{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T22:01:48Z","timestamp":1790373708121,"version":"4.1.0"},"reference-count":50,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2015,9,30]],"date-time":"2015-09-30T00:00:00Z","timestamp":1443571200000},"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":["RO1AA021775"],"award-info":[{"award-number":["RO1AA021775"]}],"id":[{"id":"10.13039\/100000027","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Alcoholism Clin &amp; Exp Res"],"published-print":{"date-parts":[[2015,11]]},"abstract":"Background<\/jats:title>Many alcoholics display moderate to severe cognitive dysfunction accompanied by brain pathology. A factor confounded with prolonged heavy alcohol consumption is poor nutrition, and many alcoholics are thiamine deficient. Thus, thiamine deficiency (TD<\/jats:styled-content>) has emerged as a key factor underlying alcohol\u2010related brain damage (ARBD<\/jats:styled-content>). TD<\/jats:styled-content> in humans can lead to Wernicke Encephalitis that can progress into Wernicke\u2013Korsakoff syndrome and these disorders have a high prevalence among alcoholics. Animal models are critical for determining the exact contributions of ethanol (EtOH)\u2010 and TD<\/jats:styled-content>\u2010induced neurotoxicity, as well as the interactions of those factors to brain and cognitive dysfunction.<\/jats:p><\/jats:sec>Methods<\/jats:title>Adult rats were randomly assigned to 1 of 6 treatment conditions: chronic EtOH treatment (CET<\/jats:styled-content>) where rats consumed a 20% v\/v solution of EtOH over 6\u00a0months; severe pyrithiamine\u2010induced TD<\/jats:styled-content> (PTD<\/jats:styled-content>\u2010moderate acute stage); moderate PTD<\/jats:styled-content> (PTD<\/jats:styled-content>\u2010early acute stage); moderate PTD<\/jats:styled-content> followed by CET<\/jats:styled-content> (PTD<\/jats:styled-content>\u2010CET<\/jats:styled-content>); moderate PTD<\/jats:styled-content> during CET<\/jats:styled-content> (CET<\/jats:styled-content>\u2010PTD<\/jats:styled-content>); and pair\u2010fed (PF) control. After recovery from treatment, all rats were tested on spontaneous alternation and attentional set\u2010shifting. After behavioral testing, brains were harvested for determination of mature brain\u2010derived neurotrophic factor (BDNF<\/jats:styled-content>) and thalamic pathology.<\/jats:p><\/jats:sec>Results<\/jats:title>Moderate TD<\/jats:styled-content> combined with CET<\/jats:styled-content>, regardless of treatment order, produced significant impairments in spatial memory, cognitive flexibility, and reductions in brain plasticity as measured by BDNF<\/jats:styled-content> levels in the frontal cortex and hippocampus. These alterations are greater than those seen in moderate TD<\/jats:styled-content> alone, and the synergistic effects of moderate TD<\/jats:styled-content> with CET<\/jats:styled-content> lead to a unique cognitive profile. However, CET<\/jats:styled-content> did not exacerbate thalamic pathology seen after moderate TD<\/jats:styled-content>.<\/jats:p><\/jats:sec>Conclusions<\/jats:title>These data support the emerging theory that subclinical TD<\/jats:styled-content> during chronic heavy alcohol consumption is critical for the development of significant cognitive impairment associated with ARBD<\/jats:styled-content>.<\/jats:p><\/jats:sec>","DOI":"10.1111\/acer.12859","type":"journal-article","created":{"date-parts":[[2015,9,30]],"date-time":"2015-09-30T06:12:18Z","timestamp":1443593538000},"page":"2143-2153","source":"Crossref","is-referenced-by-count":60,"title":["Interactions Between Chronic Ethanol Consumption and Thiamine Deficiency on Neural Plasticity, Spatial Memory, and Cognitive Flexibility"],"prefix":"10.1111","volume":"39","author":[{"given":"Lindsey C.","family":"Vedder","sequence":"first","affiliation":[{"name":"Department of Psychology Behavioral Neuroscience Program Binghamton University 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