@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}
}
@misc{KaminskiSchlagenhaufRappetal.2018,
  author    = {Kaminski, Jakob and Schlagenhauf, Florian and Rapp, Michael Armin and Awasthi, Swapnil and Ruggeri, Barbara and Deserno, Lorenz and Laura, Daedelow and Banaschewski, Tobias and Bokde, Arun and Quinlan, Erin Burke and Buechel, Christian and Bromberg, Uli 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 and Froehner, Juliane and Walter, Henrik and Whelan, Robert and Ripke, Stephan and Schumann, Gunter and Heinz, Andreas},
  title     = {Variance in Dopaminergic Markers},
  series = {Biological psychiatry : a journal of psychiatric neuroscience and therapeutics ; a publication of the Society of Biological Psychiatry},
  volume    = {83},
  journal   = {Biological psychiatry : a journal of psychiatric neuroscience and therapeutics ; a publication of the Society of Biological Psychiatry},
  number    = {9},
  publisher = {Elsevier},
  address   = {New York},
  organization    = {IMAGEN Consortium},
  issn      = {0006-3223},
  doi       = {10.1016/j.biopsych.2018.02.311},
  pages     = {S118 -- S118},
  year      = {2018},
  language  = {en}
}
@misc{KaminskiSchlagenhaufRappetal.2018,
  author    = {Kaminski, Jakob A. and Schlagenhauf, Florian and Rapp, Michael Armin 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 Armin 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}
}
@misc{RodriguezSillkeSteinhoffBojarskietal.2019,
  author    = {Rodriguez-Sillke, Yasmina and Steinhoff, U. and Bojarski, Christian and Lissner, Donata and Schumann, Michael and Branchi, F. and Siegmund, Britta and Glauben, Rainer},
  title     = {Deep immune profiling of human Peyer´s Patches in patients of inflammatory bowel diseases},
  series = {European journal of immunology},
  volume    = {49},
  journal   = {European journal of immunology},
  publisher = {Wiley},
  address   = {Weinheim},
  issn      = {0014-2980},
  doi       = {10.1002/eji.201970300},
  pages     = {203 -- 204},
  year      = {2019},
  language  = {en}
}
@inproceedings{RolfBergesHubwieseretal.2010,
  author    = {Rolf, Arno and Berges, Marc and Hubwieser, Peter and Kehrer, Timo and Kelter, Udo and Romeike, Ralf and Frenkel, Marcus and Karsten, Weicker and Reinhardt, Wolfgang and Mascher, Michael and G{\"u}l, Senol and Magenheim, Johannes and Raimer, Stephan and Diethelm, Ira and D{\"u}nnebier, Malte and Gabor, Kiss and Susanne, Boll and Rolf, Meinhardt and Gronewold, Sabine and Krekeler, Larissa and Jahnke, Isa and Haertel, Tobias and Mattick, Volker and Lettow, Karsten and Hafer, J{\"o}rg and Ludwig, Joachim and Schumann, Marlen and Laroque, Christoph and Schulte, Jonas and Urban, Diana},
  title     = {HDI2010 - Tagungsband der 4. Fachtagung zur "Hochschuldidaktik Informatik"},
  editor    = {Engbring, Dieter and Keil, Reinhard and Magenheim, Johannes and Selke, Harald},
  publisher = {Universit{\"a}tsverlag Potsdam},
  address   = {Potsdam},
  isbn      = {978-3-86956-100-4},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus-49167},
  pages     = {105},
  year      = {2010},
  abstract  = {Mit der 4. Tagung zur Hochschuldidaktik Informatik wird eine Reihe fortgesetzt, die ihren Anfang 1998 in Stuttgart unter der {\"U}berschrift „Informatik und Ausbildung" genommen hat. Seither dienen diese Tagungen den Lehrenden im Bereich der Hochschulinformatik als Forum der Information und des Diskurses {\"u}ber aktuelle didaktische und bildungspolitische Entwicklungen im Bereich der Informatikausbildung. Aktuell z{\"a}hlen dazu insbesondere Fragen der Bildungsrelevanz informatischer Inhalte und der Herausforderung durch eine st{\"a}rkere Kompetenzorientierung in der Informatik. Die eingereichten Beitr{\"a}ge zur HDI 2010 in Paderborn veranschaulichen unterschiedliche Bem{\"u}hungen, sich mit relevanten Problemen der Informatikdidaktik an Hochschulen in Deutschland (und z. T. auch im Ausland) auseinanderzusetzen. Aus der Breite des Spektrums der Einreichungen ergaben sich zugleich Probleme bei der Begutachtung. Letztlich konnten von den zahlreichen Einreichungen nur drei die Gutachter so {\"u}berzeugen, dass sie uneingeschr{\"a}nkt in ihrer Langfassung akzeptiert wurden. Neun weitere Einreichungen waren trotz Kritik {\"u}berwiegend positiv begutachtet worden, so dass wir diese als Kurzfassung bzw. Diskussionspapier in die Tagung aufgenommen haben.},
  language  = {de}
}
@misc{Schumann2019,
  type      = {Master Thesis},
  author    = {Schumann, Michael},
  title     = {Extraterrestrische Ex-zentriker},
  doi       = {10.25932/publishup-43420},
  url       = {http://nbn-resolving.de/urn:nbn:de:kobv:517-opus4-434203},
  school      = {Universit{\"a}t Potsdam},
  pages     = {93},
  year      = {2019},
  abstract  = {Seit ihrem Beginn ist die Raumfahrt Untersuchungsgegenstand verschiedenster Disziplinen. Auch die Philosophie hat seither eine kritische Perspektive auf diese Aktivit{\"a}t eingenommen. Und doch fehlt es bislang eines philosophisch-systematischen Zugangs, mit einem genuin ‚anthropologischen' Gesichtspunkt. Diese L{\"u}cke wird immer offensichtlicher, seitdem sich, nach Entdeckung der ersten Exoplaneten, neue ‚Astro-wissenschaften' (z.B. Astrobiologe, Astrokognition, Astrosoziologie) gebildet haben, die explizit Menschen als Raumfahrer voraussetzen bzw. menschliche Eigenschaften auf ihre ‚Abl{\"o}sbarkeit' hin diskutieren. Mit vorliegender Masterarbeit soll der Versuch gemacht werden, die notwendigen Pr{\"a}suppositionen, f{\"u}r das Verst{\"a}ndnis von Menschen als ‚raumfahrende Lebewesen', aufzudecken, ohne naturalistische oder kulturalistische Verk{\"u}rzungen zu betreiben. Zu diesem Zweck wird der systematische Rahmen von Helmuth Plessners Philosophischer Anthropologie gew{\"a}hlt, da dieser eine umfassende ‚spezies-neutrale' (d.h. es erlaubt {\"u}ber Menschen, Tiere und Extraterrestriker gleichermaßen nachzudenken, ohne ‚anthropozentrische' oder ‚speziesistische' Vorurteile zu machen) Untersuchung des infrage stehenden Sachverhaltes bietet. Um diesen Rahmen zu exemplifizieren, und w{\"a}hrenddessen den philosophisch-systematischen Ansatz zur Raumfahrt zu elaborieren, der raumfahrende Extraterrestriker ohne Anthropomorphisierung konzeptualisieren, wie auch den Umgang mit Extraterrestrikern in ethischer und politischer Hinsicht ber{\"u}cksichtigen kann, werden die Themenkreise der Astrobiologie, Astroethik und Astropolitik in einzelnen Kapiteln besprochen. Abschließend ist, entgegen aller Erwartung, der gew{\"a}hlte Ansatz als ‚kritisch-posthumanistische' Option zu verteidigen.},
  language  = {de}
}
@misc{RodriguezSillkeSchumannLissneretal.2020,
  author    = {Rodr{\´i}guez Sillke, Yasmina and Schumann, Michael and Lissner, Donata and Branchi, Frederica and Glauben, Rainer and Siegmund, Britta},
  title     = {Small intestinal inflammation but not colitis drives pro-inflammatory nutritional antigen-specific T-cell response},
  series = {Journal of Crohn's and Colitis},
  volume    = {14},
  journal   = {Journal of Crohn's and Colitis},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {1873-9946},
  doi       = {10.1093/ecco-jcc/jjz203.172},
  pages     = {S154 -- S155},
  year      = {2020},
  abstract  = {Background: Inflammatory bowel disease (IBD) represents a dysregulation of the mucosal immune system. The pathogenesis of Crohn's disease (CD) and ulcerative colitis (UC) is linked to the loss of intestinal tolerance and barrier function. The healthy mucosal immune system has previously been shown to be inert against food antigens. Since the small intestine is the main contact surface for antigens and therefore the immunological response, the present study served to analyse food-antigen-specific T cells in the peripheral blood of IBD patients. Methods: Peripheral blood mononuclear cells of CD, with an affected small intestine, and UC (colitis) patients, either active or in remission, were stimulated with the following food antigens: gluten, soybean, peanut and ovalbumin. Healthy controls and celiac disease patients were included as controls. Antigen-activated CD4+ T cells in the peripheral blood were analysed by a magnetic enrichment of CD154+ effector T cells and a cytometric antigen-reactive T-cell analysis ('ARTE' technology) followed by characterisation of the ef- fector response. Results: The effector T-cell response of antigen-specific T cells were compared between CD with small intestinal inflammation and UC where inflammation was restricted to the colon. Among all tested food antigens, the highest frequency of antigen-specific T cells (CD4+CD154+) was found for gluten. Celiac disease patients were included as control, since gluten has been identified as the disease- causing antigen. The highest frequency of gluten antigen-specific T cells was revealed in active CD when compared with UC, celiac disease on a gluten-free diet (GFD) and healthy controls. Ovalbuminspecific T cells were almost undetectable, whereas the reaction to soybean and peanut was slightly higher. But again, the strong- est reaction was observed in CD with small intestinal involvement compared with UC. Remarkably, in celiac disease on a GFD only antigen-specific cells for gluten were detected. These gluten-specific T cells were characterised by up-regulation of the pro-inflammatory cytokines IFN-γ, IL-17A and TNF-α. IFN-g was exclusively elevated in CD patients with active disease. Gluten-specific T-cells expressing IL-17A were increased in all IBD patients. Furthermore, T cells of CD patients, independent of disease activity, revealed a high expression of the pro-inflammatory cytokine TNF-α. Conclusion: The 'ARTE'-technique allows to analyse and quantify food antigen specific T cells in the peripheral blood of IBD patients indicating a potential therapeutic insight. These data provide evidence that small intestinal inflammation in CD is key for the development of a systemic pro-inflammatory effector T-cell response driven by food antigens.},
  language  = {en}
}
@article{HolzBoeckerSchlierBuchmannetal.2017,
  author    = {Holz, Nathalie E. and Boecker-Schlier, Regina and Buchmann, Arlette F. and Blomeyer, Dorothea and Jennen-Steinmetz, Christine and Baumeister, Sarah and Plichta, Michael M. and Cattrell, Anna and Schumann, Gunter and Esser, G{\"u}nter and Schmidt, Martin and Buitelaar, Jan and Meyer-Lindenberg, Andreas and Banaschewski, Tobias and Brandeis, Daniel and Laucht, Manfred},
  title     = {Ventral striatum and amygdala activity as convergence sites for early adversity and conduct disorder},
  series = {Frontiers in human neuroscience},
  volume    = {12},
  journal   = {Frontiers in human neuroscience},
  number    = {2},
  publisher = {Oxford Univ. Press},
  address   = {Oxford},
  issn      = {1749-5016},
  doi       = {10.1093/scan/nsw120},
  pages     = {261 -- 272},
  year      = {2017},
  abstract  = {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.},
  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}
}
@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      = {0006-3223},
  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}
}
@misc{AwasthiKaminskiRappetal.2019,
  author    = {Awasthi, Swapnil and Kaminski, Jakob and Rapp, Michael Armin and Schlagenhauf, Florian and Walter, Henrik and Ruggeri, Barbara and Ripke, Stephan and Schumann, Gunter and Heinz, Andreas},
  title     = {A neural signature of malleability},
  series = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  volume    = {29},
  journal   = {European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology},
  publisher = {Elsevier},
  address   = {Amsterdam},
  issn      = {0924-977X},
  doi       = {10.1016/j.euroneuro.2017.08.139},
  pages     = {S858 -- S859},
  year      = {2019},
  abstract  = {General intelligence has a substantial genetic background in children, adolescents, and adults, but environmental factors also strongly correlate with cognitive performance as evidenced by a strong (up to one SD) increase in average intelligence test results in the second half of the previous century. This change occurred in a period apparently too short to accommodate radical genetic changes. It is highly suggestive that environmental factors interact with genotype by possible modification of epigenetic factors that regulate gene expression and thus contribute to individual malleability. This modification might as well be reflected in recent observations of an association between dopamine-dependent encoding of reward prediction errors and cognitive capacity, which was modulated by adverse life events.},
  language  = {en}
}