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The current studies determine the effect of an in vivo methionine sulfoxidation of A\u03b2 through ablation of the methionine sulfoxide reductase A (MsrA) in a mouse model of AD, a mouse that overexpresses amyloid precursor protein (APP) and A\u03b2 in neurons. Lack of MsrA fosters the formation of methionine sulfoxide in proteins, and thus its ablation in the AD-mouse model will increase the formation of methionine sulfoxide in A\u03b2. Indeed, the novel MsrA-deficient APP mice ( APP<jats:sup>+<\/jats:sup>\/ MsrAKO) exhibited higher levels of soluble A\u03b2 in brain compared with APP<jats:sup>+<\/jats:sup> mice. Furthermore, mitochondrial respiration and the activity of cytochrome c oxidase were compromised in the APP<jats:sup>+<\/jats:sup>\/ MsrAKO compared with control mice. These results suggest that lower MsrA activity modifies A\u03b2 solubility properties and causes mitochondrial dysfunction, and augmenting its activity may be beneficial in delaying AD progression. <\/jats:p>","DOI":"10.1152\/ajpendo.00453.2015","type":"journal-article","created":{"date-parts":[[2016,1,19]],"date-time":"2016-01-19T23:54:24Z","timestamp":1453247664000},"page":"E388-E393","source":"Crossref","is-referenced-by-count":37,"title":["Methionine sulfoxide reductase A affects \u03b2-amyloid solubility and mitochondrial function in a mouse model of Alzheimer's disease"],"prefix":"10.1152","volume":"310","author":[{"given":"Jackob","family":"Moskovitz","sequence":"first","affiliation":[{"name":"Department of Pharmacology and Toxicology, School of Pharmacy, University of Kansas, Lawrence, Kansas"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fang","family":"Du","sequence":"additional","affiliation":[{"name":"Department of Pharmacology and Toxicology, School of 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