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.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","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","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.journal","Schizophrenia Bulletin"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Meyer, J."],["dc.contributor.author","Falkai, Peter Gaston"],["dc.date.accessioned","2018-11-07T08:32:30Z"],["dc.date.available","2018-11-07T08:32:30Z"],["dc.date.issued","2009"],["dc.format.extent","92"],["dc.identifier.isi","000263964700269"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17353"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.publisher.place","Oxford"],["dc.relation.conference","12th International Congress on Schizophrenia Research"],["dc.relation.eventlocation","San Diego, CA"],["dc.relation.issn","0586-7614"],["dc.title","ASSOCIATION OF THE BRAIN-DERIVED NEUROTROPHIC FACTOR (BDNF) VAL66MET POLYMORPHISM WITH HIPPOCAMPAL N-ACETYL ASPARTATE (NAA/CHO) LEVEL AND VERBAL MEMORY CAPACITY"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]

[["dc.bibliographiccitation.journal","European Psychiatry"],["dc.bibliographiccitation.volume","23"],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Reith, W."],["dc.contributor.author","Moeller, Hans-Juergen"],["dc.contributor.author","Bondy, Brigitta"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T11:16:30Z"],["dc.date.available","2018-11-07T11:16:30Z"],["dc.date.issued","2008"],["dc.format.extent","S19"],["dc.identifier.doi","10.1016/j.eurpsy.2008.01.068"],["dc.identifier.isi","000254987800066"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/54601"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier France-editions Scientifiques Medicales Elsevier"],["dc.publisher.place","Paris"],["dc.relation.issn","0924-9338"],["dc.title","Influences of snap-25 polymorphisms on cognition and MRS spectra in psychoses and OCD"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","188"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","199"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Guse, Birgit"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Ecker, Ullrich K. H."],["dc.contributor.author","Heimes, Janina"],["dc.contributor.author","Galea, Joseph Michael"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Scherk, Harald"],["dc.date.accessioned","2018-11-07T09:42:18Z"],["dc.date.available","2018-11-07T09:42:18Z"],["dc.date.issued","2014"],["dc.description.abstract","Objectives. Impairments in memory and executive function are key components of schizophrenia. These disturbances have been linked to several subcortical and cortical networks. For example, anatomical and functional changes in the hippocampus have been linked to deficits in these cognitive domains. However, the association between hippocampal morphometry, neurochemistry and function is controversial. Therefore, we aimed to investigate the relationship between hippocampal anomalies and their functional relevance. Methods. Fifty-seven first-episode schizophrenia patients (FE-SZ) and 61 healthy control subjects (HC) participated in this study. Hippocampal volumes were investigated using structural magnetic resonance imaging (sMRI) and hippocampal neurochemistry was determined using proton magnetic resonance spectroscopy (1H MRS). Verbal memory was used as a hippocampus-dependent cognitive task whereas working memory and cognitive flexibility assessed frontal lobe function. Results. FE-SZ presented smaller volumes of the left hippocampus, with a significant correlation between left hippocampal volume and verbal memory performance (immediate recall). There was also an inverse correlation between neurochemical ratios (NAA/Cho and Cho/Cr) and verbal memory (delayed recognition). Tests of cognitive flexibility and working memory were not correlated with MRI and 1H MRS values. Compared to HC, FE-SZ demonstrated reduced performance in all of the assessed neurocognitive domains. Conclusions. These results point to a relationship between verbal memory and hippocampal integrity in schizophrenia patients which might be independent from deficits in other memory domains. Disturbed verbal memory functions in FE-SZ might be linked specifically to hippocampal function."],["dc.description.sponsorship","Deutsche Forschungsgemeinschaft (DFG) [HA 6091/1-1]"],["dc.identifier.doi","10.3109/15622975.2011.620002"],["dc.identifier.isi","000332798400003"],["dc.identifier.pmid","22047183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33925"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","1814-1412"],["dc.relation.issn","1562-2975"],["dc.title","Hippocampal integrity and neurocognition in first-episode schizophrenia: A multidimensional study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","285"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","294"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Scherk, Harald"],["dc.contributor.author","Backens, Martin"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Usher, Juliana"],["dc.contributor.author","Kemmer, Claudia"],["dc.contributor.author","Reith, Wolfgang"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Gruber, Oliver"],["dc.date.accessioned","2018-11-07T08:35:37Z"],["dc.date.available","2018-11-07T08:35:37Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective. Prefrontal and anterior cingulate cortical regions are assumed to be involved in the pathophysiology of mood regulation. Reduced prefrontal and anterior cingulate function indicated by decreased N-acetyl-aspartate (NAA) levels in patients with bipolar disorder has been reported inconsistently. A positive correlation between lithium serum level and NAA concentrations has been found previously. The aim of this study was to re-investigate prefrontal and anterior cingulate neurochemistry in a sample of euthymic patients with bipolar I disorder. Methods. NAA, choline (Cho), creatine (Cr) and myo-inositol (Ins) in left dorsolateral prefrontal cortex and left anterior cingulate cortex were measured in 33 euthymic patients with bipolar I disorder and 29 healthy comparison subjects by using proton magnetic resonance spectroscopy ([(1)H]MRS). Results. Metabolic ratios did not differ between patients with bipolar I disorder and comparison subjects in prefrontal and anterior cingulate cortex neither in the total sample nor in the pairwise matched sub-sample. We could not observe an association between lithium level and NAA ratios. Lithium treated patients demonstrated unchanged NAA or myo-inositol ratios compared to alternatively treated patients. Conclusion. In contrast to prior findings, we could not observe any metabolic alterations in euthymic patients with bipolar disorder."],["dc.description.sponsorship","Saarland University Hospital, Germany (HOM-FOR) [A/2003/21]"],["dc.identifier.doi","10.3109/15622970701472086"],["dc.identifier.isi","000273002200005"],["dc.identifier.pmid","19921970"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18110"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Taylor & Francis Ltd"],["dc.relation.issn","1562-2975"],["dc.title","Cortical neurochemistry 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"]]