Interactions between chronic ethanol consumption and thiamine deficiency on neural plasticity spatial memory and cognitive flexibility

摘要

BackgroundMany 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) has emerged as a key factor underlying alcohol–related brain damage (ARBD). TD in humans can lead to Wernicke Encephalitis that can progress into Wernicke–Korsakoff Syndrome and these disorders have a high prevalence among alcoholics. Animal models are critical for determining the exact contributions of ethanol- and TD-induced neurotoxicity, as well as the interactions of those factors to brain and cognitive dysfunction.