Now showing 1 - 10 of 11
  • 2008Journal Article
    [["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"]]
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  • 2013Journal Article
    [["dc.bibliographiccitation.firstpage","74"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neuropsychobiology"],["dc.bibliographiccitation.lastpage","83"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Schneider, Marc"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Ruge, Diane"],["dc.contributor.author","Retz, Wolfgang"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Rösler, Michael"],["dc.date.accessioned","2018-11-07T09:30:13Z"],["dc.date.available","2018-11-07T09:30:13Z"],["dc.date.issued","2013"],["dc.description.abstract","Background: First-episode schizophrenia (FE-SZ) and attention deficit hyperactivity disorder (ADHD) are both neuropsychiatric disorders associated with an impaired dopaminergic transmission. Though displaying different clinical phenotypes, a common pathophysiological pathway is discussed controversially. Several studies using transcranial magnetic stimulation (TMS) revealed abnormalities in human motor cortex excitability in both schizophrenia and ADHD patients. Studies on cortical excitability comparing these two diseases directly are lacking. Method: In this study, a total of 94 subjects were analyzed.Twenty-five FE-SZ patients were directly compared with 28 ADHD patients and 41 healthy controls (HC). We investigated cortical excitability (inhibitory and facilitatory networks) with single- and paired-pulse TMS to the left and right motor cortex. Results: Compared to HC, FE-SZ/ADHD patients displayed an impaired cortical inhibition over the left hemisphere. Apart from an enhanced intracortical facilitation, FE-SZ patients did not differ compared to ADHD patients in the main outcome measures. Both patient groups presented a dysfunctional hemispheric pattern of cortical inhibition and facilitation in comparison with HC. Conclusion: The results of this study indicate a pattern of cortical disinhibition and abnormal hemispheric balance of intracortical excitability networks in two different psychiatric diseases. These effects might be associated with an imbalance in GABAergic and dopaminergic transmission and might provide evidence for a common pathophysiological pathway of both diseases. Copyright (C) 2013 S. Karger AG, Basel"],["dc.identifier.doi","10.1159/000343912"],["dc.identifier.isi","000315615000003"],["dc.identifier.pmid","23295893"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10824"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31253"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1423-0224"],["dc.relation.issn","0302-282X"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A Similar but Distinctive Pattern of Impaired Cortical Excitability in First-Episode Schizophrenia and ADHD"],["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"]]
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  • 2010Journal Article
    [["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"]]
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  • 2019Journal Article
    [["dc.bibliographiccitation.artnumber","284"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Translational Psychiatry"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Keeser, Daniel"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Raabe, Florian"],["dc.contributor.author","Degenhardt, Franziska"],["dc.contributor.author","Rossner, Moritz J."],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Cantuti-Castelvetri, Ludovico"],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Falkai, Peter Gaston"],["dc.date.accessioned","2019-12-18T14:16:43Z"],["dc.date.available","2019-12-18T14:16:43Z"],["dc.date.issued","2019"],["dc.description.abstract","Hippocampal volume decrease is a structural hallmark of schizophrenia (SCZ), and convergent evidence from postmortem and imaging studies suggests that it may be explained by changes in the cytoarchitecture of the cornu ammonis 4 (CA4) and dentate gyrus (DG) subfields. Increasing evidence indicates that aerobic exercise increases hippocampal volume in CA subfields and improves cognition in SCZ patients. Previous studies showed that the effects of exercise on the hippocampus might be connected to the polygenic burden of SCZ risk variants. However, little is known about cell type-specific genetic contributions to these structural changes. In this secondary analysis, we evaluated the modulatory role of cell type-specific SCZ polygenic risk scores (PRS) on volume changes in the CA1, CA2/3, and CA4/DG subfields over time. We studied 20 multi-episode SCZ patients and 23 healthy controls who performed aerobic exercise, and 21 multi-episode SCZ patients allocated to a control intervention (table soccer) for 3 months. Magnetic resonance imaging-based assessments were performed with FreeSurfer at baseline and after 3 months. The analyses showed that the polygenic burden associated with oligodendrocyte precursor cells (OPC) and radial glia (RG) significantly influenced the volume changes between baseline and 3 months in the CA4/DG subfield in SCZ patients performing aerobic exercise. A higher OPC- or RG-associated genetic risk burden was associated with a less pronounced volume increase or even a decrease in CA4/DG during the exercise intervention. We hypothesize that SCZ cell type-specific polygenic risk modulates the aerobic exercise-induced neuroplastic processes in the hippocampus."],["dc.identifier.doi","10.1038/s41398-019-0618-z"],["dc.identifier.pmid","31712617"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16922"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62762"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.eissn","2158-3188"],["dc.relation.issn","2158-3188"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Polygenic burden associated to oligodendrocyte precursor cells and radial glia influences the hippocampal volume changes induced by aerobic exercise in schizophrenia patients"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]
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  • 2009Journal Article
    [["dc.bibliographiccitation.firstpage","278"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","283"],["dc.bibliographiccitation.volume","259"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Woelwer, Wolfgang"],["dc.contributor.author","Gaebel, Wolfgang"],["dc.contributor.author","Riesbeck, Mathias"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Klosterkoetter, Joachim"],["dc.contributor.author","Schneider, Frank"],["dc.contributor.author","Buchkremer, Gerd"],["dc.contributor.author","Möller, Hans-Jürgen"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Bender, Stefan"],["dc.contributor.author","Schloesser, Ralf G. M."],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T11:25:57Z"],["dc.date.available","2018-11-07T11:25:57Z"],["dc.date.issued","2009"],["dc.description.abstract","Subtle structural brain abnormalities are an established finding in first-episode psychosis. Nevertheless their relationship to the clinical course of schizophrenia is controversially discussed. In a multicentre study 45 first-episode schizophrenia patients (FE-SZ) underwent standardized MRI scanning and were followed up to 1 year. In 32 FE-SZ volumetric measurement of three regions of interests (ROIs) potentially associated with disease course, hippocampus, lateral ventricle and the anterior limb of the internal capsule (ALIC) could be performed. The subgroups of FE-SZ with good (12 patients) and poor outcome (11 patients), defined by a clinically relevant change of the PANSS score, were compared with regard to these volumetric measures. Multivariate analysis of covariance revealed a significant reduced maximal cross sectional area of the left ALIC in FE-SZ with clinically relevant deterioration compared to those with stable psychopathology. There were no differences in the other selected ROIs between the two subgroups. In conclusion, reduced maximal area of ALIC, which can be interpreted as a disturbance of fronto-thalamic connectivity, is associated with poor outcome during the 1 year course of first-episode schizophrenia."],["dc.identifier.doi","10.1007/s00406-008-0867-y"],["dc.identifier.isi","000265574000004"],["dc.identifier.pmid","19224108"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6732"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56746"],["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","Internal capsule size associated with outcome in first-episode schizophrenia"],["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"]]
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  • 2010Journal Article
    [["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"]]
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  • 2012Journal Article
    [["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"]]
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  • 2011Journal Article
    [["dc.bibliographiccitation.firstpage","459"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","465"],["dc.bibliographiccitation.volume","261"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","McIntosh, Andrew M."],["dc.contributor.author","Droese, Uta-Aglaia"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Lawrie, Stephen M."],["dc.contributor.author","Moorhead, Thomas William"],["dc.contributor.author","Tepest, Ralf"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Wobrock, Thomas"],["dc.date.accessioned","2018-11-07T08:50:53Z"],["dc.date.available","2018-11-07T08:50:53Z"],["dc.date.issued","2011"],["dc.description.abstract","Cortical development and folding seems to be under environmental as well as genetic control. The aim of our study was to estimate the genetic influence on gyrification and cortical volumes, comparing prefrontal gyrification index (GI) in monozygotic (MZ) and dizygotic (DZ) twin pairs, and unrelated pairs. Twenty-four subjects (6 pairs of MZ and 6 pairs of DZ twins) were included in this study. Prefrontal cortical folding (gyrification) was measured by an automated and manual version of the gyrification index (A-GI, M-GI) according to previously published protocols. MR-imaging was performed and 3 representative slices were selected from coronar MR-imaging scans. The volumes of the total brain, temporal lobes, prefrontal lobes, and cerebellum were analyzed, too. To evaluate similarity in GI, absolute differences in GI, and brain volumes as well as intraclass correlations of twin pairs were compared with regard to twin status. Finally, a control group of unrelated pairs was assembled from the first two study groups and analyzed. Compared to unrelated pairs, twin pairs exhibited more similarity concerning different brain volumes and a trend to more similarity concerning A-GI. MZ twins did not present more similarity concerning GI (automatically and manually measured) and volume measurements compared to DZ twins. Different factors, like intrauterine factors, postnatal development conditions, and especially environmental factors might account for the differences between related and unrelated pairs. The nonexistence of a pronounced similarity in MZ twins compared to DZ twins concerning prefrontal GI raises questions about the extent of genetic influence on GI."],["dc.identifier.doi","10.1007/s00406-011-0198-2"],["dc.identifier.isi","000297619700002"],["dc.identifier.pmid","21336867"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7122"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/21799"],["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","Prefrontal cortex gyrification index in twins: an MRI study"],["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"]]
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  • 2010Journal Article
    [["dc.bibliographiccitation.firstpage","353"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Psychopharmacology"],["dc.bibliographiccitation.lastpage","363"],["dc.bibliographiccitation.volume","208"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Wolff-Menzler, Claus"],["dc.contributor.author","Guse, Birgit"],["dc.contributor.author","Lang, Nicolas"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Ecker, Ullrich K. H."],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T08:46:37Z"],["dc.date.available","2018-11-07T08:46:37Z"],["dc.date.issued","2010"],["dc.description.abstract","There is a high prevalence of substance use disorder (SUD) in first-episode schizophrenia (SZ), but its contribution to the underlying SZ pathophysiology remains unclear. Several studies using transcranial magnetic stimulation (TMS) have observed abnormalities in human motor cortex (M1) excitability in SZ. Studies on cortical excitability comparing SZ patients with and without comorbid substance abuse are lacking. A total of 29 first-episode SZ patients participated in this study; 12 had a history of comorbid cannabis abuse (SZ-SUD) and 17 did not (SZ-NSUD). We applied TMS to right and left M1 areas to assess the resting motor threshold (RMT), short-interval cortical inhibition (SICI), intracortical facilitation (ICF), and the contralateral cortical silent period (CSP). In SICI and ICF conditions, right M1 stimulation led to significantly higher motor evoked potential ratios in SZ-SUD compared to SZ-NSUD. This suggests lower cortical inhibition and increased ICF in first-episode SZ with previous cannabis abuse. There were no group differences in RMT and CSP duration. Neither were there any significant correlations between psychopathology (as indexed by Positive and Negative Syndrome Scale), disease characteristics, the extent of cannabis abuse, and TMS parameters (SICI, ICF, and CSP). Comorbid cannabis abuse may potentiate the reduced intracortical inhibition and enhanced ICF observed in first-episode SZ patients in some previous studies. This finding suggests an increased alteration of GABA(A) and NMDA receptor activity in cannabis-abusing first-episode patients as compared to schizophrenia patients with no history of substance abuse. This may constitute a distinct vulnerability factor in this special population."],["dc.identifier.doi","10.1007/s00213-009-1736-8"],["dc.identifier.isi","000273627400002"],["dc.identifier.pmid","19997844"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4025"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20737"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0033-3158"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Increased cortical inhibition deficits in first-episode schizophrenia with comorbid cannabis abuse"],["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"]]
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  • 2009Journal Article
    [["dc.bibliographiccitation.firstpage","143"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","150"],["dc.bibliographiccitation.volume","259"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Frommann, Nicole"],["dc.contributor.author","Woelwer, Wolfgang"],["dc.contributor.author","Gaebel, Wolfgang"],["dc.date.accessioned","2018-11-07T08:31:01Z"],["dc.date.available","2018-11-07T08:31:01Z"],["dc.date.issued","2009"],["dc.description.abstract","Chronic alcohol abuse leads to morphological changes of the brain. We investigated if these volumetric changes are reversible after a period of abstinence. For this reason 41 male and 15 female alcohol patients underwent MRI-scanning after in-patient detoxification (baseline) entering alcoholism treatment programs, and between 6 and 9 months later (follow-up), in a phase of convalescence. Additionally, 29 male and 16 female control subjects were examined. The MRI-scans were delineated and the resulting regions of interest, volumes of lateral ventricles and prefrontal lobes were expressed relatively to total brain volume. Compared to control subjects alcohol patients showed bilaterally decreased prefrontal lobes (11% reduction) and increased lateral ventricles (up to 42% enlargement). The extent of the ventricular increase was depending on patient's additional psychiatric diagnosis, showing smaller lateral ventricles in patients with additional personality disorder. While at follow-up the size of prefrontal lobes remained unchanged, volumes of the lateral ventricles decreased (5-6% reduction) in alcohol patients with abstinence and improved drinking behavior, especially in patients that underwent only one detoxification. The extent of the ventricular enlargement correlated with the elevation of alcohol related laboratory measures (mean corpuscular volume, gamma-glutamyl transpeptidase). In conclusion this study confirms the hypothesis that alcoholism causes brain damages that are partially reversible. It should be analyzed in further studies with larger sample sizes, if complete brain regeneration is possible maintaining abstinence over a longer period."],["dc.description.sponsorship","BMBF [01 EB 9408]"],["dc.identifier.doi","10.1007/s00406-008-0846-3"],["dc.identifier.isi","000265382900003"],["dc.identifier.pmid","19165528"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6730"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17026"],["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","Effects of abstinence on brain morphology in alcoholism"],["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"]]
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