Trost, Sarah Makbule

[["dc.bibliographiccitation.firstpage","839"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","840"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Zilles, D."],["dc.contributor.author","Koller, M."],["dc.contributor.author","Methfessel, I."],["dc.contributor.author","Trost, S."],["dc.contributor.author","Simon, A."],["dc.date.accessioned","2020-12-10T14:08:35Z"],["dc.date.available","2020-12-10T14:08:35Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00115-018-0559-4"],["dc.identifier.eissn","1433-0407"],["dc.identifier.issn","0028-2804"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70495"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.haserratum","/handle/2/70497"],["dc.title","Ethik, Evidenz und Elektrokonvulsionstherapie"],["dc.title.alternative","Ethics, evidence and electroconvulsive therapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1062"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","1062"],["dc.bibliographiccitation.volume","89"],["dc.contributor.author","Zilles, D."],["dc.contributor.author","Koller, M."],["dc.contributor.author","Methfessel, I."],["dc.contributor.author","Trost, S."],["dc.contributor.author","Simon, A."],["dc.date.accessioned","2020-12-10T14:08:36Z"],["dc.date.available","2020-12-10T14:08:36Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1007/s00115-018-0595-0"],["dc.identifier.eissn","1433-0407"],["dc.identifier.issn","0028-2804"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70497"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-354"],["dc.relation.iserratumof","/handle/2/70495"],["dc.title","Erratum zu: Ethik, Evidenz und Elektrokonvulsionstherapie"],["dc.title.alternative","Erratum to: Ethics, evidence and electroconvulsive therapy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","erratum_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","50"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.lastpage","56"],["dc.bibliographiccitation.volume","92"],["dc.contributor.author","Zilles-Wegner, David"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Walliser, Karoline"],["dc.contributor.author","Saager, Leif"],["dc.contributor.author","Horn, Sebastian"],["dc.contributor.author","Ernst, Mareike"],["dc.date.accessioned","2021-04-14T08:24:49Z"],["dc.date.available","2021-04-14T08:24:49Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1007/s00115-020-00960-7"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/81434"],["dc.language.iso","de"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","1433-0407"],["dc.relation.issn","0028-2804"],["dc.title","Elektrokonvulsionstherapie in der Schwangerschaft: Fallbericht und interdisziplinäre Behandlungsvorschläge"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.contributor.author","Belz, Michael"],["dc.contributor.author","Hessmann, Philipp"],["dc.contributor.author","Vogelgsang, Jonathan"],["dc.contributor.author","Schmidt, Ulrike"],["dc.contributor.author","Ruhleder, Mirjana"],["dc.contributor.author","Signerski-Krieger, Jörg"],["dc.contributor.author","Radenbach, Katrin"],["dc.contributor.author","Trost, Sarah"],["dc.contributor.author","Schott, Björn H."],["dc.contributor.author","Bartels, Claudia"],["dc.date.accessioned","2021-06-01T09:42:51Z"],["dc.date.available","2021-06-01T09:42:51Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract The Covid-19 pandemic highly impacts mental health worldwide. Patients with psychiatric disorders are a vulnerable risk population for worsening of their condition and relapse of symptoms. This study investigates the pandemic-related course of psychosocial burden in patients with pre-existing mental disorders. With the newly developed Goettingen psychosocial Burden and Symptom Inventory (Goe-BSI) psychosocial burden has been traced retrospectively (1) before the pandemic (beginning of 2020), (2) at its beginning under maximum lockdown conditions (March 2020), and (3) for the current state after maximum lockdown conditions (April/May 2020). The Goe-BSI also integrates the Adjustment Disorder New Module (ADNM-20), assesses general psychiatric symptoms, and resilience. A total of 213 patients covering all major psychiatric disorders (ICD-10 F0-F9) were interviewed once in the time range from April, 24th until May 11th, 2020. Across all diagnoses patients exhibited a distinct pattern with an initial rise followed by a decline of psychosocial burden ( p  < 0.001, partial η 2  = 0.09; Bonferroni-corrected pairwise comparisons between all three time-points: p  < 0.05 to 0.001). Female gender and high ADNM-20 scores were identified as risk factors for higher levels and an unfavorable course of psychosocial burden over time. Most psychiatric symptoms remained unchanged. Trajectories of psychosocial burden vary in parallel to local lockdown restrictions and seem to reflect an adaptive stress response. For female patients with pre-existing mental disorders and patients with high-stress responses, timely and specific treatment should be scheduled. With the continuation of the pandemic, monitoring of long-term effects is of major importance, especially when long incubation times for the development of mental health issues are considered."],["dc.identifier.doi","10.1007/s00406-021-01268-6"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/85373"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-425"],["dc.relation.eissn","1433-8491"],["dc.relation.issn","0940-1334"],["dc.title","Evolution of psychosocial burden and psychiatric symptoms in patients with psychiatric disorders during the Covid-19 pandemic"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["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 prüfen"],["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"]]

[["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 prüfen"],["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"]]

[["dc.bibliographiccitation.firstpage","153"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain imaging and behavior"],["dc.bibliographiccitation.lastpage","182"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Thompson, Paul M."],["dc.contributor.author","Stein, Jason L."],["dc.contributor.author","Medland, Sarah E."],["dc.contributor.author","Hibar, Derrek P."],["dc.contributor.author","Arias-Vasquez, Alejandro"],["dc.contributor.author","Renteria, Miguel E."],["dc.contributor.author","Toro, Roberto"],["dc.contributor.author","Jahanshad, Neda"],["dc.contributor.author","Schumann, Gunter"],["dc.contributor.author","Franke, Barbara"],["dc.contributor.author","Trost, Sarah"],["dc.date.accessioned","2019-07-09T11:41:33Z"],["dc.date.available","2019-07-09T11:41:33Z"],["dc.date.issued","2014-06-01"],["dc.description.abstract","The Enhancing NeuroImaging Genetics through Meta-Analysis (ENIGMA) Consortium is a collaborative network of researchers working together on a range of large-scale studies that integrate data from 70 institutions worldwide. Organized into Working Groups that tackle questions in neuroscience, genetics, and medicine, ENIGMA studies have analyzed neuroimaging data from over 12,826 subjects. In addition, data from 12,171 individuals were provided by the CHARGE consortium for replication of findings, in a total of 24,997 subjects. By meta-analyzing results from many sites, ENIGMA has detected factors that affect the brain that no individual site could detect on its own, and that require larger numbers of subjects than any individual neuroimaging study has currently collected. ENIGMA's first project was a genome-wide association study identifying common variants in the genome associated with hippocampal volume or intracranial volume. Continuing work is exploring genetic associations with subcortical volumes (ENIGMA2) and white matter microstructure (ENIGMA-DTI). Working groups also focus on understanding how schizophrenia, bipolar illness, major depression and attention deficit/hyperactivity disorder (ADHD) affect the brain. We review the current progress of the ENIGMA Consortium, along with challenges and unexpected discoveries made on the way."],["dc.identifier.doi","10.1007/s11682-013-9269-5"],["dc.identifier.fs","610752"],["dc.identifier.pmid","24399358"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12172"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58451"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1931-7565"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.mesh","Brain Mapping"],["dc.subject.mesh","Cooperative Behavior"],["dc.subject.mesh","Genome-Wide Association Study"],["dc.subject.mesh","Humans"],["dc.subject.mesh","Meta-Analysis as Topic"],["dc.subject.mesh","Neuroimaging"],["dc.title","The ENIGMA Consortium: large-scale collaborative analyses of neuroimaging and genetic data."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["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 prüfen"],["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"]]

[["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 prüfen"],["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"]]

[["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 prüfen"],["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"]]