{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,29]],"date-time":"2026-09-29T12:03:15Z","timestamp":1790683395758,"version":"4.1.0"},"reference-count":42,"publisher":"National Academy of Sciences","issue":"13","content-domain":{"domain":["www.pnas.org"],"crossmark-restriction":true},"short-container-title":["Proc. Natl. Acad. Sci. U.S.A."],"published-print":{"date-parts":[[2014,4]]},"abstract":"<jats:title>Significance<\/jats:title>\n                  <jats:p>\n                    Suppression of NAD\n                    <jats:sup>+<\/jats:sup>\n                    -dependent sirtuin 1 (SIRT1) is linked to dementia or Alzheimer\u2019s disease (AD) and the metabolic syndrome (MS). Because advanced glycation end products (AGEs) promote MS and neurotoxicity, we conducted studies of C57BL6 mice fed isocaloric diets containing defined AGEs [methyl-glyoxal derivatives (MG)] to determine whether food AGEs promote AD and MS. MG\n                    <jats:sup>+<\/jats:sup>\n                    -fed, but not MG\n                    <jats:sup>\u2212<\/jats:sup>\n                    -fed, mice developed brain SIRT1 deficiency, amyloid-\u03b2 deposits, cognitive and motor deficits, and MS. These findings were validated in older healthy humans with high baseline circulating MG levels by a time-dependent decline in cognition and insulin sensitivity. The data suggest that food-derived AGEs, an environmental factor, contribute to both AD and MS by causing chronic SIRT1 suppression. Importantly, reduction of food-derived AGEs is feasible and may provide an effective treatment strategy for both these epidemics.\n                  <\/jats:p>","DOI":"10.1073\/pnas.1316013111","type":"journal-article","created":{"date-parts":[[2014,2,24]],"date-time":"2014-02-24T21:44:15Z","timestamp":1393278255000},"page":"4940-4945","update-policy":"https:\/\/doi.org\/10.1073\/pnas.cm10313","source":"Crossref","is-referenced-by-count":151,"title":["Oral glycotoxins are a modifiable cause of dementia and the metabolic syndrome in mice and humans"],"prefix":"10.1073","volume":"111","author":[{"given":"Weijing","family":"Cai","sequence":"first","affiliation":[{"name":"Department of aGeriatrics, Division of Experimental Diabetes,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jaime","family":"Uribarri","sequence":"additional","affiliation":[{"name":"Medicine,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Li","family":"Zhu","sequence":"additional","affiliation":[{"name":"Department of aGeriatrics, Division of Experimental Diabetes,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Xue","family":"Chen","sequence":"additional","affiliation":[{"name":"Department of aGeriatrics, Division of Experimental Diabetes,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Shobha","family":"Swamy","sequence":"additional","affiliation":[{"name":"Department of aGeriatrics, Division of Experimental Diabetes,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhengshan","family":"Zhao","sequence":"additional","affiliation":[{"name":"Department of aGeriatrics, Division of Experimental Diabetes,"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Fabrizio","family":"Grosjean","sequence":"additional","affiliation":[{"name":"Department of aGeriatrics, Division of Experimental Diabetes,"},{"name":"Division of Nephrology, Department of Medicine, University of Pavia, 27100 Pavia, Italy;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Calogera","family":"Simonaro","sequence":"additional","affiliation":[{"name":"Human Genetics, and"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"George A.","family":"Kuchel","sequence":"additional","affiliation":[{"name":"Division of Nephrology, Department of Medicine, University of Pavia, 27100 Pavia, Italy;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Michal","family":"Schnaider-Beeri","sequence":"additional","affiliation":[{"name":"Psychiatry, The Icahn School of Medicine at Mount Sinai, New York, NY 10029;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark","family":"Woodward","sequence":"additional","affiliation":[{"name":"UConn Center on Aging, University of Connecticut Health Center, CT 06030; 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