Gruber, Oliver

[["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"]]

[["dc.bibliographiccitation.firstpage","455"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","464"],["dc.bibliographiccitation.volume","260"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","McIntosh, Andrew M."],["dc.contributor.author","Kraft, Susanne"],["dc.contributor.author","Klinghardt, Anne"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Reith, Wolfgang"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Lawrie, Stephen M."],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Moorhead, Thomas William"],["dc.date.accessioned","2018-11-07T08:39:38Z"],["dc.date.available","2018-11-07T08:39:38Z"],["dc.date.issued","2010"],["dc.description.abstract","Structural magnetic resonance imaging (MRI) studies reveal evidence for brain abnormalities in obsessive-compulsive disorder (OCD), for instance, reduction of gray matter volume in the prefrontal cortex. Disturbances of gyrification in the prefrontal cortex have been described several times in schizophrenia pointing to a neurodevelopmental etiology, while gyrification has not been studied so far in OCD patients. In 26 OCD patients and 38 healthy control subjects MR-imaging was performed. Prefrontal cortical folding (gyrification) was measured bilaterally by an automated version of the automated-gyrification index (A-GI), a ratio reflecting the extent of folding, from the slice containing the inner genu of the corpus callosum up to the frontal pole. Analysis of covariance (ANCOVA, independent factor diagnosis, covariates age, duration of education) demonstrated that compared with control subjects, patients with OCD displayed a significantly reduced A-GI in the left hemisphere (p = 0.021) and a trend for a decreased A-GI in the right hemisphere (p = 0.076). Significant correlations between prefrontal lobe volume and A-GI were only observed in controls, but not in OCD patients. In conclusion, prefrontal hypogyrification in OCD patients may be a structural correlate of the impairment in executive function of this patient group and may point to a neurodevelopmental origin of this disease."],["dc.identifier.doi","10.1007/s00406-009-0096-z"],["dc.identifier.isi","000281947000003"],["dc.identifier.pmid","20112027"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5776"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/19044"],["dc.notes.intern","Merged from goescholar"],["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.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Reduced prefrontal gyrification in obsessive-compulsive disorder"],["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"]]

[["dc.bibliographiccitation.firstpage","212"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","217"],["dc.bibliographiccitation.volume","259"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Menzel, Patrick"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Kemmer, Claudia"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Reith, Wolfgang"],["dc.contributor.author","Meyer, Jobst"],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T08:29:07Z"],["dc.date.available","2018-11-07T08:29:07Z"],["dc.date.issued","2009"],["dc.description.abstract","Functional imaging studies in healthy individuals revealed an association between 5-HTTLPR genotype and neuronal activity in the amygdala. The aim of this study was firstly to investigate a possible overall impact of the 5-HTTLPR on amygdala volume in patients with bipolar disorder and healthy individuals and secondly to test a diagnosis specific influence of the 5-HTTLPR on amygdala volume. We performed a region of interest analysis of amygdala volume in 37 patients with bipolar I disorder and 37 healthy control subjects. The 5-HTTLPR genotype of each proband was determined and the subjects were separated according to 5-HTTLPR genotype and for statistical analyses the groups SS and SL were combined and compared with the group LL. This study shows that carriers of the short allele (SL or SS) of the 5-HTTLPR polymorphism exhibit a relatively increased volume of the right amygdala compared to homozygous L-allele carriers irrespective of diagnosis status. However, further analyses with the factors genotype and diagnosis were not able to reproduce this result. The present findings are consistent with the view that the 5-HTTLPR polymorphism might modulate neuronal size or number in the amygdala. It would be worthwhile investigating the relationship between serotonin transporter function and amygdala function and volume in further studies."],["dc.identifier.doi","10.1007/s00406-008-0853-4"],["dc.identifier.isi","000265383100003"],["dc.identifier.pmid","19224115"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6731"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16573"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0940-1334"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","5-HTTLPR genotype influences amygdala volume"],["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"]]

[["dc.bibliographiccitation.firstpage","601"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","607"],["dc.bibliographiccitation.volume","260"],["dc.contributor.author","Radenbach, Katrin E."],["dc.contributor.author","Flaig, V."],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Scherk, Harald"],["dc.date.accessioned","2018-11-07T08:36:09Z"],["dc.date.available","2018-11-07T08:36:09Z"],["dc.date.issued","2010"],["dc.description.abstract","There are several hypotheses on functional neuronal networks that modulate mood states and which might form the neuroanatomical basis of bipolar disorder. The thalamus has been reported to be a key structure within the circuits that modulate mood states and might thus play an important role within the aetiology of the bipolar affective disorder. Nevertheless, structural brain imaging studies on the thalamus volume of bipolar patients have shown heterogeneous results. Using structural MRI scanning, we compared the thalamus volume of 41 euthymic bipolar patients to the thalamus volume of 41 well-matched healthy controls. Taking the concomitant medication as a co-variable within the patient group, the analysis of variance revealed a significantly smaller relative volume of the right thalamus in patients not treated with lithium when compared with healthy controls. In contrast, there are no significant differences concerning the thalamus volume between all euthymic bipolar patients and healthy controls. The study only shows findings of a transverse section. No longitudinal analysis was performed. More detailed information on patients' pharmacological histories could not be obtained. In conclusion, this result may be interpreted as an indication of the impact of the thalamus in the pathogenesis of the bipolar I disorder and emphasises the need for further longitudinal studies in bipolar patients with special attention paid to the concomitant medication, in particular to the role of lithium."],["dc.description.sponsorship","Saarland University Hospital, Germany [HOMFOR A/2003/21]"],["dc.identifier.doi","10.1007/s00406-010-0100-7"],["dc.identifier.isi","000284898200005"],["dc.identifier.pmid","20127489"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5975"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18242"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0940-1334"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Thalamic volumes in patients with bipolar disorder"],["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"]]

[["dc.bibliographiccitation.firstpage","345"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","349"],["dc.bibliographiccitation.volume","258"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Kemmer, Claudia"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Reith, Wolfgang"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T11:12:22Z"],["dc.date.available","2018-11-07T11:12:22Z"],["dc.date.issued","2008"],["dc.description.abstract","Background Structural brain imaging is assumed to be a key method to elucidate the underlying neuropathology of bipolar disorder. However, magnetic resonance imaging studies using region of interest analysis and voxel-based morphometry (VBM) revealed quite inconsistent findings. Hence, there is no clear evidence so far for core regions of cortical or subcortical structural abnormalities in bipolar disorder. The aim of this study was to investigate grey and white matter volumes in a large sample of patients with bipolar I disorder. Methods Thirty-five patients with bipolar I disorder and 32 healthy controls matched with respect to gender, handedness and education participated in the study. MRI scanning was performed and an optimized VBM analysis was conducted. Results We could not observe any significant differences of grey or white matter volumes between patients with bipolar disorder and healthy control subjects. Additional analyses did not reveal significant correlations between grey or white matter volume with number of manic or depressive episodes, duration of illness, existence of psychotic symptoms, and treatment with lithium or antipsychotics. Conclusions With this VBM study we were not able to identify core regions of structural abnormalities in bipolar disorder."],["dc.identifier.doi","10.1007/s00406-007-0801-8"],["dc.identifier.isi","000258654900004"],["dc.identifier.pmid","18347837"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6733"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53647"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0940-1334"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","No change to grey and white matter volumes in bipolar I disorder patients"],["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"]]

[["dc.bibliographiccitation.firstpage","133"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","ARCH GEN PSYCHIATRY"],["dc.bibliographiccitation.lastpage","143"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Pajonk, Frank-Gerald"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Berner, Dorothea"],["dc.contributor.author","Kaizl, Inge"],["dc.contributor.author","Kierer, Astrid"],["dc.contributor.author","Müller, Stephanie"],["dc.contributor.author","Oest, Martin"],["dc.contributor.author","Meyer, Tim"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Thornton, Allen E."],["dc.contributor.author","Honer, Willam G."],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2019-07-10T08:13:32Z"],["dc.date.available","2019-07-10T08:13:32Z"],["dc.date.issued","2010"],["dc.description.abstract","Context: Hippocampal volume is lower than expected in patients with schizophrenia; however, whether this represents a fixed deficit is uncertain. Exercise is a stimulus to hippocampal plasticity. Objective: To determine whether hippocampal volume would increase with exercise in humans and whether this effect would be related to improved aerobic fitness. Design: Randomized controlled study. Setting: Patients attending a day hospital program or an outpatient clinic. Patients or Other Participants: Male patients with chronic schizophrenia and matched healthy subjects. Interventions: Aerobic exercise training (cycling) and playing table football (control group) for a period of 3 months. Main Outcome Measures: Magnetic resonance imaging of the hippocampus. Secondary outcome measures were magnetic resonance spectroscopy, neuropsychological (Rey Auditory Verbal Learning Test, Corsi blocktapping test), and clinical (Positive and Negative Syndrome Scale) features. Results: Following exercise training, relative hippocampal volume increased significantly in patients (12%) and healthy subjects (16%), with no change in the nonexercise group of patients (−1%). Changes in hippocampal volume in the exercise group were correlated with improvements in aerobic fitness measured by change in maximum oxygen consumption (r=0.71; P=.003). In the schizophrenia exercise group (but not the controls), change in hippocampal volume was associated with a 35% increase in the N-acetylaspartate to creatine ratio in the hippocampus. Finally, improvement in test scores for short-term memory in the combined exercise and nonexercise schizophrenia group was correlated with change in hippocampal volume (r=0.51; P .05). Conclusion: These results indicate that in both healthy subjects and patients with schizophrenia hippocampal volume is plastic in response to aerobic exercise."],["dc.identifier.fs","575536"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6145"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61270"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Hippocampal Plasticity in Response to Exercise in Schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","23"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","31"],["dc.bibliographiccitation.volume","262"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Ekawardhani, Savira"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Reith, Wolfgang"],["dc.contributor.author","Meyer, Jobst"],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T09:13:53Z"],["dc.date.available","2018-11-07T09:13:53Z"],["dc.date.issued","2012"],["dc.description.abstract","The brain-derived neurotrophic factor (BDNF) is a key regulator of synaptic plasticity and has been suggested to be involved in the pathophysiology and pathogenesis of psychotic disorders, with particular emphasis on dysfunctions of the hippocampus. The aim of the present study was to replicate and to extend prior findings of BDNF val66met genotype effects on hippocampal volume and N-acetyl aspartate (NAA) levels. Hundred and fifty-eight caucasians (66 schizophrenic, 45 bipolar, and 47 healthy subjects; 105 subjects underwent MRI and 103 MRS scanning) participated in the study and were genotyped with regard to the val66met polymorphism (rs6265) of the BDNF gene. Hippocampal volumes were determined using structural magnetic resonance imaging (MRI), and measures of biochemical markers were taken using proton magnetic resonance spectroscopy (H-1-MRS) in the hippocampus and other brain regions. Verbal memory was assessed as a behavioral index of hippocampal function. BDNF genotype did not impact hippocampal volumes. Significant genotype effects were found on metabolic markers specifically in the left hippocampus. In particular, homozygous carriers of the met-allele exhibited significantly lower NAA/Cre and (Glu + Gln)/Cre metabolic ratios compared with val/val homozygotes, independently of psychiatric diagnoses. BDNF genotype had a numerical, but nonsignificant effect on verbal memory performance. These findings provide first in vivo evidence for an effect of the functional BDNF val66met polymorphism on the glutamate system in human hippocampus."],["dc.identifier.doi","10.1007/s00406-011-0214-6"],["dc.identifier.isi","000300058000004"],["dc.identifier.pmid","21509595"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8066"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27273"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0940-1334"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Association of the brain-derived neurotrophic factor val66met polymorphism with magnetic resonance spectroscopic markers in the human hippocampus: in vivo evidence for effects on the glutamate system"],["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"]]