@article{SchroederVanDerVenWarloetal.2000, author = {Schr{\"o}der, Rolf and VanDerVen, Peter F. M. and Warlo, Irene and Schumann, H. and F{\"u}rst, Dieter Oswald and Bl{\"u}mke, Ingmar and Goebel, Hans H. and Schmidt, M. C. and Hatzfeld, Mechthild}, title = {A member of the armadillo multigene family, is a constituent of sarcomeric I-bands in human skeletal muscle}, year = {2000}, language = {en} } @article{LauchtBeckerFranketal.2008, author = {Laucht, Manfred and Becker, Katja and Frank, Josef and Schmidt, Martin H. and Esser, G{\"u}nter and Treutlein, Jens and Skowronek, Markus H. and Schumann, Gunter}, title = {Genetic variation in dopamine pathways differentially associated with smoking progression in adolescence}, issn = {0890-8567}, doi = {10.1097/Chi.0b013e31816bff77}, year = {2008}, abstract = {Objective: To clarify the nature of the association between dopamine genes and smoking by examining whether genetic variability in components of the dopamine pathway could explain refined phenotypes in adolescent smoking progression. Method: Data are from an ongoing prospective study of the long-term outcome of early risk factors studied since birth. At age 15 years, 220 participants (108 males, 112 females) completed a self-report questionnaire measuring smoking behavior and were genotyped for five dopamine gene variants. Results: Smoking initiation was related to allelic variation in the dopamine D-4 receptor gene (DRD4), whereas smoking continuation and dependence showed association with the dopamine D-2 receptor gene (DRD2). Adolescents with the seven-repeat allele of the common DRD4 exon 3 polymorphism had rates of ever smoking that were significantly higher than in those with other genotypes. Once smoking started, carriers of the T allele of a single nucleotide polymorphism of DRD2 (rs4648317) reported higher rates of current smoking and scored higher on nicotine dependence than their allelic counterparts. Among current smokers, intention to quit was significantly lower in adolescents homozygous for the 10-repeat allele of the common dopamine transporter 3 untranslated region polymorphism. Conclusions: Our results provide preliminary evidence of genetic influences on different stages of smoking and suggest the importance of specific dopamine genes in smoking progression in adolescence.}, language = {en} } @article{NockeSchumannBoehm2004, author = {Nocke, T. and Schumann, H. and B{\"o}hm, Uwe}, title = {Methods for the visualization of clustered climate data}, issn = {0943-4062}, year = {2004}, abstract = {Increasing amounts of large climate data require new analysis techniques. The area of data mining investigates new paradigms and methods including factors like scalability, flexibility and problem abstraction for large data sets. The field of visual data mining in particular offers valuable methods for analyzing large amounts of data intuitively. In this paper we describe our approach of integrating cluster analysis and visualization methods for the exploration of climate data. We integrated cluster algorithms, appropriate visualization techniques and sophisticated interaction paradigms into a general framework}, language = {en} } @article{KoenigAblerAgartzetal.2020, author = {Koenig, Julian and Abler, Birgit and Agartz, Ingrid and akerstedt, Torbjorn and Andreassen, Ole A. and Anthony, Mia and Baer, Karl-Juergen and Bertsch, Katja and Brown, Rebecca C. and Brunner, Romuald and Carnevali, Luca and Critchley, Hugo D. and Cullen, Kathryn R. and de Geus, Eco J. C. and de la Cruz, Feliberto and Dziobek, Isabel and Ferger, Marc D. and Fischer, Hakan and Flor, Herta and Gaebler, Michael and Gianaros, Peter J. and Giummarra, Melita J. and Greening, Steven G. and Guendelman, Simon and Heathers, James A. J. and Herpertz, Sabine C. and Hu, Mandy X. and Jentschke, Sebastian and Kaess, Michael and Kaufmann, Tobias and Klimes-Dougan, Bonnie and Koelsch, Stefan and Krauch, Marlene and Kumral, Deniz and Lamers, Femke and Lee, Tae-Ho and Lekander, Mats and Lin, Feng and Lotze, Martin and Makovac, Elena and Mancini, Matteo and Mancke, Falk and Mansson, Kristoffer N. T. and Manuck, Stephen B. and Mather, Mara and Meeten, Frances and Min, Jungwon and Mueller, Bryon and Muench, Vera and Nees, Frauke and Nga, Lin and Nilsonne, Gustav and Ordonez Acuna, Daniela and Osnes, Berge and Ottaviani, Cristina and Penninx, Brenda W. J. H. and Ponzio, Allison and Poudel, Govinda R. and Reinelt, Janis and Ren, Ping and Sakaki, Michiko and Schumann, Andy and Sorensen, Lin and Specht, Karsten and Straub, Joana and Tamm, Sandra and Thai, Michelle and Thayer, Julian F. and Ubani, Benjamin and van Der Mee, Denise J. and van Velzen, Laura S. and Ventura-Bort, Carlos and Villringer, Arno and Watson, David R. and Wei, Luqing and Wendt, Julia and Schreiner, Melinda Westlund and Westlye, Lars T. and Weymar, Mathias and Winkelmann, Tobias and Wu, Guo-Rong and Yoo, Hyun Joo and Quintana, Daniel S.}, title = {Cortical thickness and resting-state cardiac function across the lifespan}, series = {Psychophysiology : journal of the Society for Psychophysiological Research}, volume = {58}, journal = {Psychophysiology : journal of the Society for Psychophysiological Research}, number = {7}, publisher = {Wiley}, address = {Hoboken}, issn = {0048-5772}, doi = {10.1111/psyp.13688}, pages = {16}, year = {2020}, abstract = {Understanding the association between autonomic nervous system [ANS] function and brain morphology across the lifespan provides important insights into neurovisceral mechanisms underlying health and disease. Resting-state ANS activity, indexed by measures of heart rate [HR] and its variability [HRV] has been associated with brain morphology, particularly cortical thickness [CT]. While findings have been mixed regarding the anatomical distribution and direction of the associations, these inconsistencies may be due to sex and age differences in HR/HRV and CT. Previous studies have been limited by small sample sizes, which impede the assessment of sex differences and aging effects on the association between ANS function and CT. To overcome these limitations, 20 groups worldwide contributed data collected under similar protocols of CT assessment and HR/HRV recording to be pooled in a mega-analysis (N = 1,218 (50.5\% female), mean age 36.7 years (range: 12-87)). Findings suggest a decline in HRV as well as CT with increasing age. CT, particularly in the orbitofrontal cortex, explained additional variance in HRV, beyond the effects of aging. This pattern of results may suggest that the decline in HRV with increasing age is related to a decline in orbitofrontal CT. These effects were independent of sex and specific to HRV; with no significant association between CT and HR. Greater CT across the adult lifespan may be vital for the maintenance of healthy cardiac regulation via the ANS-or greater cardiac vagal activity as indirectly reflected in HRV may slow brain atrophy. Findings reveal an important association between CT and cardiac parasympathetic activity with implications for healthy aging and longevity that should be studied further in longitudinal research.}, language = {en} } @article{RotheMetzBoeweetal.1994, author = {Rothe, Heinz-J{\"u}rgen and Metz, Anna-Marie and B{\"o}we, H. and Schumann, J.}, title = {Kundenzufriedenheit : der Einfluss von Stabilit{\"a}t des Kontakts zwischen Unternehmensmitarbeitern und Kunden}, isbn = {3-87988-810-8}, year = {1994}, language = {de} } @article{BuchmannSchmidBlomeyeretal.2009, author = {Buchmann, Arlette F. and Schmid, Brigitte and Blomeyer, Dorothea and Becker, Katja and Treutlein, Jens and Zimmermann, Ulrich S. and Jennen-Steinmetz, Christine and Schmidt, Martin H. and Esser, G{\"u}nter and Banaschewski, Tobias and Rietschel, Marcella and Schumann, Gunter and Laucht, Manfred}, title = {Impact of age at first drink on vulnerability to alcohol-related problems : testing the marker hypothesis in a prospective study of young adults}, issn = {0022-3956}, doi = {10.1016/j.jpsychires.2009.02.006}, year = {2009}, abstract = {There is ample evidence that the early initiation of alcohol use is a risk factor for the development of later alcohol-related problems. The purpose of the current study was to examine whether this association can be explained by indicators of a common underlying susceptibility or whether age at drinking onset may be considered as an independent predictor of later drinking behavior, suggesting a potential causal relationship. Participants were drawn from a prospective cohort study of the long-term outcomes of early risk factors followed up from birth onwards. Structured interviews were administered to 304 participants to assess age at first drink and current drinking behavior. Data on risk factors, including early family adversity, parental alcohol use, childhood psychopathology and stressful life events, were repeatedly collected during childhood using standardized parent interviews. In addition, information on genotype was considered. Results confirmed previous work demonstrating that hazardous alcohol consumption is related to early-adolescent drinking onset. A younger age of first drink was significantly predicted by 5-HTTLPR genotype and the degree of preceding externalizing symptoms, and both factors were related to increased consumption or harmful alcohol use at age 19. However, even after controlling for these potential explanatory factors, earlier age at drinking onset remained a strong predictor of heavy alcohol consumption in young adulthood. The present longitudinal study adds to the current literature indicating that the early onset - adult hazardous drinking association cannot solely be attributed to shared genetic and psychopathologic risk factors as examined in this study.}, language = {en} } @article{BlomeyerTreutleinEsseretal.2007, author = {Blomeyer, Dorothea and Treutlein, Jens and Esser, G{\"u}nter and Schmidt, Martin H. and Schumann, Gunter and Laucht, Manfred}, title = {Interaction between CRHR1 gene and stressful life events predicts adolescent heavy alcohol use}, issn = {0006-3223}, year = {2007}, abstract = {Background: Recent animal research suggests that alterations in the corticotropin releasing hormone receptor 1 (CRHR1) may lead to heavy alcohol use following repeated stress. The aim of this study was to examine interactions between two haplotype-tagging single nucleotide polymorphisms (SNPs) covering the CRHR1 gene and adverse life events on heavy drinking in adolescents. Methods: Data were available from the Mannheim Study of Children at Risk, an ongoing cohort study of the long-term outcome of early risk factors followed since birth. At age 15 years, 280 participants (135 males, 145 females) completed a self-report questionnaire measuring alcohol use and were genotyped for two SNPs (rs242938, rs1876831) of CRHR1. Assessment of negative life events over the past three years was obtained by a standardized interview with the parents. Results: Adolescents homozygous for the C allele of rs1876831 drank higher maximum amounts of alcohol per occasion and had greater lifetime rates of heavy drinking in relation to negative life events than individuals carrying the T allele. No gene X environment interactions were found for regular drinking and between rs242938 and stressful life events. Conclusions: These findings provide first evidence in humans that the CRHR1 gene interacts with exposure to stressful life events to predict heavy alcohol use in adolescents.}, language = {en} } @article{BlomeyerBuchmannLascorzetal.2013, author = {Blomeyer, Dorothea and Buchmann, Arlette F. and Lascorz, Jesus and Zimmermann, Ulrich S. and Esser, G{\"u}nter and Desrivieres, Sylvane and Schmidt, Martin H. and Banaschewski, Tobias and Schumann, Gunter and Laucht, Manfred}, title = {Association of PER2 genotype and stressful life events with alcohol drinking in young adults}, series = {PLoS one}, volume = {8}, journal = {PLoS one}, number = {3}, publisher = {PLoS}, address = {San Fransisco}, issn = {1932-6203}, doi = {10.1371/journal.pone.0059136}, pages = {7}, year = {2013}, abstract = {Background: Clock genes govern circadian rhythms and shape the effect of alcohol use on the physiological system. Exposure to severe negative life events is related to both heavy drinking and disturbed circadian rhythmicity. The aim of this study was 1) to extend previous findings suggesting an association of a haplotype tagging single nucleotide polymorphism of PER2 gene with drinking patterns, and 2) to examine a possible role for an interaction of this gene with life stress in hazardous drinking. Methods: Data were collected as part of an epidemiological cohort study on the outcome of early risk factors followed since birth. At age 19 years, 268 young adults (126 males, 142 females) were genotyped for PER2 rs56013859 and were administered a 45-day alcohol timeline follow-back interview and the Alcohol Use Disorders Identification Test (AUDIT). Life stress was assessed as the number of severe negative life events during the past four years reported in a questionnaire and validated by interview. Results: Individuals with the minor G allele of rs56013859 were found to be less engaged in alcohol use, drinking at only 72\% of the days compared to homozygotes for the major A allele. Moreover, among regular drinkers, a gene x environment interaction emerged (p = .020). While no effects of genotype appeared under conditions of low stress, carriers of the G allele exhibited less hazardous drinking than those homozygous for the A allele when exposed to high stress. Conclusions: These findings may suggest a role of the circadian rhythm gene PER2 in both the drinking patterns of young adults and in moderating the impact of severe life stress on hazardous drinking in experienced alcohol users. However, in light of the likely burden of multiple tests, the nature of the measures used and the nominal evidence of interaction, replication is needed before drawing firm conclusions.}, language = {en} } @book{RanaMohapatraSidorovaetal.2022, author = {Rana, Kaushik and Mohapatra, Durga Prasad and Sidorova, Julia and Lundberg, Lars and Sk{\"o}ld, Lars and Lopes Grim, Lu{\´i}s Fernando and Sampaio Gradvohl, Andr{\´e} Leon and Cremerius, Jonas and Siegert, Simon and Weltzien, Anton von and Baldi, Annika and Klessascheck, Finn and Kalancha, Svitlana and Lichtenstein, Tom and Shaabani, Nuhad and Meinel, Christoph and Friedrich, Tobias and Lenzner, Pascal and Schumann, David and Wiese, Ingmar and Sarna, Nicole and Wiese, Lena and Tashkandi, Araek Sami and van der Walt, Est{\´e}e and Eloff, Jan H. P. and Schmidt, Christopher and H{\"u}gle, Johannes and Horschig, Siegfried and Uflacker, Matthias and Najafi, Pejman and Sapegin, Andrey and Cheng, Feng and Stojanovic, Dragan and Stojnev Ilić, Aleksandra and Djordjevic, Igor and Stojanovic, Natalija and Predic, Bratislav and Gonz{\´a}lez-Jim{\´e}nez, Mario and de Lara, Juan and Mischkewitz, Sven and Kainz, Bernhard and van Hoorn, Andr{\´e} and Ferme, Vincenzo and Schulz, Henning and Knigge, Marlene and Hecht, Sonja and Prifti, Loina and Krcmar, Helmut and Fabian, Benjamin and Ermakova, Tatiana and Kelkel, Stefan and Baumann, Annika and Morgenstern, Laura and Plauth, Max and Eberhard, Felix and Wolff, Felix and Polze, Andreas and Cech, Tim and Danz, Noel and Noack, Nele Sina and Pirl, Lukas and Beilharz, Jossekin Jakob and De Oliveira, Roberto C. L. and Soares, F{\´a}bio Mendes and Juiz, Carlos and Bermejo, Belen and M{\"u}hle, Alexander and Gr{\"u}ner, Andreas and Saxena, Vageesh and Gayvoronskaya, Tatiana and Weyand, Christopher and Krause, Mirko and Frank, Markus and Bischoff, Sebastian and Behrens, Freya and R{\"u}ckin, Julius and Ziegler, Adrian and Vogel, Thomas and Tran, Chinh and Moser, Irene and Grunske, Lars and Sz{\´a}rnyas, G{\´a}bor and Marton, J{\´o}zsef and Maginecz, J{\´a}nos and Varr{\´o}, D{\´a}niel and Antal, J{\´a}nos Benjamin}, title = {HPI Future SOC Lab - Proceedings 2018}, number = {151}, editor = {Meinel, Christoph and Polze, Andreas and Beins, Karsten and Strotmann, Rolf and Seibold, Ulrich and R{\"o}dszus, Kurt and M{\"u}ller, J{\"u}rgen}, publisher = {Universit{\"a}tsverlag Potsdam}, address = {Potsdam}, isbn = {978-3-86956-547-7}, issn = {1613-5652}, doi = {10.25932/publishup-56371}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-563712}, publisher = {Universit{\"a}t Potsdam}, pages = {x, 277}, year = {2022}, abstract = {The "HPI Future SOC Lab" is a cooperation of the Hasso Plattner Institute (HPI) and industry partners. Its mission is to enable and promote exchange and interaction between the research community and the industry partners. The HPI Future SOC Lab provides researchers with free of charge access to a complete infrastructure of state of the art hard and software. This infrastructure includes components, which might be too expensive for an ordinary research environment, such as servers with up to 64 cores and 2 TB main memory. The offerings address researchers particularly from but not limited to the areas of computer science and business information systems. Main areas of research include cloud computing, parallelization, and In-Memory technologies. This technical report presents results of research projects executed in 2018. Selected projects have presented their results on April 17th and November 14th 2017 at the Future SOC Lab Day events.}, language = {en} } @misc{XieJiaRollsetal.2021, author = {Xie, Chao and Jia, Tianye and Rolls, Edmund T. and Robbins, Trevor W. and Sahakian, Barbara J. and Zhang, Jie and Liu, Zhaowen and Cheng, Wei and Luo, Qiang and Zac Lo, Chun-Yi and Schumann, Gunter and Feng, Jianfeng and Wang, He and Banaschewski, Tobias and Barker, Gareth J. and Bokde, Arun L.W. and B{\"u}chel, Christian and Quinlan, Erin Burke and Desrivi{\`e}res, Sylvane and Flor, Herta and Grigis, Antoine and Garavan, Hugh and Gowland, Penny and Heinz, Andreas and Hohmann, Sarah and Ittermann, Bernd and Martinot, Jean-Luc and Paill{\`e}re Martinot, Marie-Laure and Nees, Frauke and Papadopoulos Orfanos, Dimitri and Paus, Tom{\´a}š and Poustka, Luise and Fr{\"o}hner, Juliane H. and Smolka, Michael N. and Walter, Henrik and Whelan, Robert}, title = {Reward versus nonreward sensitivity of the medial versus lateral orbitofrontal cortex relates to the severity of depressive symptoms}, series = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, journal = {Zweitver{\"o}ffentlichungen der Universit{\"a}t Potsdam : Humanwissenschaftliche Reihe}, number = {3}, issn = {1866-8364}, doi = {10.25932/publishup-55788}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-557882}, pages = {13}, year = {2021}, abstract = {BACKGROUND: The orbitofrontal cortex (OFC) is implicated in depression. The hypothesis investigated was whether the OFC sensitivity to reward and nonreward is related to the severity of depressive symptoms. METHODS: Activations in the monetary incentive delay task were measured in the IMAGEN cohort at ages 14 years (n = 1877) and 19 years (n = 1140) with a longitudinal design. Clinically relevant subgroups were compared at ages 19 (high-severity group: n = 116; low-severity group: n = 206) and 14. RESULTS: The medial OFC exhibited graded activation increases to reward, and the lateral OFC had graded activation increases to nonreward. In this general population, the medial and lateral OFC activations were associated with concurrent depressive symptoms at both ages 14 and 19 years. In a stratified high-severity depressive symptom group versus control group comparison, the lateral OFC showed greater sensitivity for the magnitudes of activations related to nonreward in the high-severity group at age 19 (p = .027), and the medial OFC showed decreased sensitivity to the reward magnitudes in the high-severity group at both ages 14 (p = .002) and 19 (p = .002). In a longitudinal design, there was greater sensitivity to nonreward of the lateral OFC at age 14 for those who exhibited high depressive symptom severity later at age 19 (p = .003). CONCLUSIONS: Activations in the lateral OFC relate to sensitivity to not winning, were associated with high depressive symptom scores, and at age 14 predicted the depressive symptoms at ages 16 and 19. Activations in the medial OFC were related to sensitivity to winning, and reduced reward sensitivity was associated with concurrent high depressive symptom scores.}, language = {en} } @misc{KaminskiSchlagenhaufRappetal.2018, author = {Kaminski, Jakob A. and Schlagenhauf, Florian and Rapp, Michael A. and Awasthi, Swapnil and Ruggeri, Barbara and Deserno, Lorenz and Banaschewski, Tobias and Bokde, Arun L. W. and Bromberg, Uli and B{\"u}chel, Christian and Quinlan, Erin Burke and Desrivi{\`e}res, Sylvane and Flor, Herta and Frouin, Vincent and Garavan, Hugh and Gowland, Penny and Ittermann, Bernd and Martinot, Jean-Luc and Paill{\`e}re Martinot, Marie-Laure and Nees, Frauke and Papadopoulos Orfanos, Dimitri and Paus, Tom{\´a}š and Poustka, Luise and Smolka, Michael N. and Fr{\"o}hner, Juliane H. and Walter, Henrik and Whelan, Robert and Ripke, Stephan and Schumann, Gunter and Heinz, Andreas}, title = {Epigenetic variance in dopamine D2 receptor}, series = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, journal = {Postprints der Universit{\"a}t Potsdam : Mathematisch-Naturwissenschaftliche Reihe}, number = {950}, issn = {1866-8372}, doi = {10.25932/publishup-42568}, url = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-425687}, pages = {13}, year = {2018}, abstract = {Genetic and environmental factors both contribute to cognitive test performance. A substantial increase in average intelligence test results in the second half of the previous century within one generation is unlikely to be explained by genetic changes. One possible explanation for the strong malleability of cognitive performance measure is that environmental factors modify gene expression via epigenetic mechanisms. Epigenetic factors may help to understand the recent observations of an association between dopamine-dependent encoding of reward prediction errors and cognitive capacity, which was modulated by adverse life events. The possible manifestation of malleable biomarkers contributing to variance in cognitive test performance, and thus possibly contributing to the "missing heritability" between estimates from twin studies and variance explained by genetic markers, is still unclear. Here we show in 1475 healthy adolescents from the IMaging and GENetics (IMAGEN) sample that general IQ (gIQ) is associated with (1) polygenic scores for intelligence, (2) epigenetic modification of DRD2 gene, (3) gray matter density in striatum, and (4) functional striatal activation elicited by temporarily surprising reward-predicting cues. Comparing the relative importance for the prediction of gIQ in an overlapping subsample, our results demonstrate neurobiological correlates of the malleability of gIQ and point to equal importance of genetic variance, epigenetic modification of DRD2 receptor gene, as well as functional striatal activation, known to influence dopamine neurotransmission. Peripheral epigenetic markers are in need of confirmation in the central nervous system and should be tested in longitudinal settings specifically assessing individual and environmental factors that modify epigenetic structure.}, language = {en} } @article{KaminskiSchlagenhaufRappetal.2018, author = {Kaminski, Jakob A. and Schlagenhauf, Florian and Rapp, Michael A. and Awasthi, Swapnil and Ruggeri, Barbara and Deserno, Lorenz and Banaschewski, Tobias and Bokde, Arun L. W. and Bromberg, Uli and B{\"u}chel, Christian and Quinlan, Erin Burke and Desrivieres, Sylvane and Flor, Herta and Frouin, Vincent and Garavan, Hugh and Gowland, Penny and Ittermann, Bernd and Martinot, Jean-Luc and Martinot, Marie-Laure Paillere and Nees, Frauke and Orfanos, Dimitri Papadopoulos and Paus, Tomas and Poustka, Luise and Smolka, Michael N. and Fr{\"o}hner, Juliane H. and Walter, Henrik and Whelan, Robert and Ripke, Stephan and Schumann, Gunter and Heinz, Andreas}, title = {Epigenetic variance in dopamine D2 receptor}, series = {Translational Psychiatry}, volume = {8}, journal = {Translational Psychiatry}, publisher = {Nature Publ. Group}, address = {New York}, organization = {IMAGEN Consortium}, issn = {2158-3188}, doi = {10.1038/s41398-018-0222-7}, pages = {11}, year = {2018}, abstract = {Genetic and environmental factors both contribute to cognitive test performance. A substantial increase in average intelligence test results in the second half of the previous century within one generation is unlikely to be explained by genetic changes. One possible explanation for the strong malleability of cognitive performance measure is that environmental factors modify gene expression via epigenetic mechanisms. Epigenetic factors may help to understand the recent observations of an association between dopamine-dependent encoding of reward prediction errors and cognitive capacity, which was modulated by adverse life events. The possible manifestation of malleable biomarkers contributing to variance in cognitive test performance, and thus possibly contributing to the "missing heritability" between estimates from twin studies and variance explained by genetic markers, is still unclear. Here we show in 1475 healthy adolescents from the IMaging and GENetics (IMAGEN) sample that general IQ (gIQ) is associated with (1) polygenic scores for intelligence, (2) epigenetic modification of DRD2 gene, (3) gray matter density in striatum, and (4) functional striatal activation elicited by temporarily surprising reward-predicting cues. Comparing the relative importance for the prediction of gIQ in an overlapping subsample, our results demonstrate neurobiological correlates of the malleability of gIQ and point to equal importance of genetic variance, epigenetic modification of DRD2 receptor gene, as well as functional striatal activation, known to influence dopamine neurotransmission. Peripheral epigenetic markers are in need of confirmation in the central nervous system and should be tested in longitudinal settings specifically assessing individual and environmental factors that modify epigenetic structure.}, language = {en} } @article{XieJiaRollsetal.2021, author = {Xie, Chao and Jia, Tianye and Rolls, Edmund T. and Robbins, Trevor W. and Sahakian, Barbara J. and Zhang, Jie and Liu, Zhaowen and Cheng, Wei and Luo, Qiang and Zac Lo, Chun-Yi and Schumann, Gunter and Feng, Jianfeng and Wang, He and Banaschewski, Tobias and Barker, Gareth J. and Bokde, Arun L.W. and B{\"u}chel, Christian and Quinlan, Erin Burke and Desrivi{\`e}res, Sylvane and Flor, Herta and Grigis, Antoine and Garavan, Hugh and Gowland, Penny and Heinz, Andreas and Hohmann, Sarah and Ittermann, Bernd and Martinot, Jean-Luc and Paill{\`e}re Martinot, Marie-Laure and Nees, Frauke and Papadopoulos Orfanos, Dimitri and Paus, Tom{\´a}š and Poustka, Luise and Fr{\"o}hner, Juliane H. and Smolka, Michael N. and Walter, Henrik and Whelan, Robert}, title = {Reward versus nonreward sensitivity of the medial versus lateral orbitofrontal cortex relates to the severity of depressive symptoms}, series = {Biological Psychiatry: Cognitive Neuroscience and Neuroimaging}, volume = {6}, journal = {Biological Psychiatry: Cognitive Neuroscience and Neuroimaging}, number = {3}, publisher = {Elsevier Science}, address = {Amsterdam}, issn = {2451-9022}, doi = {10.1016/j.bpsc.2020.08.017}, pages = {259 -- 269}, year = {2021}, abstract = {BACKGROUND: The orbitofrontal cortex (OFC) is implicated in depression. The hypothesis investigated was whether the OFC sensitivity to reward and nonreward is related to the severity of depressive symptoms. METHODS: Activations in the monetary incentive delay task were measured in the IMAGEN cohort at ages 14 years (n = 1877) and 19 years (n = 1140) with a longitudinal design. Clinically relevant subgroups were compared at ages 19 (high-severity group: n = 116; low-severity group: n = 206) and 14. RESULTS: The medial OFC exhibited graded activation increases to reward, and the lateral OFC had graded activation increases to nonreward. In this general population, the medial and lateral OFC activations were associated with concurrent depressive symptoms at both ages 14 and 19 years. In a stratified high-severity depressive symptom group versus control group comparison, the lateral OFC showed greater sensitivity for the magnitudes of activations related to nonreward in the high-severity group at age 19 (p = .027), and the medial OFC showed decreased sensitivity to the reward magnitudes in the high-severity group at both ages 14 (p = .002) and 19 (p = .002). In a longitudinal design, there was greater sensitivity to nonreward of the lateral OFC at age 14 for those who exhibited high depressive symptom severity later at age 19 (p = .003). CONCLUSIONS: Activations in the lateral OFC relate to sensitivity to not winning, were associated with high depressive symptom scores, and at age 14 predicted the depressive symptoms at ages 16 and 19. Activations in the medial OFC were related to sensitivity to winning, and reduced reward sensitivity was associated with concurrent high depressive symptom scores.}, language = {en} }