@article{LauchtSkowronekBeckeretal.2008,
  author    = {Laucht, Manfred and Skowronek, Markus H. and Becker, Katja and Schulze, Thomas G. and Schmidt, Martin H. and Esser, G{\"u}nter and Rietschel, Marcella},
  title     = {Environmental risk factors and attention-deficit : hyperactivity discorder symptoms ; reply},
  issn      = {0003-990X},
  year      = {2008},
  language  = {en}
}
@article{LauchtSkowronekBeckeretal.2007,
  author    = {Laucht, Manfred and Skowronek, Markus H. and Becker, Katja and Schmidt, Martin H. and Esser, G{\"u}nter and Rietschel, Marcella and Schulze, Thomas G.},
  title     = {Interacting effects of the dopamine transporter gene and psychosocial adversity on attention-deficit/ hyperactivity disorder symptoms among 15-year-olds from high-risk community sample},
  issn      = {0003-990X},
  year      = {2007},
  abstract  = {Context: Recent evidence suggests that gene X environment interactions could explain the inconsistent findings of association studies relating the dopamine transporter (DAT1) gene with attention-deficit/hyperactivity disorder (ADHD). 1bjective: To examine whether psychosocial adversity moderated the effect of genetic variation in DAT1 on ADHD symptoms in. adolescents from a high-risk community sample. Design: Prospective cohort study. Setting: Data were taken from the Mannheim Study of Children at Risk, an ongoing longitudinal study of the long-term outcomes of early risk factors followed up from birth on. Participants: Three hundred five adolescents (146 boys, 159 girls) participated in a follow-up assessment at age 15 years. Main Outcome Measures: Measures of ADHD symptoms according to DSM-IV were obtained using standardized structural interviews with adolescents and their parents. Psychosocial adversity was determined according to an "enriched" family adversity index as proposed by Rutter and Quinton. DNA was genotyped for the common DAT1 40-base pair (bp) variable number of tandem repeats (VNTR) polymorphism in the 3' untranslated region; 3 previously described single nucleotide polymorphisms in exon 15, intron 9, and exon 9; and a novel 30-bp VNTR polymorphism in intron 8. Results: Adolescents homozygous for the 10-repeat allele of the 40-bp VNTR polymorphism who grew up in greater psychosocial adversity exhibited significantly more inattention and hyperactivity-impulsivity than adolescents with other genotypes or who lived in less adverse family conditions (significant interaction, P=.013-017). This gene X environment interaction was also observed in individuals homozygous for the 6-repeat allele of the 30-bp VNTR polymorphism and the haplotype comprising both markers. Conclusions: These findings provide initial evidence that environmental risks as described by the Rutter Family Adversity Index moderate the impact of the DAT1 gene on ADHD symptoms, suggesting a DAT1 effect only in those individuals exposed to psychosocial adversity.},
  language  = {en}
}
@article{ZhengLuanSofianopoulouetal.2020,
  author    = {Zheng, Ju-Sheng and Luan, Jian'an and Sofianopoulou, Eleni and Imamura, Fumiaki and Stewart, Isobel D. and Day, Felix R. and Pietzner, Maik and Wheeler, Eleanor and Lotta, Luca A. and Gundersen, Thomas E. and Amiano, Pilar and Ardanaz, Eva and Chirlaque, Maria-Dolores and Fagherazzi, Guy and Franks, Paul W. and Kaaks, Rudolf and Laouali, Nasser and Mancini, Francesca Romana and Nilsson, Peter M. and Onland-Moret, N. Charlotte and Olsen, Anja and Overvad, Kim and Panico, Salvatore and Palli, Domenico and Ricceri, Fulvio and Rolandsson, Olov and Spijkerman, Annemieke M. W. and Sanchez, Maria-Jose and Schulze, Matthias Bernd and Sala, Nuria and Sieri, Sabina and Tjonneland, Anne and Tumino, Rosario and van der Schouw, Yvonne T. and Weiderpass, Elisabete and Riboli, Elio and Danesh, John and Butterworth, Adam S. and Sharp, Stephen J. and Langenberg, Claudia and Forouhi, Nita G. and Wareham, Nicholas J.},
  title     = {Plasma vitamin C and type 2 diabetes},
  series = {Diabetes care},
  volume    = {44},
  journal   = {Diabetes care},
  number    = {1},
  publisher = {American Diabetes Association},
  address   = {Alexandria},
  issn      = {0149-5992},
  doi       = {10.2337/dc20-1328},
  pages     = {98 -- 106},
  year      = {2020},
  abstract  = {OBJECTIVE: Higher plasma vitamin C levels are associated with lower type 2 diabetes risk, but whether this association is causal is uncertain. To investigate this, we studied the association of genetically predicted plasma vitamin C with type 2 diabetes. RESEARCH DESIGN AND METHODS: We conducted genome-wide association studies of plasma vitamin C among 52,018 individuals of European ancestry to discover novel genetic variants. We performed Mendelian randomization analyses to estimate the association of genetically predicted differences in plasma vitamin C with type 2 diabetes in up to 80,983 case participants and 842,909 noncase participants. We compared this estimate with the observational association between plasma vitamin C and incident type 2 diabetes, including 8,133 case participants and 11,073 noncase participants. RESULTS: We identified 11 genomic regions associated with plasma vitamin C (P < 5 x 10(-8)), with the strongest signal at SLC23A1, and 10 novel genetic loci including SLC23A3, CHPT1, BCAS3, SNRPF, RER1, MAF, GSTA5, RGS14, AKT1, and FADS1. Plasma vitamin C was inversely associated with type 2 diabetes (hazard ratio per SD 0.88; 95\% CI 0.82, 0.94), but there was no association between genetically predicted plasma vitamin C (excluding FADS1 variant due to its apparent pleiotropic effect) and type 2 diabetes (1.03; 95\% CI 0.96, 1.10). CONCLUSIONS: These findings indicate discordance between biochemically measured and genetically predicted plasma vitamin C levels in the association with type 2 diabetes among European populations. The null Mendelian randomization findings provide no strong evidence to suggest the use of vitamin C supplementation for type 2 diabetes prevention.},
  language  = {en}
}
@article{FoerstnerBoettgerMoldavskietal.2023,
  author    = {F{\"o}rstner, Bernd Rainer and B{\"o}ttger, Sarah Jane and Moldavski, Alexander and Bajbouj, Malek and Pfennig, Andrea and Manook, Andre and Ising, Marcus and Pittig, Andre and Heinig, Ingmar and Heinz, Andreas and Mathiak, Klaus and Schulze, Thomas G. and Schneider, Frank and Kamp-Becker, Inge and Meyer-Lindenberg, Andreas and Padberg, Frank and Banaschewski, Tobias and Bauer, Michael and Rupprecht, Rainer and Wittchen, Hans-Ulrich and Rapp, Michael A. and Tschorn, Mira},
  title     = {The associations of positive and negative valence systems, cognitive systems and social processes on disease severity in anxiety and depressive disorders},
  series = {Frontiers in psychiatry},
  volume    = {14},
  journal   = {Frontiers in psychiatry},
  publisher = {Frontiers Research Foundation},
  address   = {Lausanne},
  issn      = {1664-0640},
  doi       = {10.3389/fpsyt.2023.1161097},
  pages     = {10},
  year      = {2023},
  abstract  = {Background Anxiety and depressive disorders share common features of mood dysfunctions. This has stimulated interest in transdiagnostic dimensional research as proposed by the Research Domain Criteria (RDoC) approach by the National Institute of Mental Health (NIMH) aiming to improve the understanding of underlying disease mechanisms. The purpose of this study was to investigate the processing of RDoC domains in relation to disease severity in order to identify latent disorder-specific as well as transdiagnostic indicators of disease severity in patients with anxiety and depressive disorders. Methods Within the German research network for mental disorders, 895 participants (n = 476 female, n = 602 anxiety disorder, n = 257 depressive disorder) were recruited for the Phenotypic, Diagnostic and Clinical Domain Assessment Network Germany (PD-CAN) and included in this cross-sectional study. We performed incremental regression models to investigate the association of four RDoC domains on disease severity in patients with affective disorders: Positive (PVS) and Negative Valance System (NVS), Cognitive Systems (CS) and Social Processes (SP). Results The results confirmed a transdiagnostic relationship for all four domains, as we found significant main effects on disease severity within domain-specific models (PVS: \& beta; = -0.35; NVS: \& beta; = 0.39; CS: \& beta; = -0.12; SP: \& beta; = -0.32). We also found three significant interaction effects with main diagnosis showing a disease-specific association. Limitations The cross-sectional study design prevents causal conclusions. Further limitations include possible outliers and heteroskedasticity in all regression models which we appropriately controlled for. Conclusion Our key results show that symptom burden in anxiety and depressive disorders is associated with latent RDoC indicators in transdiagnostic and disease-specific ways.},
  language  = {en}
}
@article{FoerstnerTschornReinosoSchilleretal.2022,
  author    = {F{\"o}rstner, Bernd R. and Tschorn, Mira and Reinoso-Schiller, Nicolas and Maričić, Lea Mascarell and R{\"o}cher, Erik and Kalman, Janos L. and Stroth, Sanna and Mayer, Annalina V. and Schwarz, Kristina and Kaiser, Anna and Pfennig, Andrea and Manook, Andr{\´e} and Ising, Marcus and Heinig, Ingmar and Pittig, Andre and Heinz, Andreas and Mathiak, Klaus and Schulze, Thomas G. and Schneider, Frank and Kamp-Becker, Inge and Meyer-Lindenberg, Andreas and Padberg, Frank and Banaschewski, Tobias and Bauer, Michael and Rupprecht, Rainer and Wittchen, Hans-Ulrich and Rapp, Michael A.},
  title     = {Mapping research domain criteria using a transdiagnostic mini-RDoC assessment in mental disorders: a confirmatory factor analysis},
  series = {European archives of psychiatry and clinical neuroscience},
  volume    = {273},
  journal   = {European archives of psychiatry and clinical neuroscience},
  number    = {3},
  publisher = {Springer Nature},
  address   = {Heidelberg},
  issn      = {0940-1334},
  doi       = {10.1007/s00406-022-01440-6},
  pages     = {527 -- 539},
  year      = {2022},
  abstract  = {This study aimed to build on the relationship of well-established self-report and behavioral assessments to the latent constructs positive (PVS) and negative valence systems (NVS), cognitive systems (CS), and social processes (SP) of the Research Domain Criteria (RDoC) framework in a large transnosological population which cuts across DSM/ICD-10 disorder criteria categories. One thousand four hundred and thirty one participants (42.1\% suffering from anxiety/fear-related, 18.2\% from depressive, 7.9\% from schizophrenia spectrum, 7.5\% from bipolar, 3.4\% from autism spectrum, 2.2\% from other disorders, 18.4\% healthy controls, and 0.2\% with no diagnosis specified) recruited in studies within the German research network for mental disorders for the Phenotypic, Diagnostic and Clinical Domain Assessment Network Germany (PD-CAN) were examined with a Mini-RDoC-Assessment including behavioral and self-report measures. The respective data was analyzed with confirmatory factor analysis (CFA) to delineate the underlying latent RDoC-structure. A revised four-factor model reflecting the core domains positive and negative valence systems as well as cognitive systems and social processes showed a good fit across this sample and showed significantly better fit compared to a one factor solution. The connections between the domains PVS, NVS and SP could be substantiated, indicating a universal latent structure spanning across known nosological entities. This study is the first to give an impression on the latent structure and intercorrelations between four core Research Domain Criteria in a transnosological sample. We emphasize the possibility of using already existing and well validated self-report and behavioral measurements to capture aspects of the latent structure informed by the RDoC matrix.},
  language  = {en}
}