{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T02:52:43Z","timestamp":1790477563623,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2018,11,11]],"date-time":"2018-11-11T00:00:00Z","timestamp":1541894400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/501100008641","name":"Chung Shan Medical University","doi-asserted-by":"publisher","award":["NCHU\u2010CSMU\u201010503"],"award-info":[{"award-number":["NCHU\u2010CSMU\u201010503"]}],"id":[{"id":"10.13039\/501100008641","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004663","name":"Ministry of Science and Technology, Taiwan","doi-asserted-by":"publisher","award":["MOST 106\u20102320\u2010B\u2010040\u2010021\u2010MY3"],"award-info":[{"award-number":["MOST 106\u20102320\u2010B\u2010040\u2010021\u2010MY3"]}],"id":[{"id":"10.13039\/501100004663","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Journal Cellular Physiology"],"published-print":{"date-parts":[[2019,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p>Alzheimer's disease (AD) is one of the most prevalent neurodegenerative disorders. Its pathology is associated with the deposition of amyloid \u03b2 (A\u03b2), an abnormal extracellular peptide. Moreover, its pathological progression is closely accompanied by neuroinflammation. Specifically, A\u03b2\u2010associated microglial overactivation may have the central role in AD pathogenesis. Interestingly, arginine metabolism may contribute to the equilibrium between M1 and M2 microglia. However, little is known about the involvement of arginine metabolism in A\u03b2\u2010induced microglial neuroinflammation and neurotoxicity. Moreover, the underlying mechanism by which A\u03b2 induces the transition of microglia to the M1 phenotype remains unclear. In this study, we investigated the role of A\u03b2 in mediating microglial activation and polarization both in vitro and in vivo. Our results demonstrated that under the A\u03b2 treatment, ornithine decarboxylase (ODC), a rate\u2010limiting enzyme in the regulation of arginine catabolism, regulates microglial activation by altering the antizyme (AZ)\u2009+\u20091 ribosomal frameshift. Furthermore, the restoration of ODC protein expression levels has profound effects on inhibition of A\u03b2\u2010induced M1 markers and thus attenuates microglial\u2010mediated cytotoxicity. Altogether, our findings suggested that A\u03b2 may contribute to M1\u2010like activation by disrupting the balance between ODC and AZ in microglia.<\/jats:p>","DOI":"10.1002\/jcp.27659","type":"journal-article","created":{"date-parts":[[2018,11,12]],"date-time":"2018-11-12T06:13:27Z","timestamp":1542003207000},"page":"9733-9745","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":21,"title":["A\u03b2 stimulates microglial activation through antizyme\u2010dependent downregulation of ornithine decarboxylase"],"prefix":"10.1002","volume":"234","author":[{"given":"Yu\u2010Wen","family":"Cheng","sequence":"first","affiliation":[{"name":"Department of Internal Medicine Yuanli Lee's General Hospital, Lee's Medical Corporation Miaoli Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chun\u2010Cheng","family":"Chang","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine Dajia Lee's General 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