Poustka, Luise

[["dc.bibliographiccitation.firstpage","1680"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Autism Research"],["dc.bibliographiccitation.lastpage","1692"],["dc.bibliographiccitation.volume","12"],["dc.contributor.affiliation","Banaschewski, Tobias; 2\r\nDepartment of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim\r\nHeidelberg University\r\nMannheim Germany"],["dc.contributor.affiliation","Dziobek, Isabel; 3\r\nBerlin School of Mind and Brain and Institute of Psychology\r\nHumboldt‐Universität zu Berlin\r\nBerlin Germany"],["dc.contributor.affiliation","Brandeis, Daniel; 2\r\nDepartment of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim\r\nHeidelberg University\r\nMannheim Germany"],["dc.contributor.affiliation","Poustka, Luise; 2\r\nDepartment of Child and Adolescent Psychiatry and Psychotherapy, Central Institute of Mental Health, Medical Faculty Mannheim\r\nHeidelberg University\r\nMannheim Germany"],["dc.contributor.affiliation","Freitag, Christine M.; 1\r\nDepartment of Child and Adolescent Psychiatry, Psychosomatics and Psychotherapy\r\nUniversity Hospital, Goethe University Frankfurt am Main\r\nFrankfurt Germany"],["dc.contributor.author","Bast, Nico"],["dc.contributor.author","Banaschewski, Tobias"],["dc.contributor.author","Dziobek, Isabel"],["dc.contributor.author","Brandeis, Daniel"],["dc.contributor.author","Poustka, Luise"],["dc.contributor.author","Freitag, Christine M."],["dc.date.accessioned","2019-11-25T15:27:33Z"],["dc.date.accessioned","2021-10-27T13:21:35Z"],["dc.date.available","2019-11-25T15:27:33Z"],["dc.date.available","2021-10-27T13:21:35Z"],["dc.date.issued","2019"],["dc.date.updated","2022-02-09T13:22:08Z"],["dc.description.abstract","Progression of pupil dilation (PD) in response to visual stimuli may indicate distinct internal processes. No study has been performed on PD progression during a social cognition task. Here, we describe PD progression during the Movie for the Assessment of Social Cognition (MASC) test in n = 23 adolescents with Autism Spectrum Disorder (ASD) and n = 24 age, IQ and sex-matched neurotypical controls (NTC). The MASC consists of 43 video sequences depicting human social interactions, each followed by a multiple-choice question concerning characters' mental states. PD progression data were extracted by eye tracking and controlled for fixation behavior. Segmenting PD progression during video sequences by principal component analysis, three sequential PD components were unveiled. In ASD compared with NTC, a distinct PD progression was observed with increased constriction amplitude, increased dilation latency, and increased dilation amplitude that correlated with PD progression components. These components predicted social cognition performance. The first and second PD components correlated positively with MASC behavioral performance in ASD but negatively in NTC. These PD components may be interpreted as indicators of sensory-perceptual processing and attention function. In ASD, aberrant sensory-perceptual processing and attention function could contribute to attenuated social cognition performance. This needs to be tested by additional studies combining the respective cognitive tests and the outlined PD progression analysis. Phasic activity of the locus coeruleus-norepinephrine system is discussed as putatively shared underlying mechanism. Autism Res2019. © 2019 The Authors. Autism Research published by International Society for Autism Research published by Wiley Periodicals, Inc. LAY SUMMARY: In adolescents with autism, we found an altered pupil dilation during watching scenes of human interactions. Early pupil dilation correlated positively with the number of correct answers to questions about the shown human interactions. Our findings suggest that aberrant sensory processing and attention function may contribute to altered social cognition in autism."],["dc.description.sponsorship","Innovative Medicines Initiative Joint Undertaking"],["dc.identifier.doi","10.1002/aur.2178"],["dc.identifier.eissn","1939-3806"],["dc.identifier.issn","1939-3792"],["dc.identifier.pmid","31347301"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16726"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92033"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.publisher","John Wiley & Sons, Inc."],["dc.relation.eissn","1939-3806"],["dc.relation.issn","1939-3806"],["dc.relation.issn","1939-3792"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Pupil Dilation Progression Modulates Aberrant Social Cognition in Autism Spectrum Disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","435"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","JAMA Psychiatry"],["dc.bibliographiccitation.volume","76"],["dc.contributor.author","Luo, Qiang"],["dc.contributor.author","Chen, Qiang"],["dc.contributor.author","Wang, Wenjia"],["dc.contributor.author","Desrivières, Sylvane"],["dc.contributor.author","Quinlan, Erin Burke"],["dc.contributor.author","Jia, Tianye"],["dc.contributor.author","Macare, Christine"],["dc.contributor.author","Robert, Gabriel H."],["dc.contributor.author","Cui, Jing"],["dc.contributor.author","Guedj, Mickaël"],["dc.contributor.author","Palaniyappan, Lena"],["dc.contributor.author","Kherif, Ferath"],["dc.contributor.author","Banaschewski, Tobias"],["dc.contributor.author","Bokde, Arun L. W."],["dc.contributor.author","Büchel, Christian"],["dc.contributor.author","Flor, Herta"],["dc.contributor.author","Frouin, Vincent"],["dc.contributor.author","Garavan, Hugh"],["dc.contributor.author","Gowland, Penny"],["dc.contributor.author","Heinz, Andreas"],["dc.contributor.author","Ittermann, Bernd"],["dc.contributor.author","Martinot, Jean-Luc"],["dc.contributor.author","Artiges, Eric"],["dc.contributor.author","Paillère-Martinot, Marie-Laure"],["dc.contributor.author","Nees, Frauke"],["dc.contributor.author","Orfanos, Dimitri Papadopoulos"],["dc.contributor.author","Poustka, Luise"],["dc.contributor.author","Fröhner, Juliane H."],["dc.contributor.author","Smolka, Michael N."],["dc.contributor.author","Walter, Henrik"],["dc.contributor.author","Whelan, Robert"],["dc.contributor.author","Callicott, Joseph H."],["dc.contributor.author","Mattay, Venkata S."],["dc.contributor.author","Pausova, Zdenka"],["dc.contributor.author","Dartigues, Jean-François"],["dc.contributor.author","Tzourio, Christophe"],["dc.contributor.author","Crivello, Fabrice"],["dc.contributor.author","Berman, Karen F."],["dc.contributor.author","Li, Fei"],["dc.contributor.author","Paus, Tomáš"],["dc.contributor.author","Weinberger, Daniel R."],["dc.contributor.author","Murray, Robin M."],["dc.contributor.author","Schumann, Gunter"],["dc.contributor.author","Feng, Jianfeng"],["dc.date.accessioned","2019-07-09T11:51:24Z"],["dc.date.available","2019-07-09T11:51:24Z"],["dc.date.issued","2019"],["dc.description.abstract","Importance: Deviation from normal adolescent brain development precedes manifestations of many major psychiatric symptoms. Such altered developmental trajectories in adolescents may be linked to genetic risk for psychopathology. Objective: To identify genetic variants associated with adolescent brain structure and explore psychopathologic relevance of such associations. Design, Setting, and Participants: Voxelwise genome-wide association study in a cohort of healthy adolescents aged 14 years and validation of the findings using 4 independent samples across the life span with allele-specific expression analysis of top hits. Group comparison of the identified gene-brain association among patients with schizophrenia, unaffected siblings, and healthy control individuals. This was a population-based, multicenter study combined with a clinical sample that included participants from the IMAGEN cohort, Saguenay Youth Study, Three-City Study, and Lieber Institute for Brain Development sample cohorts and UK biobank who were assessed for both brain imaging and genetic sequencing. Clinical samples included patients with schizophrenia and unaffected siblings of patients from the Lieber Institute for Brain Development study. Data were analyzed between October 2015 and April 2018. Main Outcomes and Measures: Gray matter volume was assessed by neuroimaging and genetic variants were genotyped by Illumina BeadChip. Results: The discovery sample included 1721 adolescents (873 girls [50.7%]), with a mean (SD) age of 14.44 (0.41) years. The replication samples consisted of 8690 healthy adults (4497 women [51.8%]) from 4 independent studies across the life span. A nonsynonymous genetic variant (minor T allele of rs13107325 in SLC39A8, a gene implicated in schizophrenia) was associated with greater gray matter volume of the putamen (variance explained of 4.21% in the left hemisphere; 8.66; 95% CI, 6.59-10.81; P = 5.35 × 10-18; and 4.44% in the right hemisphere; t = 8.90; 95% CI, 6.75-11.19; P = 6.80 × 10-19) and also with a lower gene expression of SLC39A8 specifically in the putamen (t127 = -3.87; P = 1.70 × 10-4). The identified association was validated in samples across the life span but was significantly weakened in both patients with schizophrenia (z = -3.05; P = .002; n = 157) and unaffected siblings (z = -2.08; P = .04; n = 149). Conclusions and Relevance: Our results show that a missense mutation in gene SLC39A8 is associated with larger gray matter volume in the putamen and that this association is significantly weakened in schizophrenia. These results may suggest a role for aberrant ion transport in the etiology of psychosis and provide a target for preemptive developmental interventions aimed at restoring the functional effect of this mutation."],["dc.identifier.doi","10.1001/jamapsychiatry.2018.4126"],["dc.identifier.pmid","30649180"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16122"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59943"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/720270/EU//HBP SGA1"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/695313/EU//STRATIFY"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602450/EU//IMAGEMEND"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/603016/EU//MATRICS"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Association of a Schizophrenia-Risk Nonsynonymous Variant With Putamen Volume in Adolescents"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0216152"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","PLOS ONE"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Albaugh, Matthew D."],["dc.contributor.author","Hudziak, James. J."],["dc.contributor.author","Orr, Catherine"],["dc.contributor.author","Spechler, Philip A."],["dc.contributor.author","Chaarani, Bader"],["dc.contributor.author","Mackey, Scott"],["dc.contributor.author","Lepage, Claude"],["dc.contributor.author","Fonov, Vladimir"],["dc.contributor.author","Rioux, Pierre"],["dc.contributor.author","Evans, Alan C."],["dc.contributor.author","Banaschewski, Tobias"],["dc.contributor.author","Bokde, Arun L. W."],["dc.contributor.author","Bromberg, Uli"],["dc.contributor.author","Büchel, Christian"],["dc.contributor.author","Quinlan, Erin Burke"],["dc.contributor.author","Desrivières, Sylvane"],["dc.contributor.author","Flor, Herta"],["dc.contributor.author","Grigis, Antoine"],["dc.contributor.author","Gowland, Penny"],["dc.contributor.author","Heinz, Andreas"],["dc.contributor.author","Ittermann, Bernd"],["dc.contributor.author","Martinot, Jean-Luc"],["dc.contributor.author","Martinot, Marie-Laure Paillère"],["dc.contributor.author","Nees, Frauke"],["dc.contributor.author","Orfanos, Dimitri Papadopoulos"],["dc.contributor.author","Paus, Tomáš"],["dc.contributor.author","Poustka, Luise"],["dc.contributor.author","Millenet, Sabina"],["dc.contributor.author","Fröhner, Juliane H."],["dc.contributor.author","Smolka, Michael N."],["dc.contributor.author","Walter, Henrik"],["dc.contributor.author","Whelan, Robert"],["dc.contributor.author","Schumann, Gunter"],["dc.contributor.author","Potter, Alexandra S."],["dc.contributor.author","Garavan, Hugh"],["dc.date.accessioned","2019-07-09T11:51:17Z"],["dc.date.available","2019-07-09T11:51:17Z"],["dc.date.issued","2019"],["dc.description.abstract","In structural neuroimaging studies, reduced cerebral cortical thickness in orbital and ventromedial prefrontal regions is frequently interpreted as reflecting an impaired ability to downregulate neuronal activity in the amygdalae. Unfortunately, little research has been conducted in order to test this conjecture. We examine the extent to which amygdalar reactivity is associated with cortical thickness in a population-based sample of adolescents. Data were obtained from the IMAGEN study, which includes 2,223 adolescents. While undergoing functional neuroimaging, participants passively viewed video clips of a face that started from a neutral expression and progressively turned angry, or, instead, turned to a second neutral expression. Left and right amygdala ROIs were used to extract mean BOLD signal change for the angry minus neutral face contrast for all subjects. T1-weighted images were processed through the CIVET pipeline (version 2.1.0). In variable-centered analyses, local cortical thickness was regressed against amygdalar reactivity using first and second-order linear models. In a follow-up person-centered analysis, we defined a \"high reactive\" group of participants based on mean amygdalar BOLD signal change for the angry minus neutral face contrast. Between-group differences in cortical thickness were examined (\"high reactive\" versus all other participants). A significant association was revealed between the continuous measure of amygdalar reactivity and bilateral ventromedial prefrontal cortical thickness in a second-order linear model (p < 0.05, corrected). The \"high reactive\" group, in comparison to all other participants, possessed reduced cortical thickness in bilateral orbital and ventromedial prefrontal cortices, bilateral anterior temporal cortices, left caudal middle temporal gyrus, and the left inferior and middle frontal gyri (p < 0.05, corrected). Results are consistent with non-human primate studies, and provide empirical support for an association between reduced prefrontal cortical thickness and amygdalar reactivity. Future research will likely benefit from investigating the degree to which psychopathology qualifies relations between prefrontal cortical structure and amygdalar reactivity."],["dc.identifier.doi","10.1371/journal.pone.0216152"],["dc.identifier.pmid","31048888"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16093"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59915"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/695313/EU//STRATIFY"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602450/EU//IMAGEMEND"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/603016/EU//MATRICS"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Amygdalar reactivity is associated with prefrontal cortical thickness in a large population-based sample of adolescents"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","101804"],["dc.bibliographiccitation.journal","NeuroImage: Clinical"],["dc.bibliographiccitation.volume","22"],["dc.contributor.author","Ruan, Hongtao"],["dc.contributor.author","Zhou, Yunyi"],["dc.contributor.author","Luo, Qiang"],["dc.contributor.author","Robert, Gabriel H."],["dc.contributor.author","Desrivières, Sylvane"],["dc.contributor.author","Quinlan, Erin Burke"],["dc.contributor.author","Liu, ZhaoWen"],["dc.contributor.author","Banaschewski, Tobias"],["dc.contributor.author","Bokde, Arun L.W."],["dc.contributor.author","Bromberg, Uli"],["dc.contributor.author","Büchel, Christian"],["dc.contributor.author","Flor, Herta"],["dc.contributor.author","Frouin, Vincent"],["dc.contributor.author","Garavan, Hugh"],["dc.contributor.author","Gowland, Penny"],["dc.contributor.author","Heinz, Andreas"],["dc.contributor.author","Ittermann, Bernd"],["dc.contributor.author","Martinot, Jean-Luc"],["dc.contributor.author","Martinot, Marie-Laure Paillère"],["dc.contributor.author","Nees, Frauke"],["dc.contributor.author","Orfanos, Dimitri Papadopoulos"],["dc.contributor.author","Poustka, Luise"],["dc.contributor.author","Hohmann, Sarah"],["dc.contributor.author","Fröhner, Juliane H."],["dc.contributor.author","Smolka, Michael N."],["dc.contributor.author","Walter, Henrik"],["dc.contributor.author","Whelan, Robert"],["dc.contributor.author","Li, Fei"],["dc.contributor.author","Schumann, Gunter"],["dc.contributor.author","Feng, Jianfeng"],["dc.date.accessioned","2019-07-09T11:51:49Z"],["dc.date.available","2019-07-09T11:51:49Z"],["dc.date.issued","2019"],["dc.description.abstract","Adolescent binge drinking has been associated with higher risks for the development of many health problems throughout the lifespan. Adolescents undergo multiple changes that involve the co-development processes of brain, personality and behavior; therefore, certain behavior, such as alcohol consumption, can have disruptive effects on both brain development and personality maturation. However, these effects remain unclear due to the scarcity of longitudinal studies. In the current study, we used multivariate approaches to explore discriminative features in brain functional architecture, personality traits, and genetic variants in 19-year-old individuals (n = 212). Taking advantage of a longitudinal design, we selected features that were more drastically altered in drinkers with an earlier onset of binge drinking. With the selected features, we trained a hierarchical model of support vector machines using a training sample (n = 139). Using an independent sample (n = 73), we tested the model and achieved a classification accuracy of 71.2%. We demonstrated longitudinally that after the onset of binge drinking the developmental trajectory of improvement in impulsivity slowed down. This study identified the disrupting effects of adolescent binge drinking on the developmental trajectories of both brain and personality."],["dc.identifier.doi","10.1016/j.nicl.2019.101804"],["dc.identifier.pmid","30991616"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16200"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60018"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/H2020/695313/EU//STRATIFY"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/602450/EU//IMAGEMEND"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/115300/EU//EU-AIMS"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/321580/EU//ERANID"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/610691/EU//BRIDGET"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Adolescent binge drinking disrupts normal trajectories of brain functional organization and personality maturation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]