TY  - JOUR
A1  - Boecker-Schlier, Regina
A1  - Holz, Nathalie E.
A1  - Buchmann, Arlette F.
A1  - Blomeyer, Dorothea
A1  - Plichta, Michael M.
A1  - Jennen-Steinmetz, Christine
A1  - Wolf, Isabella
A1  - Baumeister, Sarah
A1  - Treutleind, Jens
A1  - Rietschel, Marcella
A1  - Meyer-Lindenberg, Andreas
A1  - Banaschewski, Tobias
A1  - Brandeis, Daniel
A1  - Laucht, Manfred
T1  - Interaction between COMT Val(158)Met polymorphism and childhood adversity affects reward processing in adulthood
JF  - NeuroImage : a journal of brain function
N2  - 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.
KW  - Reward processing
KW  - COMT Val(158)Met polymorphism
KW  - Childhood adversity
KW  - Gene-environment interaction
KW  - Functional magnetic resonance imaging
KW  - Electroencephalography
Y1  - 2016
U6  - https://doi.org/10.1016/j.neuroimage.2016.02.006
SN  - 1053-8119
SN  - 1095-9572
VL  - 132
SP  - 556
EP  - 570
PB  - Elsevier
CY  - San Diego
ER  - 
TY  - JOUR
A1  - Laucht, Manfred
A1  - Treutlein, Jens
A1  - Blomeyer, Dorothea
A1  - Buchmann, Arlette F.
A1  - Schmidt, Martin H.
A1  - Esser, Günter
A1  - Jennen-Steinmetz, Christine
A1  - Rietschel, Marcella
A1  - Banaschewski, Tobias
T1  - Interactive effects of corticotropin-releasing hormone receptor 1 gene and childhood adversity on depressive symptoms in young adults findings from a longitudinal study
JF  - European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology
N2  - Accumulating research suggests a moderating role for the corticotropin-releasing hormone receptor 1 gene (CRHR1) in the association between childhood adversity and adult depression. The present study aims to replicate recent findings using different genetic variants and measures of early adversity assessed both prospectively and retrospectively. Data were collected in the context of an ongoing epidemiological cohort study following the outcome of early risk factors from birth into adulthood. 300 participants (137 males, 163 females) were genotyped for four CRHR1 SNPs (rs7209436, rs110402, rs242924, and rs17689882) and completed the Beck Depression Inventory at ages 19, 22 and 23 years. Childhood adversity was assessed using the Childhood Trauma Questionnaire and by a standardized parent interview yielding an index of family adversity. Our results indicate that CRHR1 and childhood adversity interacted to predict depressive symptoms in young adults. Specifically, we found that the impact of childhood maltreatment on adult depressive symptoms was significantly higher in individuals (i) with two copies of the CRHR1 TAT haplotype, and (ii) homozygous for the G allele of rs17689882. The interaction was demonstrated for exposure to childhood maltreatment as assessed by retrospective self-report, but not to prospectively ascertain objective family adversity. The present study partially replicates recent findings of a CRHR1 by childhood adversity interaction with regard to adult depression highlighting the subjective characteristics of the environmental pathogen that is operative in this interaction.
KW  - Corticotropin-releasing hormone receptor 1 gene
KW  - Depression
KW  - Maltreatment
KW  - Family adversity
KW  - Young adults
KW  - Gene-environment interaction
Y1  - 2013
U6  - https://doi.org/10.1016/j.euroneuro.2012.06.002
SN  - 0924-977X
VL  - 23
IS  - 5
SP  - 358
EP  - 367
PB  - Elsevier
CY  - Amsterdam
ER  -