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Here, we found that amyloid (A)\u2010\u03b2 treatment downregulated brain and muscle aryl hydrocarbon receptor nuclear translocator\u2010like (BMAL) 1 through the hypermethylation of its promoter region in HT22 cells and that the inhibition of DNA methylation ameliorated circadian rhythm disorders and restored BMAL1 protein expression by reversing its hypermethylation in APPswe\/PSEN1dE9 (APP\/PS1) mice. Critically, increased levels of interleukin (IL)\u201017A contributed to BMAL1 downregulation through the hypermethylation of its promoter region, thus leading to circadian disruptions in APP\/PS1 mice. Moreover, we revealed that the mitogen\u2010activated protein kinase (MAPK) pathway was responsible for IL\u201017A\u2010induced DNA methyltransferase (DNMT) 1 upregulation. Taken together, we elucidate a new mechanism connecting IL\u201017A with altered DNA methylation of\n                    <jats:italic>Bmal1<\/jats:italic>\n                    , which results in circadian disturbances in an AD mouse model.\n                  <\/jats:p>","DOI":"10.1111\/jcmm.70546","type":"journal-article","created":{"date-parts":[[2025,4,10]],"date-time":"2025-04-10T10:02:07Z","timestamp":1744279327000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":5,"title":["<scp>IL<\/scp>\n                    \u2010\n                    <scp>17A<\/scp>\n                    Induces Circadian Disruptions Through the Epigenetic Repression of\n                    <scp>BMAL1<\/scp>\n                    in Mice With Alzheimer's 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