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We recently showed that the carbonic anhydrase inhibitor (\n                    <jats:styled-content style=\"fixed-case\">CAI<\/jats:styled-content>\n                    ) methazolamide (\n                    <jats:styled-content style=\"fixed-case\">MTZ<\/jats:styled-content>\n                    ) prevents amyloid \u03b2 (A\u03b2)\u2010mediated onset of apoptosis in the mouse brain. In this study, we used\n                    <jats:styled-content style=\"fixed-case\">MTZ<\/jats:styled-content>\n                    and, for the first time, the analog\n                    <jats:styled-content style=\"fixed-case\">CAI<\/jats:styled-content>\n                    acetazolamide (\n                    <jats:styled-content style=\"fixed-case\">ATZ<\/jats:styled-content>\n                    ) in neuronal and cerebral vascular cells challenged with A\u03b2, to clarify their protective effects and mitochondrial molecular mechanism of action. The\n                    <jats:styled-content style=\"fixed-case\">CAI<\/jats:styled-content>\n                    s selectively inhibited mitochondrial dysfunction pathways induced by A\u03b2, without affecting metabolic function.\n                    <jats:styled-content style=\"fixed-case\">ATZ<\/jats:styled-content>\n                    was effective at concentrations 10 times lower than\n                    <jats:styled-content style=\"fixed-case\">MTZ<\/jats:styled-content>\n                    . Both\n                    <jats:styled-content style=\"fixed-case\">MTZ<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">ATZ<\/jats:styled-content>\n                    prevented mitochondrial membrane depolarization and H\n                    <jats:sub>2<\/jats:sub>\n                    O\n                    <jats:sub>2<\/jats:sub>\n                    generation, with no effects on intracellular\n                    <jats:styled-content style=\"fixed-case\">pH<\/jats:styled-content>\n                    or\n                    <jats:styled-content style=\"fixed-case\">ATP<\/jats:styled-content>\n                    production. Importantly, the drugs did not primarily affect calcium homeostasis. This work suggests a new role for carbonic anhydrases (\n                    <jats:styled-content style=\"fixed-case\">CA<\/jats:styled-content>\n                    s) in the A\u03b2\u2010induced mitochondrial toxicity associated with\n                    <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                    and cerebral amyloid angiopathy (\n                    <jats:styled-content style=\"fixed-case\">CAA<\/jats:styled-content>\n                    ), and paves the way to\n                    <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                    clinical trials for\n                    <jats:styled-content style=\"fixed-case\">CAI<\/jats:styled-content>\n                    s,\n                    <jats:styled-content style=\"fixed-case\">FDA<\/jats:styled-content>\n                    \u2010approved drugs with a well\u2010known profile of brain delivery.\n                  <\/jats:p>","DOI":"10.1111\/acel.12787","type":"journal-article","created":{"date-parts":[[2018,6,6]],"date-time":"2018-06-06T01:41:32Z","timestamp":1528249292000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":97,"title":["Carbonic anhydrase inhibition selectively prevents amyloid \u03b2 neurovascular mitochondrial toxicity"],"prefix":"10.1111","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-8105-1701","authenticated-orcid":false,"given":"Mar\u00eda E.","family":"Solesio","sequence":"first","affiliation":[{"name":"Department of Basic Sciences New York University College of Dentistry New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Pablo M.","family":"Peixoto","sequence":"additional","affiliation":[{"name":"Department of Natural Sciences Baruch College Graduate Center The City University of New York New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ludovic","family":"Debure","sequence":"additional","affiliation":[{"name":"Department of Psychiatry New York University School of Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen M.","family":"Madamba","sequence":"additional","affiliation":[{"name":"Department of Natural Sciences Baruch College Graduate Center The City University of New York New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mony J.","family":"de Leon","sequence":"additional","affiliation":[{"name":"Department of Psychiatry New York University School of Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas","family":"Wisniewski","sequence":"additional","affiliation":[{"name":"Department of Neurology Center for Cognitive Neurology New York University School of Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Evgeny V.","family":"Pavlov","sequence":"additional","affiliation":[{"name":"Department of Basic Sciences New York University College of Dentistry New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-2047-222X","authenticated-orcid":false,"given":"Silvia","family":"Fossati","sequence":"additional","affiliation":[{"name":"Department of Psychiatry New York University School of Medicine New York New York"},{"name":"Department of Neurology Center for Cognitive Neurology New York University School of Medicine New York New York"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2018,6,5]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.23-12-05088.2003"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbamcr.2004.09.006"},{"key":"e_1_2_7_4_1","doi-asserted-by":"publisher","DOI":"10.1016\/S0143-4160(02)00203-8"},{"key":"e_1_2_7_5_1","doi-asserted-by":"publisher","DOI":"10.1073\/pnas.0708959104"},{"key":"e_1_2_7_6_1","doi-asserted-by":"publisher","DOI":"10.1523\/JNEUROSCI.4468-06.2007"},{"key":"e_1_2_7_7_1","doi-asserted-by":"publisher","DOI":"10.1517\/13543776.2013.782394"},{"key":"e_1_2_7_8_1","doi-asserted-by":"publisher","DOI":"10.1212\/WNL.0000000000000313"},{"key":"e_1_2_7_9_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.136.4.833"},{"key":"e_1_2_7_10_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.neurobiolaging.2004.09.022"},{"key":"e_1_2_7_11_1","doi-asserted-by":"publisher","DOI":"10.1038\/27094"},{"key":"e_1_2_7_12_1","doi-asserted-by":"publisher","DOI":"10.1083\/jcb.145.4.795"},{"key":"e_1_2_7_13_1","doi-asserted-by":"publisher","DOI":"10.1016\/j.bbabio.2009.02.021"},{"issue":"4","key":"e_1_2_7_14_1","doi-asserted-by":"crossref","first-page":"582","DOI":"10.1152\/jappl.1977.43.4.582","article-title":"Postcapillary changes in blood pH in\u00a0vivo during carbonic anhydrase inhibition","volume":"43","author":"Crandall E. 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