{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,24]],"date-time":"2026-01-24T13:38:31Z","timestamp":1769261911929,"version":"3.49.0"},"reference-count":66,"publisher":"Wiley","issue":"12","license":[{"start":{"date-parts":[[2020,11,24]],"date-time":"2020-11-24T00:00:00Z","timestamp":1606176000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"DOI":"10.13039\/100000027","name":"National Institute on Alcohol Abuse and Alcoholism","doi-asserted-by":"publisher","award":["P50AA017823"],"award-info":[{"award-number":["P50AA017823"]}],"id":[{"id":"10.13039\/100000027","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/100000027","name":"National Institute on Alcohol Abuse and Alcoholism","doi-asserted-by":"publisher","award":["RO1AA021775"],"award-info":[{"award-number":["RO1AA021775"]}],"id":[{"id":"10.13039\/100000027","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Alcoholism Clin &amp;amp; Exp Res"],"published-print":{"date-parts":[[2020,12]]},"abstract":"<jats:sec><jats:title>Background<\/jats:title><jats:p>Long\u2010term alcohol consumption has been linked to structural and functional brain abnormalities. Furthermore, with persistent exposure to ethanol (EtOH), nutrient deficiencies often develop. Thiamine deficiency is a key contributor to alcohol\u2010related brain damage and is suspected to contribute to white matter pathology. The expression of genes encoding myelin proteins in several cortical brain regions is altered with EtOH exposure. However, there is limited research regarding the impact of thiamine deficiency on myelin dysfunction.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>A rat model was used to assess the impact of moderate chronic EtOH exposure (CET; 20% EtOH in drinking water for 1 or 6\u00a0months), pyrithiamine\u2010induced thiamine deficiency treatment (PTD), both conditions combined (CET\u2010PTD), or CET with thiamine injections (CET\u00a0+\u00a0T) on myelin\u2010related gene expression (Olig1, Olig2, MBP, MAG, and MOG) in the frontal and parietal cortices and the cerebellum.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>The CET\u2010PTD treatments caused the greatest suppression in myelin\u2010related genes in the cortex. Specifically, the parietal cortex was the region that was most susceptible to PTD\u2010CET\u2010induced alterations in myelin\u2010related genes. In addition, PTD treatment, with and without CET, caused minor fluctuations in the expression of several myelin\u2010related genes in the frontal cortex. In contrast, CET alone and PTD alone suppressed several myelin\u2010related genes in the cerebellum. Regardless of the region, there was significant recovery of myelin\u2010related genes with extended abstinence and\/or thiamine restoration.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusion<\/jats:title><jats:p>Moderate chronic EtOH alone had a minor effect on the suppression of myelin\u2010related genes in the cortex; however, when combined with thiamine deficiency, the reduction was amplified. There was a suppression of myelin\u2010related genes following long\u2010term EtOH and thiamine deficiency in the cerebellum. However, the suppression in the myelin\u2010related genes mostly occurred 24\u00a0h after EtOH removal or following thiamine restoration; within 3\u00a0weeks of abstinence or thiamine recovery, gene expression rebounded.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.14484","type":"journal-article","created":{"date-parts":[[2020,10,17]],"date-time":"2020-10-17T07:57:54Z","timestamp":1602921474000},"page":"2481-2493","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":9,"title":["The Effect of Chronic Ethanol Exposure and Thiamine Deficiency on Myelin\u2010related Genes in the Cortex and the Cerebellum"],"prefix":"10.1111","volume":"44","author":[{"given":"Bradley J.","family":"Chatterton","sequence":"first","affiliation":[{"name":"From the Department of Psychology Behavioral Neuroscience Program Binghamton University State University of New York  Binghamton New York 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