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Background  Wernicke's encephalopathy‐ K orsakoff syndrome ( WE ‐ KS ) is common in alcoholics, caused by thiamine deficiency ( TD ; vitamin  B 1) and associated with lesions to the thalamus ( THAL ). Although  TD  alone can cause  WE , the high incidence in alcoholism suggests that  TD  and ethanol (EtOH) interact.    Methods  Mice in control,  TD , or EtOH groups alone or combined were studied after 5 or 10 days of treatment. THAL and entorhinal cortex ( ENT ) histochemistry and  mRNA  were assessed.    Results  Combined EtOH‐ TD  treatment for 5 days (Et OH ‐ TD 5) showed activated microglia, proinflammatory gene induction and  THAL  neurodegeneration that was greater than that found with  TD  alone ( TD 5), whereas 10 days resulted in marked  THAL  degeneration and microglial‐neuroimmune activation in both groups. In contrast, 10 days of  TD  did not cause  ENT  degeneration. Interestingly, in  ENT ,  TD 10 activated microglia and astrocytes more than Et OH ‐ TD 10. In  THAL , multiple astrocytic markers were lost consistent with glial cell loss.  TD  blocks glucose metabolism more than acetate. Acetate derived from hepatic EtOH metabolism is transported by monocarboxylic acid transporters ( MCT ) into both neurons and astrocytes that use acetyl‐CoA synthetase (AcCo AS ) to generate cellular energy from acetate.  MCT  and AcCo AS  expression in  THAL  is lower than  ENT  prompting the hypothesis that focal  THAL  degeneration is related to insufficient  MCT  and AcCo AS  in  THAL . To test this hypothesis, we administered glycerin triacetate ( GTA ) to increase blood acetate and found it protected the  THAL  from  TD ‐induced degeneration.    Conclusions  Our findings suggest that Et OH  potentiates  TD ‐induced  THAL  degeneration through neuroimmune gene induction. The findings support the hypothesis that  TD  deficiency inhibits global glucose metabolism and that a reduced ability to process acetate for cellular energy results in  THAL  focal degeneration in alcoholics contributing to the high incidence of Wernicke‐Korsakoff syndrome in alcoholism.

alcoholism: clinical and experimental research

Focal Thalamic Degeneration from Ethanol and Thiamine Deficiency is Associated with Neuroimmune Gene Induction, Microglial Activation, and Lack of Monocarboxylic Acid Transporters