TY - JOUR A1 - Holz, Nathalie E. A1 - Boecker-Schlier, Regina A1 - Buchmann, Arlette F. A1 - Blomeyer, Dorothea A1 - Jennen-Steinmetz, Christine A1 - Baumeister, Sarah A1 - Plichta, Michael M. A1 - Cattrell, Anna A1 - Schumann, Gunter A1 - Esser, Günter A1 - Schmidt, Martin A1 - Buitelaar, Jan A1 - Meyer-Lindenberg, Andreas A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Laucht, Manfred T1 - Ventral striatum and amygdala activity as convergence sites for early adversity and conduct disorder JF - Frontiers in human neuroscience N2 - Childhood family adversity (CFA) increases the risk for conduct disorder (CD) and has been associated with alterations in regions of affective processing like ventral striatum (VS) and amygdala. However, no study so far has demonstrated neural converging effects of CFA and CD in the same sample. At age 25 years, functional MRI data during two affective tasks, i.e. a reward (N = 171) and a face-matching paradigm (N = 181) and anatomical scans (N = 181) were acquired in right-handed currently healthy participants of an epidemiological study followed since birth. CFA during childhood was determined using a standardized parent interview. Disruptive behaviors and CD diagnoses during childhood and adolescence were obtained by diagnostic interview (2–19 years), temperamental reward dependence was assessed by questionnaire (15 and 19 years). CFA predicted increased CD and amygdala volume. Both exposure to CFA and CD were associated with a decreased VS response during reward anticipation and blunted amygdala activity during face-matching. CD mediated the effect of CFA on brain activity. Temperamental reward dependence was negatively correlated with CFA and CD and positively with VS activity. These findings underline the detrimental effects of CFA on the offspring's affective processing and support the importance of early postnatal intervention programs aiming to reduce childhood adversity factors. KW - childhood adversity KW - conduct disorder KW - amygdala KW - ventral striatum KW - fMRI Y1 - 2016 U6 - https://doi.org/10.1093/scan/nsw120 SN - 1749-5016 SN - 1749-5024 VL - 12 IS - 2 SP - 261 EP - 272 PB - Oxford Univ. Press CY - Oxford ER - TY - JOUR A1 - Holz, Nathalie E. A1 - Boecker-Schlier, Regina A1 - Hohm, Erika A1 - Zohsel, Katrin A1 - Buchmann, Arlette F. A1 - Blomeyer, Dorothea A1 - Jennen-Steinmetz, Christine A1 - Baumeister, Sarah A1 - Hohmann, Sarah A1 - Wolf, Isabella A1 - Plichta, Michael M. A1 - Esser, Günter A1 - Schmidt, Martin A1 - Meyer-Lindenberg, Andreas A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Laucht, Manfred T1 - The Long-Term Impact of Early Life Poverty on Orbitofrontal Cortex Volume in Adulthood: Results from a Prospective Study Over 25 Years JF - Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology N2 - Converging evidence has highlighted the association between poverty and conduct disorder (CD) without specifying neurobiological pathways. Neuroimaging research has emphasized structural and functional alterations in the orbitofrontal cortex (OFC) as one key mechanism underlying this disorder. The present study aimed to clarify the long-term influence of early poverty on OFC volume and its association with CD symptoms in healthy participants of an epidemiological cohort study followed since birth. At age 25 years, voxel-based morphometry was applied to study brain volume differences. Poverty (0 = non-exposed (N = 134), I = exposed (N = 33)) and smoking during pregnancy were determined using a standardized parent interview, and information on maternal responsiveness was derived from videotaped mother infant interactions at the age of 3 months. CD symptoms were assessed by diagnostic interview from 8 to 19 years of age. Information on life stress was acquired at each assessment and childhood maltreatment was measured using retrospective self-report at the age of 23 years. Analyses were adjusted for sex, parental psychopathology and delinquency, obstetric adversity, parental education, and current poverty. Individuals exposed to early life poverty exhibited a lower OFC volume. Moreover, we replicated previous findings of increased CD symptoms as a consequence of childhood poverty. This effect proved statistically mediated by OFC volume and exposure to life stress and smoking during pregnancy, but not by childhood maltreatment and maternal responsiveness. These findings underline the importance of studying the impact of early life adversity on brain alterations and highlight the need for programs to decrease income-related disparities. Y1 - 2015 U6 - https://doi.org/10.1038/npp.2014.277 SN - 0893-133X SN - 1740-634X VL - 40 IS - 4 SP - 996 EP - 1004 PB - Nature Publ. Group CY - London ER - TY - JOUR A1 - Ihle, Wolfgang A1 - Esser, Günter A1 - Boeck, K. A1 - Fischer, Andreas W. A1 - Schmidt, Martin H. T1 - Maladaptive coping strategies : antecedents, correlates or consequences of mental disorders? Y1 - 1999 ER - TY - JOUR A1 - Hohmann, Sarah A1 - Zohsel, Katrin A1 - Buchmann, Arlette F. A1 - Blomeyer, Dorothea A1 - Holz, Nathalie A1 - Boecker-Schlier, Regina A1 - Jennen-Steinmetz, Christine A1 - Rietschel, Marcella A1 - Witt, Stephanie H. A1 - Schmidt, Martin H. A1 - Esser, Günter A1 - Meyer-Lindenberg, Andreas A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Hohm, Erika A1 - Laucht, Manfred T1 - Interacting effect of MAOA genotype and maternal prenatal smoking on aggressive behavior in young adulthood JF - Journal of neural transmission N2 - Findings on the etiology of aggressive behavior have provided evidence for an effect both of genetic factors, such as variation in the monoamine oxidase A (MAOA) gene, and adverse environmental factors. Recent studies have supported the existence of gene × environment interactions, with early experiences playing a key role. In the present study, the effects of prenatal nicotine exposure, MAOA genotype and their interaction on aggressive behavior during young adulthood were examined. In a sample of 272 young adults (129 males, 143 females) from an epidemiological cohort study, smoking during pregnancy was measured with a standardized parent interview at the offspring’s age of 3 months. Aggressive behavior was assessed between the ages of 19 and 25 years using the Young Adult Self-Report. DNA was genotyped for the MAOA 5′ untranslated region variable number of tandem repeats polymorphism (VNTR). Results revealed a significant interaction between MAOA and smoking during pregnancy, indicating higher levels of aggressive behavior in young adults carrying the MAOA low-expressing genotype who had experienced prenatal nicotine exposure (n = 8, p = .025). In contrast, in carriers of the MAOA high-expressing genotype, maternal smoking during pregnancy had no effect on aggressive behavior during young adulthood (n = 20, p = .145). This study extends earlier findings demonstrating an interaction between MAOA genotype and prenatal nicotine exposure on aggressive behavior into young adulthood. The results point to the long-term adverse effects of smoking during pregnancy on the offspring’s mental health, possibly underlining the importance of smoking cessation during pregnancy. According to the nature of the study (particularly sample size and power), analyses are exploratory and results need to be interpreted cautiously. KW - MAOA KW - Smoking during pregnancy KW - Interaction KW - Aggression KW - Longitudinal KW - Young adulthood Y1 - 2016 U6 - https://doi.org/10.1007/s00702-016-1582-x SN - 0300-9564 SN - 1435-1463 VL - 123 SP - 885 EP - 894 PB - Springer CY - Wien ER - TY - JOUR A1 - Holz, Nathalie A1 - Boecker-Schlier, Regina A1 - Buchmann, Arlette F. A1 - Blomeyer, Dorothea A1 - Baumeister, Sarah A1 - Hohmann, Sarah A1 - Jennen-Steinmetz, Christine A1 - Wolf, Isabella A1 - Rietschel, Marcella A1 - Witt, Stephanie H. A1 - Plichta, Michael M. A1 - Meyer-Lindenberg, Andreas A1 - Schmidt, Martin H. A1 - Esser, Günter A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Laucht, Manfred T1 - Evidence for a Sex-Dependent MAOAx Childhood Stress Interaction in the Neural Circuitry of Aggression JF - Cerebral cortex N2 - Converging evidence emphasizes the role of an interaction between monoamine oxidase A (MAOA) genotype, environmental adversity, and sex in the pathophysiology of aggression. The present study aimed to clarify the impact of this interaction on neural activity in aggression-related brain systems. Functional magnetic resonance imaging was performed in 125 healthy adults from a high-risk community sample followed since birth. DNA was genotyped for the MAOA-VNTR (variable number of tandem repeats). Exposure to childhood life stress (CLS) between the ages of 4 and 11 years was assessed using a standardized parent interview, aggression by the Youth/Young Adult Self-Report between the ages of 15 and 25 years, and the VIRA-R (Vragenlijst Instrumentele En Reactieve Agressie) at the age of 15 years. Significant interactions were obtained between MAOA genotype, CLS, and sex relating to amygdala, hippocampus, and anterior cingulate cortex (ACC) response, respectively. Activity in the amygdala and hippocampus during emotional face-matching increased with the level of CLS in male MAOA-L, while decreasing in male MAOA-H, with the reverse pattern present in females. Findings in the opposite direction in the ACC during a flanker NoGo task suggested that increased emotional activity coincided with decreased inhibitory control. Moreover, increasing amygdala activity was associated with higher Y(A)SR aggression in male MAOA-L and female MAOA-H carriers. Likewise, a significant association between amygdala activity and reactive aggression was detected in female MAOA-H carriers. The results point to a moderating role of sex in the MAOAx CLS interaction for intermediate phenotypes of emotional and inhibitory processing, suggesting a possible mechanism in conferring susceptibility to violence-related disorders. KW - aggression KW - amygdala KW - fMRI KW - life stress KW - MAOA Y1 - 2016 U6 - https://doi.org/10.1093/cercor/bhu249 SN - 1047-3211 SN - 1460-2199 VL - 26 SP - 904 EP - 914 PB - Oxford Univ. Press CY - Cary ER - TY - JOUR A1 - Aarts, Alexander A. A1 - Anderson, Joanna E. A1 - Anderson, Christopher J. A1 - Attridge, Peter R. A1 - Attwood, Angela A1 - Axt, Jordan A1 - Babel, Molly A1 - Bahnik, Stepan A1 - Baranski, Erica A1 - Barnett-Cowan, Michael A1 - Bartmess, Elizabeth A1 - Beer, Jennifer A1 - Bell, Raoul A1 - Bentley, Heather A1 - Beyan, Leah A1 - Binion, Grace A1 - Borsboom, Denny A1 - Bosch, Annick A1 - Bosco, Frank A. A1 - Bowman, Sara D. A1 - Brandt, Mark J. A1 - Braswell, Erin A1 - Brohmer, Hilmar A1 - Brown, Benjamin T. A1 - Brown, Kristina A1 - Bruening, Jovita A1 - Calhoun-Sauls, Ann A1 - Callahan, Shannon P. A1 - Chagnon, Elizabeth A1 - Chandler, Jesse A1 - Chartier, Christopher R. A1 - Cheung, Felix A1 - Christopherson, Cody D. A1 - Cillessen, Linda A1 - Clay, Russ A1 - Cleary, Hayley A1 - Cloud, Mark D. A1 - Cohn, Michael A1 - Cohoon, Johanna A1 - Columbus, Simon A1 - Cordes, Andreas A1 - Costantini, Giulio A1 - Alvarez, Leslie D. Cramblet A1 - Cremata, Ed A1 - Crusius, Jan A1 - DeCoster, Jamie A1 - DeGaetano, Michelle A. A1 - Della Penna, Nicolas A1 - den Bezemer, Bobby A1 - Deserno, Marie K. A1 - Devitt, Olivia A1 - Dewitte, Laura A1 - Dobolyi, David G. A1 - Dodson, Geneva T. A1 - Donnellan, M. Brent A1 - Donohue, Ryan A1 - Dore, Rebecca A. A1 - Dorrough, Angela A1 - Dreber, Anna A1 - Dugas, Michelle A1 - Dunn, Elizabeth W. A1 - Easey, Kayleigh A1 - Eboigbe, Sylvia A1 - Eggleston, Casey A1 - Embley, Jo A1 - Epskamp, Sacha A1 - Errington, Timothy M. A1 - Estel, Vivien A1 - Farach, Frank J. A1 - Feather, Jenelle A1 - Fedor, Anna A1 - Fernandez-Castilla, Belen A1 - Fiedler, Susann A1 - Field, James G. A1 - Fitneva, Stanka A. A1 - Flagan, Taru A1 - Forest, Amanda L. A1 - Forsell, Eskil A1 - Foster, Joshua D. A1 - Frank, Michael C. A1 - Frazier, Rebecca S. A1 - Fuchs, Heather A1 - Gable, Philip A1 - Galak, Jeff A1 - Galliani, Elisa Maria A1 - Gampa, Anup A1 - Garcia, Sara A1 - Gazarian, Douglas A1 - Gilbert, Elizabeth A1 - Giner-Sorolla, Roger A1 - Glöckner, Andreas A1 - Göllner, Lars A1 - Goh, Jin X. A1 - Goldberg, Rebecca A1 - Goodbourn, Patrick T. A1 - Gordon-McKeon, Shauna A1 - Gorges, Bryan A1 - Gorges, Jessie A1 - Goss, Justin A1 - Graham, Jesse A1 - Grange, James A. A1 - Gray, Jeremy A1 - Hartgerink, Chris A1 - Hartshorne, Joshua A1 - Hasselman, Fred A1 - Hayes, Timothy A1 - Heikensten, Emma A1 - Henninger, Felix A1 - Hodsoll, John A1 - Holubar, Taylor A1 - Hoogendoorn, Gea A1 - Humphries, Denise J. A1 - Hung, Cathy O. -Y. A1 - Immelman, Nathali A1 - Irsik, Vanessa C. A1 - Jahn, Georg A1 - Jaekel, Frank A1 - Jekel, Marc A1 - Johannesson, Magnus A1 - Johnson, Larissa G. A1 - Johnson, David J. A1 - Johnson, Kate M. A1 - Johnston, William J. A1 - Jonas, Kai A1 - Joy-Gaba, Jennifer A. A1 - Kappes, Heather Barry A1 - Kelso, Kim A1 - Kidwell, Mallory C. A1 - Kim, Seung Kyung A1 - Kirkhart, Matthew A1 - Kleinberg, Bennett A1 - Knezevic, Goran A1 - Kolorz, Franziska Maria A1 - Kossakowski, Jolanda J. A1 - Krause, Robert Wilhelm A1 - Krijnen, Job A1 - Kuhlmann, Tim A1 - Kunkels, Yoram K. A1 - Kyc, Megan M. A1 - Lai, Calvin K. A1 - Laique, Aamir A1 - Lakens, Daniel A1 - Lane, Kristin A. A1 - Lassetter, Bethany A1 - Lazarevic, Ljiljana B. A1 - LeBel, Etienne P. A1 - Lee, Key Jung A1 - Lee, Minha A1 - Lemm, Kristi A1 - Levitan, Carmel A. A1 - Lewis, Melissa A1 - Lin, Lin A1 - Lin, Stephanie A1 - Lippold, Matthias A1 - Loureiro, Darren A1 - Luteijn, Ilse A1 - Mackinnon, Sean A1 - Mainard, Heather N. A1 - Marigold, Denise C. A1 - Martin, Daniel P. A1 - Martinez, Tylar A1 - Masicampo, E. J. A1 - Matacotta, Josh A1 - Mathur, Maya A1 - May, Michael A1 - Mechin, Nicole A1 - Mehta, Pranjal A1 - Meixner, Johannes A1 - Melinger, Alissa A1 - Miller, Jeremy K. A1 - Miller, Mallorie A1 - Moore, Katherine A1 - Möschl, Marcus A1 - Motyl, Matt A1 - Müller, Stephanie M. A1 - Munafo, Marcus A1 - Neijenhuijs, Koen I. A1 - Nervi, Taylor A1 - Nicolas, Gandalf A1 - Nilsonne, Gustav A1 - Nosek, Brian A. A1 - Nuijten, Michele B. A1 - Olsson, Catherine A1 - Osborne, Colleen A1 - Ostkamp, Lutz A1 - Pavel, Misha A1 - Penton-Voak, Ian S. A1 - Perna, Olivia A1 - Pernet, Cyril A1 - Perugini, Marco A1 - Pipitone, R. Nathan A1 - Pitts, Michael A1 - Plessow, Franziska A1 - Prenoveau, Jason M. A1 - Rahal, Rima-Maria A1 - Ratliff, Kate A. A1 - Reinhard, David A1 - Renkewitz, Frank A1 - Ricker, Ashley A. A1 - Rigney, Anastasia A1 - Rivers, Andrew M. A1 - Roebke, Mark A1 - Rutchick, Abraham M. A1 - Ryan, Robert S. A1 - Sahin, Onur A1 - Saide, Anondah A1 - Sandstrom, Gillian M. A1 - Santos, David A1 - Saxe, Rebecca A1 - Schlegelmilch, Rene A1 - Schmidt, Kathleen A1 - Scholz, Sabine A1 - Seibel, Larissa A1 - Selterman, Dylan Faulkner A1 - Shaki, Samuel A1 - Simpson, William B. A1 - Sinclair, H. Colleen A1 - Skorinko, Jeanine L. M. A1 - Slowik, Agnieszka A1 - Snyder, Joel S. A1 - Soderberg, Courtney A1 - Sonnleitner, Carina A1 - Spencer, Nick A1 - Spies, Jeffrey R. A1 - Steegen, Sara A1 - Stieger, Stefan A1 - Strohminger, Nina A1 - Sullivan, Gavin B. A1 - Talhelm, Thomas A1 - Tapia, Megan A1 - te Dorsthorst, Anniek A1 - Thomae, Manuela A1 - Thomas, Sarah L. A1 - Tio, Pia A1 - Traets, Frits A1 - Tsang, Steve A1 - Tuerlinckx, Francis A1 - Turchan, Paul A1 - Valasek, Milan A1 - Van Aert, Robbie A1 - van Assen, Marcel A1 - van Bork, Riet A1 - van de Ven, Mathijs A1 - van den Bergh, Don A1 - van der Hulst, Marije A1 - van Dooren, Roel A1 - van Doorn, Johnny A1 - van Renswoude, Daan R. A1 - van Rijn, Hedderik A1 - Vanpaemel, Wolf A1 - Echeverria, Alejandro Vasquez A1 - Vazquez, Melissa A1 - Velez, Natalia A1 - Vermue, Marieke A1 - Verschoor, Mark A1 - Vianello, Michelangelo A1 - Voracek, Martin A1 - Vuu, Gina A1 - Wagenmakers, Eric-Jan A1 - Weerdmeester, Joanneke A1 - Welsh, Ashlee A1 - Westgate, Erin C. A1 - Wissink, Joeri A1 - Wood, Michael A1 - Woods, Andy A1 - Wright, Emily A1 - Wu, Sining A1 - Zeelenberg, Marcel A1 - Zuni, Kellylynn T1 - Estimating the reproducibility of psychological science JF - Science N2 - Reproducibility is a defining feature of science, but the extent to which it characterizes current research is unknown. We conducted replications of 100 experimental and correlational studies published in three psychology journals using high-powered designs and original materials when available. Replication effects were half the magnitude of original effects, representing a substantial decline. Ninety-seven percent of original studies had statistically significant results. Thirty-six percent of replications had statistically significant results; 47% of original effect sizes were in the 95% confidence interval of the replication effect size; 39% of effects were subjectively rated to have replicated the original result; and if no bias in original results is assumed, combining original and replication results left 68% with statistically significant effects. Correlational tests suggest that replication success was better predicted by the strength of original evidence than by characteristics of the original and replication teams. Y1 - 2015 U6 - https://doi.org/10.1126/science.aac4716 SN - 1095-9203 SN - 0036-8075 VL - 349 IS - 6251 PB - American Assoc. for the Advancement of Science CY - Washington ER - TY - JOUR A1 - Holz, Nathalie E. A1 - Boecker-Schlier, Regina A1 - Jennen-Steinmetz, Christine A1 - Hohm, Erika A1 - Buchmann, Arlette F. A1 - Blomeyer, Dorothea A1 - Baumeister, Sarah A1 - Plichta, Michael M. A1 - Esser, Günter A1 - Schmidt, Martin A1 - Meyer-Lindenberg, Andreas A1 - Banaschewski, Tobias A1 - Brandeis, Daniel A1 - Laucht, Manfred T1 - Early maternal care may counteract familial liability for psychopathology in the reward circuitry JF - Social Cognitive and Affective Neuroscience N2 - Reward processing is altered in various psychopathologies and has been shown to be susceptible to genetic and environmental influences. Here, we examined whether maternal care may buffer familial risk for psychiatric disorders in terms of reward processing. Functional magnetic resonance imaging during a monetary incentive delay task was acquired in participants of an epidemiological cohort study followed since birth (N = 172, 25 years). Early maternal stimulation was assessed during a standardized nursing/playing setting at the age of 3 months. Parental psychiatric disorders (familial risk) during childhood and the participants’ previous psychopathology were assessed by diagnostic interview. With high familial risk, higher maternal stimulation was related to increasing activation in the caudate head, the supplementary motor area, the cingulum and the middle frontal gyrus during reward anticipation, with the opposite pattern found in individuals with no familial risk. In contrast, higher maternal stimulation was associated with decreasing caudate head activity during reward delivery and reduced levels of attention deficit hyperactivity disorder (ADHD) in the high-risk group. Decreased caudate head activity during reward anticipation and increased activity during delivery were linked to ADHD. These findings provide evidence of a long-term association of early maternal stimulation on both adult neurobiological systems of reward underlying externalizing behavior and ADHD during development. KW - maternal care KW - ADHD KW - ventral striatum KW - fMRI KW - resilience KW - aggression Y1 - 2018 U6 - https://doi.org/10.1093/scan/nsy087 SN - 1749-5016 SN - 1749-5024 VL - 13 IS - 11 SP - 1191 EP - 1201 PB - Oxford Univ. Press CY - Oxford ER -