@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} } @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} } @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{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} }