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The CAIs also improved microvascular fitness and induced protective glial pro\u2010clearance pathways, resulting in the reduction of A\u03b2 deposition. Notably, we unveiled that the mitochondrial carbonic anhydrase\u2010VB (CA\u2010VB) is upregulated in TgSwDI brains, CAA and AD+CAA human subjects, and in endothelial cells upon A\u03b2 treatment. Strikingly, CA\u2010VB silencing specifically reduces A\u03b2\u2010mediated endothelial apoptosis.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Discussion<\/jats:title>\n                    <jats:p>This work substantiates the potential application of CAIs in clinical trials for AD and CAA.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1002\/alz.13063","type":"journal-article","created":{"date-parts":[[2023,4,26]],"date-time":"2023-04-26T07:06:57Z","timestamp":1682492817000},"page":"5048-5073","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":53,"title":["FDA\u2010approved carbonic anhydrase inhibitors reduce amyloid \u03b2 pathology and improve cognition, by ameliorating cerebrovascular health and glial fitness"],"prefix":"10.1002","volume":"19","author":[{"given":"Elisa","family":"Canepa","sequence":"first","affiliation":[{"name":"Alzheimer's Center at Temple, 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