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@ARTICLE{Nieratschker:20790,
      author       = {Nieratschker, V. and Grosshans, M. and Frank, J. and
                      Strohmaier, J. and von der Goltz, C. and El-Maarri, O. and
                      Witt, S.H. and Cichon, S. and Nöthen, M.M. and Kiefer, F.
                      and Rietschel, M.},
      title        = {{E}pigenetic alteration of the dopamine transporter gene in
                      alcohol-dependent patients is associated with age},
      journal      = {Addiction biology},
      volume       = {19},
      number       = {2},
      issn         = {1355-6215},
      address      = {Hoboken, NJ [u.a.]},
      publisher    = {Wiley-Blackwell},
      reportid     = {PreJuSER-20790},
      pages        = {305–311},
      year         = {2014},
      note         = {Record converted from VDB: 12.11.2012},
      abstract     = {Chronic alcohol abuse and dependence are associated with
                      dysfunctional dopaminergic neurotransmission in
                      mesocorticolimbic circuits. Genetic and environmental
                      factors have been shown to modulate susceptibility to
                      alcohol dependence, and both may act through epigenetic
                      mechanisms that can modulate gene expression, e.g. DNA
                      methylation at CpG sites. Recent studies have suggested that
                      DNA methylation patterns may change over time. However, few
                      data are available concerning the rate of these changes in
                      specific genes. A recent study found that hypermethylation
                      of the promoter of the dopamine transporter (DAT) gene was
                      positively correlated with alcohol dependence and negatively
                      correlated with alcohol craving. The aim of the present
                      study was to replicate these findings in a larger sample of
                      alcohol-dependent patients and population-based controls
                      matched for age and sex. No difference in methylation level
                      was observed between patients and controls, and no
                      difference in methylation level was observed before and
                      after alcohol withdrawal in patients. However, patients with
                      more severe craving showed a trend towards lower DAT
                      methylation levels (P = 0.07), which is consistent with
                      previous findings. Furthermore, in our overall sample, DAT
                      methylation levels increased with age. Interestingly, a
                      separate analysis of patients suggested that this finding
                      was mainly driven by the patient group. Although the present
                      data do not clarify whether chronic alcohol abuse is
                      responsible for this phenomenon or merely enhances an
                      ageing-specific process, our findings suggest that
                      hypermethylation in alcohol-dependent patients is a
                      consequence, rather than a cause, of the disorder.},
      cin          = {INM-1},
      ddc          = {540},
      cid          = {I:(DE-Juel1)INM-1-20090406},
      pnm          = {Funktion und Dysfunktion des Nervensystems (FUEK409) /
                      89571 - Connectivity and Activity (POF2-89571)},
      pid          = {G:(DE-Juel1)FUEK409 / G:(DE-HGF)POF2-89571},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:22506971},
      UT           = {WOS:000331529100017},
      doi          = {10.1111/j.1369-1600.2012.00459.x},
      url          = {https://juser.fz-juelich.de/record/20790},
}