Alcohol and Alcoholism Advance Access originally published online on December 18, 2008
Alcohol and Alcoholism 2009 44(2):166-170; doi:10.1093/alcalc/agn101
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Molecular Genetics of Alcohol-Related Brain Damage
1 Bexley Substance Misuse Service, South London and Mausdley NHS Trust, London, UK
2 Molecular Psychiatry Laboratory, Research Department of Mental Health Sciences, Windeyer Institute of Medical Sciences, London Medical School, University College London, 46 Cleveland Street, London W1T 4JF, UK
* Corresponding author: Molecular Psychiatry Laboratory, Department of Mental Health Sciences, Windeyer Institute of Medical Sciences, University College London, 46 Cleveland Street, London W1T 4JF, UK. Tel: +44-1322-357940; Fax: +44-1322-357960; E-mail: i.guerrini{at}ucl.ac.uk
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Abstract |
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Aims: In the scientific literature it has been repeatedly hypothesized that there is a heritable susceptibility to thiamine deficiency comparable to other hereditary metabolic disorders. The aim of this paper is to review the most recent knowledge on the genetic susceptibility to the development of alcohol-related Wernicke–Korsakoff syndrome (WKS). Methods: A literature review was carried out looking at the molecular genetics studies performed in alcohol-dependent patients affected by WKS. Results: A genetic component in the pathogenesis of WKS has been postulated since the late seventies. Since then, very few genetic studies have been carried out on candidate genes such as thiamine-dependent enzymes, alcohol-metabolizing enzymes and GABA receptors. The findings are controversial and not conclusive. Several authors reported the important role of the thiamine transporters in the pathogenesis of the thiamine deficiency disorders. Our findings on SLC19A2 and SLC19A3 suggest a potential role of these two genes in the pathophysiology of alcohol-related thiamine deficiency but further studies need to be carried out. Conclusions: The WKS may be a very complex, multifactorial disorder where the interaction of multiple genes and environment plays an important role in the pathogenesis. However, it is still plausible that megaphenic gene effects are responsible for WKS susceptibility and the thiamine transport genes are good candidates for having such a role. Further genetic studies are definitely needed to investigate the association with candidate genes or linkage with hot spot areas.
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