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Recent studies in patients and mouse models suggest a putative link between hyperphosphorylated tau, a component of Alzheimer's disease\u2010related dementia (ADRD) pathology, and cerebral glucose hypometabolism. Impaired glucose metabolism reduces glucose flux through the hexosamine metabolic pathway triggering attenuated O\u2010linked N\u2010acetylglucosamine (O\u2010GlcNAc) protein modification. The goal of the current study was to investigate the link between cognitive function, tau pathology, and O\u2010GlcNAc signaling in an aging mouse model of MetS, agouti KKAy\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    . Male and female C57BL\/6, non\u2010agouti KKAy\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    , and agouti KKAy\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice were aged 12\u201318\u2009months on standard chow diet. Body weight, blood glucose, total cholesterol, and triglyceride were measured to confirm the MetS phenotype. Cognition, sensorimotor function, and emotional reactivity were assessed for each genotype followed by plasma and brain tissue collection for biochemical and molecular analyses. Body weight, blood glucose, total cholesterol, and triglyceride levels were significantly elevated in agouti KKAy\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice versus C57BL\/6 controls and non\u2010agouti KKAy\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    . Behaviorally, agouti KKAy\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    revealed impairments in sensorimotor and cognitive function versus age\u2010matched C57BL\/6 and non\u2010agouti KKAy\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice. Immunoblotting demonstrated increased phosphorylated tau accompanied with reduced O\u2010GlcNAc protein expression in hippocampal\u2010associated dorsal midbrain of female agouti KKAy\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    versus C57BL\/6 control mice. Together, these data demonstrate that impaired cognitive function and AD\u2010related pathology are associated with reduced O\u2010GlcNAc signaling in aging MetS KKAy\n                    <jats:sup>+\/\u2212<\/jats:sup>\n                    mice. Overall, our study suggests that interaction of tau pathology with O\u2010GlcNAc signaling may contribute to MetS\u2010induced cognitive dysfunction in aging.\n                  <\/jats:p>","DOI":"10.1002\/jnr.25196","type":"journal-article","created":{"date-parts":[[2023,4,9]],"date-time":"2023-04-09T14:29:20Z","timestamp":1681050560000},"page":"1324-1344","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":8,"title":["Cognitive dysfunction and increased phosphorylated tau are associated with reduced\n                    <scp>O\u2010GlcNAc<\/scp>\n                    signaling in an aging mouse model of metabolic syndrome"],"prefix":"10.1002","volume":"101","author":[{"given":"Shreya","family":"Gupta","sequence":"first","affiliation":[{"name":"Department of Integrative Medical Sciences Northeast Ohio Medical University  Rootstown Ohio USA"},{"name":"Biomedical Sciences Graduate Program Kent State University  Kent Ohio USA"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sanjay K. 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