charlestown, MA, USA"},{"name":"J Philip Kistler Stroke Research Center, Massachusetts General Hospital, Boston, MA, USA"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"179","published-online":{"date-parts":[[2026,2,24]]},"reference":[{"key":"e_1_3_3_2_2","doi-asserted-by":"publisher","DOI":"10.1016\/S1474-4422(23)00114-X"},{"key":"e_1_3_3_3_2","doi-asserted-by":"publisher","DOI":"10.1007\/s00401-016-1635-0"},{"key":"e_1_3_3_4_2","first-page":"1","article-title":"Different microvascular alterations underlie microbleeds and microinfarcts","volume":"8","author":"van Veluw SJ","year":"2019","unstructured":"van Veluw SJ, Scherlek AA, Freeze WM, et al. Different microvascular alterations underlie microbleeds and microinfarcts. 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