Gruber, Oliver

[["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","254S"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","Biological Psychiatry"],["dc.bibliographiccitation.lastpage","255S"],["dc.bibliographiccitation.volume","63"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Henseler, Ilona"],["dc.contributor.author","Tost, Heike"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T11:16:21Z"],["dc.date.available","2018-11-07T11:16:21Z"],["dc.date.issued","2008"],["dc.identifier.isi","254163700809"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54565"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Inc"],["dc.publisher.place","New york"],["dc.relation.conference","63rd Annual Convention of the Society-of-Biological-Psychiatry"],["dc.relation.eventlocation","Washington, DC"],["dc.relation.issn","0006-3223"],["dc.title","Working memory dysfunction as phenotypic marker of schizophrenic and bipolar affective psychoses: Common and differential abnormalities in brain activation"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Bipolar Disorders"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Meyer, J."],["dc.contributor.author","Kraft, Susanne"],["dc.contributor.author","Kemmer, Claudia"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T11:01:38Z"],["dc.date.available","2018-11-07T11:01:38Z"],["dc.date.issued","2007"],["dc.format.extent","95"],["dc.identifier.isi","000253284000263"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/51194"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.publisher.place","Oxford"],["dc.relation.conference","International Conference on Bipolar Disorder"],["dc.relation.eventlocation","Pittsburgh, PA"],["dc.relation.issn","1398-5647"],["dc.title","Dopamine transporter genotype influences N-acetylaspartate in left putamen"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","119"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Acta Psychiatrica Scandinavica"],["dc.bibliographiccitation.lastpage","124"],["dc.bibliographiccitation.volume","121"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Menzel, Patrick"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Kemmer, Claudia"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Scherk, Harald"],["dc.date.accessioned","2018-11-07T08:45:58Z"],["dc.date.available","2018-11-07T08:45:58Z"],["dc.date.issued","2010"],["dc.description.abstract","Objective: The amygdala plays a major role in processing emotional stimuli. Fourteen studies using structural magnetic resonance imaging (MRI) have examined the amygdala volume in paediatric and adult patients with bipolar disorder (BD) compared with healthy controls (HC) and reported inconsistent findings. Lithium has been found to increase grey matter volume, and first evidence points towards an effect on regional brain volume such as the amygdala. Method: We examined the amygdala volume of euthymic patients with BD treated with lithium (n = 15), without lithium (n = 24) and HC (n = 41) using structural MRI. Results: Patients treated with lithium exhibited in comparison to HC a larger right absolute (+17.9%, P = 0.015) and relative (+18%, P = 0.017) amygdala volume. There was no significant difference in amygdala volume between patients without lithium treatment and HC. Conclusion: Lithium appears to have a sustained effect on a central core region of emotional processing and should therefore be considered in studies examining BD."],["dc.description.sponsorship","Saarland University Hospital, Germany [HOMFOR A/2003/21]"],["dc.identifier.doi","10.1111/j.1600-0447.2009.01428.x"],["dc.identifier.isi","000273300500006"],["dc.identifier.pmid","19573050"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20576"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell Publishing, Inc"],["dc.relation.issn","0001-690X"],["dc.title","Increased right amygdala volume in lithium-treated patients with bipolar I disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","283"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Psychiatrica Scandinavica"],["dc.bibliographiccitation.lastpage","288"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Kemmer, Claudia"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T11:16:17Z"],["dc.date.available","2018-11-07T11:16:17Z"],["dc.date.issued","2008"],["dc.description.abstract","Objective: Subcortical regions such as hippocampus, thalamus and ventral putamen are assumed to be involved in the pathophysiology of mood regulation. Disturbed hippocampal neuronal function indicated by reduced N-acetyl-aspartate (NAA) levels in bipolar patients was shown by several studies. Results in thalamus and putamen are inconsistent. Method: N-acetyl-aspartate, choline (Cho), creatine (Cr) and myo-inositol (Ins) were measured in left hippocampus, left thalamus and left putamen using proton magnetic resonance spectroscopy in 13 euthymic patients with bipolar I disorder and 13 pairwise matched healthy control subjects. Metabolic ratios NAA/Cr, NAA/Cho, Cho/Cr and Ins/Cr were calculated. Results: Patients with bipolar I disorder demonstrated significantly reduced NAA/Cr in the left hippocampus compared with healthy control subjects. No alterations were found in thalamus or putamen. Conclusion: We hypothesize that this NAA/Cr reduction might reflect neuronal dysfunction in the left hippocampus in patients with bipolar disorder."],["dc.identifier.doi","10.1111/j.1600-0447.2007.01142.x"],["dc.identifier.isi","000253757000007"],["dc.identifier.pmid","18205896"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54546"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Blackwell Publishing"],["dc.relation.issn","0001-690X"],["dc.title","Neurochemical pathology in hippocampus in euthymic patients with bipolar I disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","115"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Human Brain Mapping"],["dc.bibliographiccitation.lastpage","125"],["dc.bibliographiccitation.volume","31"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Tost, Heike"],["dc.contributor.author","Henseler, Ilona"],["dc.contributor.author","Schmael, Christine"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Ende, Gabriele"],["dc.contributor.author","Ruf, Matthias"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Rietschel, Marcella"],["dc.date.accessioned","2018-11-07T08:47:46Z"],["dc.date.available","2018-11-07T08:47:46Z"],["dc.date.issued","2010"],["dc.description.abstract","Recent evidence suggests that deficits of working memory may be a promising neurocognitive endophenotype of bipolar affective disorder. However, little is known about the neurobiological correlates of these deficits. The aim of this stud), was to determine possible pathophysiological trait markers of bipolar disorder in neural circuits involved in working memory. Functional magnetic resonance imaging was performed in 18 euthymic bipolar patients and IS matched healthy volunteers using two circuit-specific experimental tasks established by prior systematic neuroimaging Studies of working memory. Both euthymic bipolar patients and healthy controls showed working memory-related brain activations that were highly consistent with findings from previous comparable neuroimaging studies in healthy subjects. While these patterns of brain activation were completely preserved in the bipolar patients, only the patients exhibited activation of the right amygdala during the articulatory rehearsal task. in the same task, functional activation in right frontal and intraparietal cortex and in the right cerebellum was significantly enhanced in the patients. These findings indicate that the right amygdala is pathologically activated in euthymic bipolar patients during performance of a circuit-specific working memory task (articulatory rehearsal). This pathophysiological abnormality appears to be a trait marker in bipolar disorders that can be observed even in the euthymic state and that seems to be largely independent of task performance and medication. Hum Brain Mapp 31:115-125, 2010. (C) 2009 Wiley-Liss, Inc."],["dc.identifier.doi","10.1002/hbm.20849"],["dc.identifier.isi","000273544700010"],["dc.identifier.pmid","19603410"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21045"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-liss"],["dc.relation.issn","1065-9471"],["dc.title","Pathological Amygdala Activation During Working Memory Performance: Evidence for a Pathophysiological Trait Marker in Bipolar Affective Disorder"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Menzel, Patrick"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T10:59:21Z"],["dc.date.available","2018-11-07T10:59:21Z"],["dc.date.issued","2007"],["dc.format.extent","228"],["dc.identifier.isi","000249873600120"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50681"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.conference","25th Symposium of the Arbeitsgemeinschaft-Neuropsychopharmakologie-und-Pharmakopsychiatrie"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0176-3679"],["dc.title","5-HTTLPR polymorphism influences amygdala volume"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Der Nervenarzt"],["dc.bibliographiccitation.volume","78"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Menzel, Patrick"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T10:57:22Z"],["dc.date.available","2018-11-07T10:57:22Z"],["dc.date.issued","2007"],["dc.format.extent","276"],["dc.identifier.isi","000253318800700"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50229"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","New york"],["dc.relation.issn","0028-2804"],["dc.title","The 5HTTLPR Genotype influences the size of Amygdala"],["dc.type","conference_abstract"],["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"]]

[["dc.bibliographiccitation.firstpage","1513"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","1518"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Zill, Peter"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Reith, Wolfgang"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Moeller, Hans-Juergen"],["dc.contributor.author","Bondy, Brigitta"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T11:09:33Z"],["dc.date.available","2018-11-07T11:09:33Z"],["dc.date.issued","2008"],["dc.description.abstract","The SNAP-25 gene is an integral part of the vesicle docking and fusion machinery that controls neurotransmitter release. Several post mortem studies revealed a reduction of SNAP-25 protein in the hippocampus of patients with schizophrenia and bipolar disorder (BD). Thirty-eight patients with schizophrenia, BD or obsessive-compulsive disorder and 17 healthy controls participated in the study. Proton magnetic resonance spectroscopy in left hippocampus was performed in each individual. Three single nucleotide polymorphisms (SNP) of the SNAP-25 gene were genotyped. Individuals with the homozygous CC genotype of the DdeI SNP presented a significantly higher ratio of N-acetyl-aspartate (NAA)/choline-containing compounds (Cho) in the left hippocampus compared to the group of individuals with the homozygous TT genotype. The SNAP-25 genotype may modulate synaptic plasticity and neurogenesis in the left hippocampus, and altered NAA/Cho ratio may be an indicator for this genetic modulation of neuronal function in the hippocampus."],["dc.description.sponsorship","Saarland University Hospital, Germany [HOMFOR A/2003/21]"],["dc.identifier.doi","10.1007/s00702-008-0103-y"],["dc.identifier.isi","000260525900004"],["dc.identifier.pmid","18726138"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/3560"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53031"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","1435-1463"],["dc.relation.issn","0300-9564"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","SNAP-25 genotype influences NAA/Cho in left hippocampus"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]