Wobrock, Thomas

[["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The International Journal of Neuropsychopharmacology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Strube, Wolfgang"],["dc.contributor.author","Nitsche, Michael A."],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Bunse, Tilmann"],["dc.contributor.author","Rein, Bettina"],["dc.contributor.author","Herrmann, Maximiliane"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Nieratschker, Vanessa"],["dc.contributor.author","Witt, Stephanie H."],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Hasan, Alkomiet"],["dc.date.accessioned","2018-11-07T10:01:13Z"],["dc.date.available","2018-11-07T10:01:13Z"],["dc.date.issued","2015"],["dc.description.abstract","Background: Brain-derived neurotrophic factor (BDNF) has been shown to be a moderator of neuroplasticity. A frequent BDNF-polymorphism (Val66Met) is associated with impairments of cortical plasticity. In patients with schizophrenia, reduced neuroplastic responses following non-invasive brain stimulation have been reported consistently. Various studies have indicated a relationship between the BDNF-Val66Met-polymorphism and motor-cortical plasticity in healthy individuals, but schizophrenia patients have yet to be investigated. The aim of this proof-of-concept study was, therefore, to test the impact of the BDNF-Val66Met-polymorphism on inhibitory and facilitatory cortical plasticity in schizophrenia patients. Methods: Cortical plasticity was investigated in 22 schizophrenia patients and 35 healthy controls using anodal and cathodal transcranial direct-current stimulation (tDCS) applied to the left primary motor cortex. Animal and human research indicates that excitability shifts following anodal and cathodal tDCS are related to molecular long-term potentiation and long-term depression. To test motor-cortical excitability before and after tDCS, well-established single-and paired-pulse transcranial magnetic stimulation protocols were applied. Results: Our analysis revealed increased glutamate-mediated intracortical facilitation in met-heterozygotes compared to val-homozygotes at baseline. Following cathodal tDCS, schizophrenia met-heterozygotes had reduced gamma-amino-butyric-acid-mediated short-interval intracortical inhibition, whereas healthy met-heterozygotes displayed the opposite effect. The BDNF-Val66Met-polymorphism did not influence single-pulse motor-evoked potential amplitudes after tDCS. Conclusions: These preliminary findings support the notion of an association of the BDNF-Val66Met-polymorphism with observable alterations in plasticity following cathodal tDCS in schizophrenia patients. This indicates a complex interaction between inhibitory intracortical interneuron-networks, cortical plasticity, and the BDNF-Val66Met-polymorphism. Further replication and validation need to be dedicated to this question to confirm this relationship."],["dc.description.sponsorship","AstraZeneca; I3G; AOK"],["dc.identifier.doi","10.1093/ijnp/pyu040"],["dc.identifier.isi","000352536800005"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11781"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/37969"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","1469-5111"],["dc.relation.issn","1461-1457"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","BDNF-Val66Met-Polymorphism Impact on Cortical Plasticity in Schizophrenia Patients: A Proof-of-Concept 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"]]

[["dc.bibliographiccitation.artnumber","121"],["dc.bibliographiccitation.journal","Frontiers in psychiatry"],["dc.bibliographiccitation.volume","4"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Bergener, Theresa"],["dc.contributor.author","Nitsche, Michael A."],["dc.contributor.author","Strube, Wolfgang"],["dc.contributor.author","Bunse, Tilmann"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Wobrock, Thomas"],["dc.date.accessioned","2019-07-09T11:40:09Z"],["dc.date.available","2019-07-09T11:40:09Z"],["dc.date.issued","2013"],["dc.description.abstract","Transcranial direct current stimulation (tDCS) is a non-invasive stimulation technique that can be applied to modulate cortical activity through induction of cortical plasticity. Since various neuropsychiatric disorders are characterized by fluctuations in cortical activity levels (e.g., schizophrenia), tDCS is increasingly investigated as a treatment tool. Several studies have shown that the induction of cortical plasticity following classical, unilateral tDCS is reduced or impaired in the stimulated and non-stimulated primary motor cortices (M1) of patients with schizophrenia. Moreover, an alternative, bilateral tDCS setup has recently been shown to modulate cortical plasticity in both hemispheres in healthy subjects, highlighting another potential treatment approach. Here we present the first study comparing the efficacy of unilateral tDCS (cathode left M1, anode right supraorbital) with simultaneous bilateral tDCS (cathode left M1, anode right M1) in patients with schizophrenia. tDCS-induced cortical plasticity was monitored by investigating motor-evoked potentials induced by single-pulse transcranial magnetic stimulation applied to both hemispheres. Healthy subjects showed a reduction of left M1 excitability following unilateral tDCS on the stimulated left hemisphere and an increase in right M1 excitability following bilateral tDCS. In schizophrenia, no plasticity was induced following both stimulation paradigms. The pattern of these results indicates a complex interplay between plasticity and connectivity that is impaired in patients with schizophrenia. Further studies are needed to clarify the biological underpinnings and clinical impact of these findings."],["dc.identifier.doi","10.3389/fpsyt.2013.00121"],["dc.identifier.fs","598800"],["dc.identifier.pmid","24109457"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10691"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58101"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1664-0640"],["dc.rights","CC BY 3.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/3.0"],["dc.title","Impairments of motor-cortex responses to unilateral and bilateral direct current stimulation in schizophrenia."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","15"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Brain Research"],["dc.bibliographiccitation.lastpage","23"],["dc.bibliographiccitation.volume","217"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Hamada, Masashi"],["dc.contributor.author","Nitsche, Michael A."],["dc.contributor.author","Ruge, Diane"],["dc.contributor.author","Galea, Joseph Michael"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Rothwell, John C."],["dc.date.accessioned","2018-11-07T09:13:07Z"],["dc.date.available","2018-11-07T09:13:07Z"],["dc.date.issued","2012"],["dc.description.abstract","Animal studies using polarising currents have shown that induction of synaptic long-term potentiation (LTP) and long-term depression (LTD) by bursts of patterned stimulation is affected by the membrane potential of the postsynaptic neurone. The aim of the present experiments was to test whether it is possible to observe similar phenomena in humans with the aim of improving present protocols of inducing synaptic plasticity for therapeutic purposes. We tested whether the LTP/LTD-like after effects of transcranial theta-burst stimulation (TBS) of human motor cortex, an analogue of patterned electrical stimulation in animals, were affected by simultaneous transcranial direct-current stimulation (tDCS), a non-invasive method of polarising cortical neurones in humans. Nine healthy volunteers were investigated in a single-blind, balanced cross-over study; continuous TBS (cTBS) was used to introduce LTD-like after effects, whereas intermittent TBS (iTBS) produced LTP-like effects. Each pattern was coupled with concurrent application of tDCS (<200 s, anodal, cathodal, sham). Cathodal tDCS increased the response to iTBS and abolished the effects of cTBS. Anodal tDCS changed the effects of cTBS towards facilitation, but had no impact on iTBS. Cortical motor thresholds and intracortical inhibitory/facilitatory networks were not altered by any of the stimulation protocols. We conclude that the after effects of TBS can be modulated by concurrent tDCS. We hypothesise that tDCS changes the membrane potential of the apical dendrites of cortical pyramidal neurones and that this changes the response to patterned synaptic input evoked by TBS. The data show that it may be possible to enhance LTP-like plasticity after TBS in the human cortex."],["dc.identifier.doi","10.1007/s00221-011-2968-5"],["dc.identifier.isi","000300580400003"],["dc.identifier.pmid","22143872"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/7295"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27099"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0014-4819"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Direct-current-dependent shift of theta-burst-induced plasticity in the human motor cortex"],["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","415"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","423"],["dc.bibliographiccitation.volume","262"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Aborowa, Richard"],["dc.contributor.author","Nitsche, Michael A."],["dc.contributor.author","Marshall, Louise"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Wobrock, Thomas"],["dc.date.accessioned","2018-11-07T09:07:26Z"],["dc.date.available","2018-11-07T09:07:26Z"],["dc.date.issued","2012"],["dc.description.abstract","Post-mortem and in vivo studies provide evidence for a link between reduced plasticity and dysconnectivity in schizophrenia patients. It has been suggested that the association between plasticity and connectivity contributes to the pathophysiology and symptomatology of schizophrenia. However, little is known about the impact of glutamate-dependent long-term depression (LTD)-like cortical plasticity on inter-hemispheric connectivity in schizophrenia patients. The aim of the present study was to investigate LTD-like cortical plasticity following excitability-diminishing cathodal transcranial direct current stimulation (tDCS) of the left primary motor cortex (M1) and its effects on the non-stimulated right M1. Eighteen schizophrenia patients and 18 matched (age, gender, handedness, and smoking status) control subjects were investigated in this study. Corticospinal excitability changes following tDCS and intra-cortical inhibitory circuits were monitored with transcranial magnetic stimulation. On the stimulated hemisphere, cathodal tDCS increased resting motor thresholds (RMT) in both groups and decreased motor-evoked potential (MEP) sizes in healthy controls to a greater extent compared to schizophrenia patients. On the non-stimulated hemisphere, RMTs were increased and MEPs were decreased only in the healthy control group. Our results confirm previous findings of reduced LTD-like plasticity in schizophrenia patients and offer hypothetical and indirect in vivo evidence for an association between LTD-like cortical plasticity and inter-hemispheric connectivity in schizophrenia patients. Moreover, our findings highlight the impact of plasticity on connectivity. Dysfunctional N-methyl d-aspartate receptors or modulation of dopaminergic transmission can explain these findings. Nevertheless, the effects of antipsychotic medication still need to be considered."],["dc.identifier.doi","10.1007/s00406-012-0298-7"],["dc.identifier.isi","000307309300006"],["dc.identifier.pmid","22318337"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8094"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/25794"],["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","Abnormal bihemispheric responses in schizophrenia patients following cathodal transcranial direct stimulation"],["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","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"]]

[["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"]]

[["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.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"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","100"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuropsychobiology"],["dc.bibliographiccitation.lastpage","107"],["dc.bibliographiccitation.volume","79"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Levold, Katrin"],["dc.contributor.author","Labusga, Marcin"],["dc.contributor.author","Keller-Varady, Katriona"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Hasan, Alkomiet"],["dc.date.accessioned","2020-12-10T18:37:50Z"],["dc.date.available","2020-12-10T18:37:50Z"],["dc.date.issued","2020"],["dc.description.abstract","Background: Aerobic endurance training has been discussed to induce brain plasticity and improve cognitive functions in healthy subjects and patients with neuropsychiatric disorders. For schizophrenia, a motor cortical inhibitory deficit has been established as one aspect of impaired plasticity, especially involving impairments in GABAergic interneuron networks, but the possibility to restore these deficits via exercise-induced plasticity has not been evaluated yet. Methods: 17 schizophrenia patients and 16 matched healthy controls underwent 3 months of aerobic endurance training (30 min, 3 times a week) on bicycle ergometers. After 6 weeks, computer-assisted cognitive remediation training (30 min, 2 times a week) was added. Transcranial magnetic stimulation of the left and right hemispheres was performed at baseline and at the end of the intervention. We evaluated the intensity to induce a motor-evoked potential of 1 mV (S1mV), the resting motor threshold (RMT), the cortical silent period (CSP) at an intensity of 120 and 150% of the individual RMT, short-latency interval intracortical inhibition (3 ms), and intracortical facilitation (7 and 15 ms). Depending on the variable and hemisphere, follow-up data was available for 7–15 schizophrenia patients and for 10–12 healthy controls. Results: Repeated measures ANOVA revealed no significant time × group interactions for any of the analyzed variables. A significant increase in S1mV and CSP duration at 150% RMT of the left hemisphere could be observed in both groups over time. Conclusion: Regular ergometer training over 3 months increases motor cortical inhibition as displayed by an increase in CSP. The increase in S1mV may also indicate a higher degree of inhibition after the intervention. We could not establish a difference between schizophrenia patients and healthy controls. Due to the limited sample size, our results have to be considered as preliminary and need to be replicated in future trials."],["dc.identifier.doi","10.1159/000489714"],["dc.identifier.eissn","1423-0224"],["dc.identifier.issn","0302-282X"],["dc.identifier.pmid","30001538"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/77108"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.publisher","S. Karger AG"],["dc.relation.eissn","1423-0224"],["dc.relation.issn","0302-282X"],["dc.rights","https://www.karger.com/Services/SiteLicenses"],["dc.title","Effects of Three Months of Aerobic Endurance Training on Motor Cortical Excitability in Schizophrenia Patients and Healthy Subjects"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]