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Trost, Sarah Makbule
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Trost, Sarah Makbule
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Trost, Sarah Makbule
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Trost, Sarah M.
Trost, S. M.
Trost, Sarah
Trost, S.
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2015Journal Article [["dc.bibliographiccitation.firstpage","127"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","136"],["dc.bibliographiccitation.volume","265"],["dc.contributor.author","Kittel-Schneider, Sarah"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Zilles, David"],["dc.contributor.author","Wolf, C."],["dc.contributor.author","Schmitt, A."],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Reif, A."],["dc.date.accessioned","2018-11-07T10:00:31Z"],["dc.date.available","2018-11-07T10:00:31Z"],["dc.date.issued","2015"],["dc.description.abstract","The diacylglycerol kinase eta (DGKH) gene, first identified in a genome-wide association study, is one of the few replicated risk genes of bipolar affective disorder (BD). Following initial positive studies, it not only was found to be associated with BD but also implicated in the etiology of other psychiatric disorders featuring affective symptoms, rendering DGKH a cross-disorder risk gene. However, the (patho-)physiological role of the encoded enzyme is still elusive. In the present study, we investigated primarily the influence of a risk haplotype on amygdala volume in patients suffering from schizophrenia or BD as well as healthy controls and four single nucleotide polymorphisms conveying risk. There was a significant association of the DGKH risk haplotype with increased amygdala volume in BD, but not in schizophrenia or healthy controls. These findings add to the notion of a role of DGKH in the pathogenesis of BD."],["dc.description.sponsorship","DFG [RTG 1253/1, RE1632/5-1]; BMBF (DZHI) [01EO1004]; IZKF [Z3-24]"],["dc.identifier.doi","10.1007/s00406-014-0513-9"],["dc.identifier.isi","000350305500005"],["dc.identifier.pmid","24958494"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37825"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1433-8491"],["dc.relation.issn","0940-1334"],["dc.title","Influence of DGKH variants on amygdala volume in patients with bipolar affective disorder and schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2014Journal Article [["dc.bibliographiccitation.firstpage","57"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","66"],["dc.bibliographiccitation.volume","265"],["dc.contributor.author","Goya-Maldonado, Roberto"],["dc.contributor.author","Weber, Kristina"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Diekhof, Esther"],["dc.contributor.author","Keil, Maria"],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2017-09-07T11:47:50Z"],["dc.date.available","2017-09-07T11:47:50Z"],["dc.date.issued","2014"],["dc.description.abstract","Depression is a debilitating psychiatric disorder characterized among other aspects by the inability to properly experience or respond to reward. However, it remains unclear whether patients with depression present impaired reward system due to abnormal modulatory mechanisms. We investigated the activation of the nucleus accumbens (NAcc), a crucial region involved in reward processing, with functional magnetic resonance imaging using the desire-reason-dilemma paradigm. This task allows tracking the activity of the NAcc during the acceptance or the rejection of previously conditioned reward stimuli. Patients were assigned into subgroups of lower (LA) or higher (HA) NAcc activation according to beta weights. LA patients presented significant hypoactivation in the ventral tegmental area in addition to bilateral ventral striatum, confirming impairments in the bottom-up input to the NAcc. Conversely, HA patients presented significant hyperactivation in prefrontal areas such as the rostral anterior cingulate cortex and the anterior ventral prefrontal cortex in addition to bilateral ventral striatum, suggesting disturbances in the top-down regulation of the NAcc. Demographic and clinical differences explaining the abnormal co-activations of midbrain and prefrontal regions were not identified. Therefore, we provide evidence for dysfunctional bottom-up processing in one potential neurobiological subtype of depression (LA) and dysfunctional top-down modulation in another subtype (HA). We suggest that the midbrain and prefrontal regions are more specific pathophysiological substrates for each depression subtype. Above all, our results encourage the segregation of patients by similar dysfunctional mechanisms of the dopaminergic system, which would finally contribute to disentangle more specific pathogeneses and guide the development of more personalized targets for future therapies."],["dc.identifier.doi","10.1007/s00406-014-0552-2"],["dc.identifier.gro","3150742"],["dc.identifier.pmid","25327829"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7532"],["dc.language.iso","en"],["dc.notes.status","zu prĂĽfen"],["dc.relation.issn","0940-1334"],["dc.title","Dissociating pathomechanisms of depression with fMRI: bottom-up or top-down dysfunctions of the reward system"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI PMID PMC2012Conference Abstract [["dc.bibliographiccitation.journal","The International Journal of Neuropsychopharmacology"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Vieker, Henning"],["dc.contributor.author","Diekhof, Esther Kristina"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Fanelli, A."],["dc.contributor.author","Jakob, K."],["dc.contributor.author","Petrovic, A."],["dc.contributor.author","Weber, K."],["dc.contributor.author","Keil, M."],["dc.contributor.author","Zilles, David"],["dc.contributor.author","Falkai, Peter Gaston"],["dc.date.accessioned","2018-11-07T09:10:04Z"],["dc.date.available","2018-11-07T09:10:04Z"],["dc.date.issued","2012"],["dc.format.extent","214"],["dc.identifier.isi","000209062500785"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26410"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.issn","1469-5111"],["dc.relation.issn","1461-1457"],["dc.title","Imaging endophenotypic biomarkers for schizophrenic and affective psychoses in key neural circuits"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2014Journal Article [["dc.bibliographiccitation.firstpage","1914"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Neuropsychopharmacology"],["dc.bibliographiccitation.lastpage","1923"],["dc.bibliographiccitation.volume","39"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Diekhof, Esther Kristina"],["dc.contributor.author","Zvonik, Kerstin"],["dc.contributor.author","Lewandowski, Mirjana"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Keil, Maria"],["dc.contributor.author","Zilles, David"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T09:38:30Z"],["dc.date.available","2018-11-07T09:38:30Z"],["dc.date.issued","2014"],["dc.description.abstract","Bipolar disorder (BD) is characterized by recurrent mood episodes ranging from severe depression to acute full-blown mania. Both states of this severe psychiatric disorder have been associated with alterations of reward processing in the brain. Here, we present results of a functional magnetic resonance imaging (fMRI) study on the neural correlates and functional interactions underlying reward gain processing and reward dismissal in favor of a long-term goal in bipolar patients. Sixteen medicated patients diagnosed with bipolar 1 disorder, euthymic to mildly depressed, and sixteen matched healthy controls performed the 'desire-reason dilemma' (DRD) paradigm demanding rejection of priorly conditioned reward stimuli to successfully pursue a superordinate goal. Both groups exhibited significant activations in reward-related brain regions, particularly in the mesolimbic reward system. However, bipolar patients showed reduced neural responses of the ventral striatum (vStr) when exploiting a reward stimulus, and exhibited a decreased suppression of the reward-related activation of the mesolimbic reward system while having to reject immediate reward in favor of the long-term goal. Further, functional interaction between the anteroventral prefrontal cortex and the vStr in the 'DRD' was significantly impaired in the bipolar group. These findings provide evidence for a reduced responsivity of the vStr to reward stimuli in BD, possibly related to clinical features like anhedonia. The disturbed top-down control of mesolimbic reward signals by prefrontal brain regions in BD can be interpreted in terms of a disease-related enhanced impulsivity, a trait marker of BD."],["dc.identifier.doi","10.1038/npp.2014.39"],["dc.identifier.isi","000337550600013"],["dc.identifier.pmid","24535101"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33078"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1740-634X"],["dc.relation.issn","0893-133X"],["dc.title","Disturbed Anterior Prefrontal Control of the Mesolimbic Reward System and Increased Impulsivity in Bipolar Disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2013Journal Article [["dc.bibliographiccitation.firstpage","53"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","63"],["dc.bibliographiccitation.volume","263"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Platz, B."],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Ekawardhani, Savira"],["dc.contributor.author","Meyer, J."],["dc.contributor.author","Reith, W."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T09:28:39Z"],["dc.date.available","2018-11-07T09:28:39Z"],["dc.date.issued","2013"],["dc.description.abstract","DTNBP1 is one of the most established susceptibility genes for schizophrenia, and hippocampal volume reduction is one of the major neuropathological findings in this severe disorder. Consistent with these findings, the encoded protein dysbindin-1 has been shown to be diminished in glutamatergic hippocampal neurons in schizophrenic patients. The aim of this study was to investigate the effects of two single nucleotide polymorphisms of DTNBP1 on grey matter volumes in human subjects using voxel-based morphometry. Seventy-two subjects were included and genotyped with respect to two single nucleotide polymorphisms of DTNBP1 (rs2619522 and rs1018381). All participants underwent structural magnetic resonance imaging (MRI). MRI data were preprocessed and statistically analysed using standard procedures as implemented in SPM5 (Statistical Parametric Mapping), in particular the voxel-based morphometry (VBM) toolbox. We found significant effects of the DTNBP1 SNP rs2619522 bilaterally in the hippocampus as well as in the anterior middle frontal gyrus and the intraparietal cortex. Carriers of the G allele showed significantly higher grey matter volumes in these brain regions than T/T homozygotes. Compatible with previous findings on a role of dysbindin in hippocampal functions as well as in major psychoses, the present study provides first direct in vivo evidence that the DTNBP1 SNP rs2619522 is associated with variation of grey matter volumes bilaterally in the hippocampus."],["dc.identifier.doi","10.1007/s00406-012-0320-0"],["dc.identifier.isi","000314296300006"],["dc.identifier.pmid","22580710"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/30828"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0940-1334"],["dc.title","The DTNBP1 (dysbindin-1) gene variant rs2619522 is associated with variation of hippocampal and prefrontal grey matter volumes in humans"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2011Conference Abstract [["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.volume","44"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Diekhof, Esther Kristina"],["dc.contributor.author","Zvonik, Kerstin"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Weber, K."],["dc.contributor.author","Petrovic, A."],["dc.contributor.author","Henseler, Ilona"],["dc.contributor.author","Zilles, David"],["dc.contributor.author","Melcher, T."],["dc.contributor.author","Keil, M."],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Falkai, Peter Gaston"],["dc.date.accessioned","2018-11-07T08:52:00Z"],["dc.date.available","2018-11-07T08:52:00Z"],["dc.date.issued","2011"],["dc.identifier.doi","10.1055/s-0031-1292483"],["dc.identifier.isi","000296086300067"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22064"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.conference","27th Symposium of the AGNP"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0176-3679"],["dc.title","Multi-functional MRI studies of disordered brain circuits in schizophrenic and affective psychoses"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI WOS2010Conference Abstract [["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Biological Psychiatry"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Reith, Wolfgang"],["dc.contributor.author","Meyer, Jobst"],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T08:43:24Z"],["dc.date.available","2018-11-07T08:43:24Z"],["dc.date.issued","2010"],["dc.format.extent","163S"],["dc.identifier.isi","000277064200517"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19956"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.conference","65th Annual Convention of the Society-of-Biological-Psychiatry"],["dc.relation.eventlocation","New Orleans, LA"],["dc.relation.issn","0006-3223"],["dc.title","Association of DISC1 Genetic Variation with Intermediate Phenotypes in Neuroimaging: Replication and Further Extension"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS2015Journal Article [["dc.bibliographiccitation.firstpage","303"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","311"],["dc.bibliographiccitation.volume","265"],["dc.contributor.author","Stegmayer, Katharina"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Henseler, Ilona"],["dc.contributor.author","Tost, Heike"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T09:56:51Z"],["dc.date.available","2018-11-07T09:56:51Z"],["dc.date.issued","2015"],["dc.description.abstract","Patients suffering from bipolar affective disorder show deficits in working memory functions. In a previous functional magnetic resonance imaging study, we observed an abnormal hyperactivity of the amygdala in bipolar patients during articulatory rehearsal in verbal working memory. In the present study, we investigated the dynamic neurofunctional interactions between the right amygdala and the brain systems that underlie verbal working memory in both bipolar patients and healthy controls. In total, 18 euthymic bipolar patients and 18 healthy controls performed a modified version of the Sternberg item-recognition (working memory) task. We used the psychophysiological interaction approach in order to assess functional connectivity between the right amygdala and the brain regions involved in verbal working memory. In healthy subjects, we found significant negative functional interactions between the right amygdala and multiple cortical brain areas involved in verbal working memory. In comparison with the healthy control subjects, bipolar patients exhibited significantly reduced functional interactions of the right amygdala particularly with the right-hemispheric, i.e., ipsilateral, cortical regions supporting verbal working memory. Together with our previous finding of amygdala hyperactivity in bipolar patients during verbal rehearsal, the present results suggest that a disturbed right-hemispheric \"cognitive-emotional\" interaction between the amygdala and cortical brain regions underlying working memory may be responsible for amygdala hyperactivation and affects verbal working memory (deficits) in bipolar patients."],["dc.identifier.doi","10.1007/s00406-014-0517-5"],["dc.identifier.isi","000354194500005"],["dc.identifier.pmid","25119145"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37050"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","1433-8491"],["dc.relation.issn","0940-1334"],["dc.title","Disturbed cortico-amygdalar functional connectivity as pathophysiological correlate of working memory deficits in bipolar affective disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details DOI PMID PMC WOS2015Journal Article [["dc.bibliographiccitation.firstpage","808"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Human Brain Mapping"],["dc.bibliographiccitation.lastpage","818"],["dc.bibliographiccitation.volume","37"],["dc.contributor.author","Goya-Maldonado, Roberto"],["dc.contributor.author","Brodmann, Katja"],["dc.contributor.author","Keil, Maria"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2017-09-07T11:47:50Z"],["dc.date.available","2017-09-07T11:47:50Z"],["dc.date.issued","2015"],["dc.description.abstract","Misdiagnosing bipolar depression can lead to very deleterious consequences of mistreatment. Although depressive symptoms may be similarly expressed in unipolar and bipolar disorder, changes in specific brain networks could be very distinct, being therefore informative markers for the differential diagnosis. We aimed to characterize specific alterations in candidate large-scale networks (frontoparietal, cingulo-opercular, and default mode) in symptomatic unipolar and bipolar patients using resting state fMRI, a cognitively low demanding paradigm ideal to investigate patients.MethodsNetworks were selected after independent component analysis, compared across 40 patients acutely depressed (20 unipolar, 20 bipolar), and 20 controls well-matched for age, gender, and education levels, and alterations were correlated to clinical parameters.ResultsDespite comparable symptoms, patient groups were robustly differentiated by large-scale network alterations. Differences were driven in bipolar patients by increased functional connectivity in the frontoparietal network, a central executive and externally-oriented network. Conversely, unipolar patients presented increased functional connectivity in the default mode network, an introspective and self-referential network, as much as reduced connectivity of the cingulo-opercular network to default mode regions, a network involved in detecting the need to switch between internally and externally oriented demands. These findings were mostly unaffected by current medication, comorbidity, and structural changes. Moreover, network alterations in unipolar patients were significantly correlated to the number of depressive episodes. Conclusion: Unipolar and bipolar groups displaying similar symptomatology could be clearly distinguished by characteristic changes in large-scale networks, encouraging further investigation of network fingerprints for clinical use."],["dc.identifier.doi","10.1002/hbm.23070"],["dc.identifier.gro","3150744"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7534"],["dc.language.iso","en"],["dc.notes.status","zu prĂĽfen"],["dc.relation.issn","1065-9471"],["dc.title","Differentiating unipolar and bipolar depression by alterations in large-scale brain networks"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]Details DOI2011Conference Abstract [["dc.bibliographiccitation.firstpage","101"],["dc.bibliographiccitation.journal","Bipolar Disorders"],["dc.bibliographiccitation.lastpage","102"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Focke, Niels K."],["dc.contributor.author","Zilles, David"],["dc.contributor.author","Schmitt, A."],["dc.contributor.author","Reith, W."],["dc.contributor.author","Meyer, J."],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T08:55:10Z"],["dc.date.available","2018-11-07T08:55:10Z"],["dc.date.issued","2011"],["dc.identifier.isi","000300102400254"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/22841"],["dc.notes.status","zu prĂĽfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Malden"],["dc.relation.conference","9th International Conference on Bipolar Disorder"],["dc.relation.eventlocation","Pittsburgh, PA"],["dc.relation.issn","1398-5647"],["dc.title","Effects of the bipolar disorder susceptibility gene CACNA1C on regional grey matter volumes: a voxel-based morphometry (VBM) study"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]Details WOS