{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,4,22]],"date-time":"2026-04-22T05:46:07Z","timestamp":1776836767662,"version":"3.51.2"},"reference-count":45,"publisher":"Wiley","issue":"10","license":[{"start":{"date-parts":[[2020,9,10]],"date-time":"2020-09-10T00:00:00Z","timestamp":1599696000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/100005440","name":"Center for Scientific Review","doi-asserted-by":"publisher","award":["NIA 1R01AG059639"],"award-info":[{"award-number":["NIA 1R01AG059639"]}],"id":[{"id":"10.13039\/100005440","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100005440","name":"Center for Scientific Review","doi-asserted-by":"publisher","award":["NINDS K22NS092688"],"award-info":[{"award-number":["NINDS K22NS092688"]}],"id":[{"id":"10.13039\/100005440","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000957","name":"Alzheimer's Association","doi-asserted-by":"publisher","award":["AARGD\u2010591887"],"award-info":[{"award-number":["AARGD\u2010591887"]}],"id":[{"id":"10.13039\/100000957","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Aging Cell"],"published-print":{"date-parts":[[2020,10]]},"abstract":"<jats:title>ABSTRACT<\/jats:title><jats:p>Cerebral amyloid angiopathy (CAA) is typified by the cerebrovascular deposition of amyloid. The mechanisms underlying the contribution of CAA to neurodegeneration are not currently understood. Although CAA is highly associated with the accumulation of \u03b2\u2010amyloid (A\u03b2), other amyloids are known to associate with the vasculature. Alzheimer's disease (AD) is characterized by parenchymal A\u03b2 deposition and intracellular accumulation of tau as neurofibrillary tangles (NFTs), affecting synapses directly, leading to behavioral and physical impairment. CAA increases with age and is present in 70%\u201397% of individuals with AD. Studies have overwhelmingly focused on the connection between parenchymal amyloid accumulation and synaptotoxicity; thus, the contribution of vascular amyloid is mostly understudied. Here, synaptic alterations induced by vascular amyloid accumulation and their behavioral consequences were characterized using a mouse model of Familial Danish dementia (FDD), a neurodegenerative disease characterized by the accumulation of Danish amyloid (ADan) in the vasculature. The mouse model (Tg\u2010FDD) displays a hyperactive phenotype that potentially arises from impairment in the GABAergic synapses, as determined by electrophysiological analysis. We demonstrated that the disruption of GABAergic synapse organization causes this impairment and provided evidence that GABAergic synapses are impaired in patients with CAA pathology. Understanding the mechanism that CAA contributes to synaptic dysfunction in AD\u2010related dementias is of critical importance for developing future therapeutic interventions.<\/jats:p>","DOI":"10.1111\/acel.13233","type":"journal-article","created":{"date-parts":[[2020,9,14]],"date-time":"2020-09-14T07:36:46Z","timestamp":1600069006000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":16,"title":["Vascular amyloid accumulation alters the gabaergic synapse and induces hyperactivity in a model of cerebral amyloid angiopathy"],"prefix":"10.1111","volume":"19","author":[{"given":"Pablo","family":"Cisternas","sequence":"first","affiliation":[{"name":"Stark Neurosciences Research Institute Indiana University School of Medicine Indianapolis IN USA"},{"name":"Department of Anatomy, Cell Biology &amp; Physiology Indiana University School of Medicine Indianapolis IN USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1129-4038","authenticated-orcid":false,"given":"Xavier","family":"Taylor","sequence":"additional","affiliation":[{"name":"Stark Neurosciences Research Institute Indiana University School of Medicine Indianapolis IN USA"},{"name":"Department of Anatomy, Cell Biology &amp; 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