@article{HolzBuchmannBoeckerSchlieretal.2015,
  author    = {Holz, Nathalie E. and Buchmann, Arlette F. and Boecker-Schlier, Regina and Blomeyer, Dorothea and Baumeister, Sarah and Wolf, Isabella and Rietschel, Marcella and Witt, Stephanie H. and Plichta, Michael M. and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Role of FKBP5 in emotion processing: results on amygdala activity, connectivity and volume},
  series = {Brain structure \& function},
  volume    = {220},
  journal   = {Brain structure \& function},
  number    = {3},
  publisher = {Springer},
  address   = {Heidelberg},
  issn      = {1863-2653},
  doi       = {10.1007/s00429-014-0729-5},
  pages     = {1355 -- 1368},
  year      = {2015},
  abstract  = {Accumulating evidence suggests a role of FKBP5, a co-chaperone regulating the glucocorticoid receptor sensitivity, in the etiology of depression and anxiety disorders. Based on recent findings of altered amygdala activity following childhood adversity, the present study aimed at clarifying the impact of genetic variation in FKBP5 on threat-related neural activity and coupling as well as morphometric alterations in stress-sensitive brain systems. Functional magnetic resonance imaging during an emotional face-matching task was performed in 153 healthy young adults (66 males) from a high-risk community sample followed since birth. Voxel-based morphometry was applied to study structural alterations and DNA was genotyped for FKBP5 rs1360780. Childhood adversity was measured using retrospective self-report (Childhood Trauma Questionnaire) and by a standardized parent interview assessing childhood family adversity. Depression was assessed by the Beck Depression Inventory. There was a main effect of FKBP5 on the left amygdala, with T homozygotes showing the highest activity, largest volume and increased coupling with the left hippocampus and the orbitofrontal cortex (OFC). Moreover, amygdala-OFC coupling proved to be associated with depression in this genotype. In addition, our results support previous evidence of a gene-environment interaction on right amygdala activity with respect to retrospective assessment of childhood adversity, but clarify that this does not generalize to the prospective assessment. These findings indicated that activity in T homozygotes increased with the level of adversity, whereas the opposite pattern emerged in C homozygotes, with CT individuals being intermediate. The present results point to a functional involvement of FKBP5 in intermediate phenotypes associated with emotional processing, suggesting a possible mechanism for this gene in conferring susceptibility to stress-related disorders.},
  language  = {en}
}
@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{BenderBanaschewskiRoessneretal.2015,
  author    = {Bender, Stephan and Banaschewski, Tobias and R{\"o}ßner, Veit and Klein, Christoph and Rietschel, Marcella and Feige, Bernd and Brandeis, Daniel and Laucht, Manfred},
  title     = {Variability of single trial brain activation predicts fluctuations in reaction time},
  series = {Biological psychology},
  volume    = {106},
  journal   = {Biological psychology},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0301-0511},
  doi       = {10.1016/j.biopsycho.2015.01.013},
  pages     = {50 -- 60},
  year      = {2015},
  abstract  = {Brain activation stability is crucial to understanding attention lapses. EEG methods could provide excellent markers to assess neuronal response variability with respect to temporal (intertrial coherence) and spatial variability (topographic consistency) as well as variations in activation intensity (low frequency variability of single trial global field power). We calculated intertrial coherence, topographic consistency and low frequency amplitude variability during target P300 in a continuous performance test in 263 15-year-olds from a cohort with psychosocial and biological risk factors. Topographic consistency and low frequency amplitude variability predicted reaction time fluctuations (RTSD) in a linear model. Higher RTSD was only associated with higher psychosocial adversity in the presence of the homozygous 6R-10R dopamine transporter haplotype. We propose that topographic variability of single trial P300 reflects noise as well as variability in evoked cortical activation patterns. Dopaminergic neuromodulation interacted with environmental and biological risk factors to predict behavioural reaction time variability. (C) 2015 Elsevier B.V. All rights reserved.},
  language  = {en}
}