@article{BoeckerSchlierHolzBuchmannetal.2016,
  author    = {Boecker-Schlier, Regina and Holz, Nathalie E. and Buchmann, Arlette F. and Blomeyer, Dorothea and Plichta, Michael M. and Jennen-Steinmetz, Christine and Wolf, Isabella and Baumeister, Sarah and Treutleind, Jens and Rietschel, Marcella and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Interaction between COMT Val(158)Met polymorphism and childhood adversity affects reward processing in adulthood},
  series = {NeuroImage : a journal of brain function},
  volume    = {132},
  journal   = {NeuroImage : a journal of brain function},
  publisher = {Elsevier},
  address   = {San Diego},
  issn      = {1053-8119},
  doi       = {10.1016/j.neuroimage.2016.02.006},
  pages     = {556 -- 570},
  year      = {2016},
  abstract  = {Background: Accumulating evidence suggests that altered dopamine transmission may increase the risk of mental disorders such as ADHD, schizophrenia or depression, possibly mediated by reward system dysfunction. This study aimed to clarify the impact of the COMT Val(158)Met polymorphism in interaction with environmental variation (G x E) on neuronal activity during reward processing. Methods: 168 healthy young adults from a prospective study conducted over 25 years participated in amonetary incentive delay task measured with simultaneous EEG-fMRI. DNA was genotyped for COMT, and childhood family adversity (CFA) up to age 11 was assessed by a standardized parent interview. Results: At reward delivery, a G x E revealed that fMRI activation for win vs. no-win trials in reward-related regions increased with the level of CFA in Met homozygotes as compared to Val/Met heterozygotes and Val homozygotes, who showed no significant effect. During the anticipation of monetary vs. verbal rewards, activation decreased with the level of CFA, which was also observed for EEG, in which the CNV declined with the level of CFA. Conclusions: These results identify convergent genetic and environmental effects on reward processing in a prospective study. Moreover, G x E effects during reward delivery suggest that stress during childhood is associated with higher reward sensitivity and reduced efficiency in processing rewarding stimuli in genetically at-risk individuals. Together with previous evidence, these results begin to define a specific system mediating interacting effects of early environmental and genetic risk factors, which may be targeted by early intervention and prevention. (C) 2016 Elsevier Inc. All rights reserved.},
  language  = {en}
}
@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}
}