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Amyloid beta\u2010peptide (1\u201342) [A\u03b2(1\u201342)], a major component of senile plaques, is neurotoxic and induces oxidative stress\n                      <jats:italic>in\u00a0vitro<\/jats:italic>\n                      and\n                      <jats:italic>in\u00a0vivo<\/jats:italic>\n                      . Redox proteomics has been used to identify proteins oxidatively modified by A\u03b2(1\u201342)\n                      <jats:italic>in\u00a0vitro<\/jats:italic>\n                      and\n                      <jats:italic>in\u00a0vivo<\/jats:italic>\n                      . In this review, we discuss these proteins in the context of those identified to be oxidatively modified in animal models of\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      , and human studies including familial\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      , pre\u2010clinical\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      (\n                      <jats:styled-content style=\"fixed-case\">PCAD<\/jats:styled-content>\n                      ), mild cognitive impairment (\n                      <jats:styled-content style=\"fixed-case\">MCI<\/jats:styled-content>\n                      ), early\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      , late\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      , Down syndrome (\n                      <jats:styled-content style=\"fixed-case\">DS<\/jats:styled-content>\n                      ), and\n                      <jats:styled-content style=\"fixed-case\">DS<\/jats:styled-content>\n                      with\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      (\n                      <jats:styled-content style=\"fixed-case\">DS<\/jats:styled-content>\n                      \/\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      ). These redox proteomics studies indicate that A\u03b2(1\u201342)\u2010mediated oxidative stress occurs early in\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      pathogenesis and results in altered antioxidant and cellular detoxification defenses, decreased energy yielding metabolism and mitochondrial dysfunction, excitotoxicity, loss of synaptic plasticity and cell structure, neuroinflammation, impaired protein folding and degradation, and altered signal transduction. Improved access to biomarker imaging and the identification of lifestyle interventions or treatments to reduce A\u03b2 production could be beneficial in preventing or delaying the progression of\n                      <jats:styled-content style=\"fixed-case\">AD<\/jats:styled-content>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:label\/>\n                    <jats:p>\n                      <jats:boxed-text content-type=\"graphic\" position=\"anchor\">\n                        <jats:graphic xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" mimetype=\"image\/png\" position=\"anchor\" specific-use=\"enlarged-web-image\" xlink:href=\"graphic\/jnc14589-fig-0007-m.png\">\n                          <jats:alt-text>image<\/jats:alt-text>\n                        <\/jats:graphic>\n                      <\/jats:boxed-text>\n                      <jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" xlink:href=\"http:\/\/onlinelibrary.wiley.com\/journal\/10.1111\/(ISSN)1471-4159\/homepage\/special_issues.htm\">This article is part of the special issue \"Proteomics\"<\/jats:ext-link>\n                      .\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/jnc.14589","type":"journal-article","created":{"date-parts":[[2018,9,16]],"date-time":"2018-09-16T00:59:14Z","timestamp":1537059554000},"page":"459-487","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":107,"title":["Redox proteomics and amyloid \u03b2\u2010peptide: insights into Alzheimer disease"],"prefix":"10.1111","volume":"151","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3254-5286","authenticated-orcid":false,"given":"D. 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