@article{HeinrichBuchmannZohseletal.2015,
  author    = {Heinrich, Angela and Buchmann, Arlette F. and Zohsel, Katrin and Dukal, Helene and Frank, Josef and Treutlein, Jens and Nieratschker, Vanessa and Witt, Stephanie H. and Brandeis, Daniel and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Laucht, Manfred and Rietschel, Marcella},
  title     = {Alterations of Glucocorticoid Receptor Gene Methylation in Externalizing Disorders During Childhood and Adolescence},
  series = {Behavior genetics : an international journal devoted to research in the inheritance of behavior in animals and man},
  volume    = {45},
  journal   = {Behavior genetics : an international journal devoted to research in the inheritance of behavior in animals and man},
  number    = {5},
  publisher = {Springer},
  address   = {New York},
  issn      = {0001-8244},
  doi       = {10.1007/s10519-015-9721-y},
  pages     = {529 -- 536},
  year      = {2015},
  abstract  = {Epigenetic modulations are a hypothesized link between environmental factors and the development of psychiatric disorders. Research has suggested that patients with depression or bipolar disorder exhibit higher methylation levels in the glucocorticoid receptor gene NR3C1. We aimed to investigate whether NR3C1 methylation changes are similarly associated with externalizing disorders such as aggressive behavior and conduct disorder. NR3C1 exon 1F methylation was analyzed in young adults with a lifetime diagnosis of an externalizing disorder (N = 68) or a depressive disorder (N = 27) and healthy controls (N = 124) from the Mannheim Study of Children at Risk. The externalizing disorders group had significantly lower NR3C1 methylation levels than the lifetime depressive disorder group (p = 0.009) and healthy controls (p = 0.001) This report of lower methylation levels in NR3C1 in externalizing disorders may indicate a mechanism through which the differential development of externalizing disorders as opposed to depressive disorders might occur.},
  language  = {en}
}
@article{HohmannHohmTreutleinetal.2015,
  author    = {Hohmann, Sarah and Hohm, Erika and Treutlein, Jens and Blomeyer, Dorothea and Jennen-Steinmetz, Christine and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Association of norepinephrine transporter (NET, SLC6A2) genotype with ADHD-related phenotypes: Findings of a longitudinal study from birth to adolescence},
  series = {Psychiatry research : the official publication of the International Society for Neuroimaging in Psychiatry},
  volume    = {226},
  journal   = {Psychiatry research : the official publication of the International Society for Neuroimaging in Psychiatry},
  number    = {2-3},
  publisher = {Elsevier},
  address   = {Clare},
  issn      = {0165-1781},
  doi       = {10.1016/j.psychres.2014.12.029},
  pages     = {425 -- 433},
  year      = {2015},
  abstract  = {Variation in the gene encoding for the norepinephrine transporter (NET, SLC6A2) has repeatedly been linked with ADHD, although there is some inconsistency regarding the association with specific genes. The variants for which most consistent association has been found are the NET variants rs3785157 and rs28386840. Here, we tested for their association with ADHD diagnosis and ADHD-related phenotypes during development in a longitudinal German community sample. Children were followed from age 4 to age 15, using diagnostic interviews to assess ADHD. Between the ages of 8 and 15 years, the Child Behavior Checklist (CBCL) was administered to the primary caregivers. The continuous performance task (CPT) was performed at age 15. Controlling for possible confounders, we found that homozygous carriers of the major A allele of the functional promoter variant rs28386840 displayed a higher rate of ADHD lifetime diagnosis. Moreover, homozygous carriers of the minor T allele of rs3785157 were more likely to develop ADHD and showed higher scores on the CBCL externalizing behavior scales. Additionally, we found that individuals heterozygous for rs3785157 made fewer omission errors in the CPT than homozygotes. This is the first longitudinal study to report associations between specific NET variants and ADHD-related phenotypes during the course of development. (C) 2015 Elsevier Ireland Ltd. All rights reserved.},
  language  = {en}
}