Gruber, Oliver

[["dc.bibliographiccitation.firstpage","126"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","134"],["dc.bibliographiccitation.volume","1301"],["dc.contributor.author","Parlapani, Eleni"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Erdmann, Andrea"],["dc.contributor.author","Bernstein, Hans-Gert"],["dc.contributor.author","Breunig, Barbara"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Petroianu, Georg A."],["dc.contributor.author","von Wilmsdorff, Martina"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Honer, William G."],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T11:22:01Z"],["dc.date.available","2018-11-07T11:22:01Z"],["dc.date.issued","2009"],["dc.description.abstract","There is evidence for migrational disturbances in the entorhinal cortex (ERC) in schizophrenia that supports a neurodevelopmental origin of the disorder. Since impaired myelin basic protein (MBP) gene expression during the migration phase could lead to abnormalities in final laminar position, we performed layer specific measurements of MBP expression in the ERC and hypothesised that migrational disturbances of pre-alpha-cell clusters relate to decreased MBP expression. Paraffin embedded sections of the left entorhinal cortex of 16 schizophrenia patients and 10 control subjects were stained for MBP using routine immunohistochemistry. on each section representative regions of interest were scanned to attain optimal quality images of the gray matter. Results were correlated to previous published disturbed dispersion of pre-alpha-cell clusters in adjacent brain sections. Mean MBP stain-intensity was significantly reduced in schizophrenia patients. Absolute MBP stain-intensity was significantly reduced in layers III and IV in patients. A significant correlation of MBP stain-intensity with the distance of the deep pole of the pre-alpha-cell cluster from the gray white matter junction was observed in the ERC of schizophrenia patients. The present data provide evidence for reduced MBP expression in the ERC in schizophrenia, which implies deficits in axonal myelination and disturbed connectivity. MBP gene is expressed in oligodendrocytes and neuronal populations during embryonic development, which are important in establishing the structure of the cerebral cortex. Correlation between reduced MBP as a sign of down-regulated MBP gene expression and disorganization of pre-alpha-cell clusters supports a neurodevelopmental origin of pathological processes in schizophrenia. (C) 2009 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.brainres.2009.09.007"],["dc.identifier.isi","000272100200014"],["dc.identifier.pmid","19747901"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/55908"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","0006-8993"],["dc.title","Association between myelin basic protein expression and left entorhinal cortex pre-alpha cell layer disorganization in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","89"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Revista de psiquiatria clínica"],["dc.bibliographiccitation.lastpage","96"],["dc.bibliographiccitation.volume","36"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Otto, Sylvia"],["dc.contributor.author","Jatzko, Alexander"],["dc.contributor.author","Ruf, Matthias"],["dc.contributor.author","Demirakca, Traute"],["dc.contributor.author","Tost, Heike"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Parlapani, Eleni"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Braus, Dieter F."],["dc.date.accessioned","2018-11-07T08:35:29Z"],["dc.date.available","2018-11-07T08:35:29Z"],["dc.date.issued","2009"],["dc.description.abstract","Objectives: In first-episode schizophrenia patients, functional magnetic resonance imaging (fMRI) has shown prefronto-parietal dysfunction during acoustic and visual stimulation. The aim of this study was to investigate the prefronto-parietal network in elderly schizophrenia patients using the same paradigm. Additionally, we hypothesized favourable effects on brain activation by the atypical antipsychotic clozapine compared to typical neuroleptics. Methods: We investigated 18 elderly, chronic schizophrenia patients and 21 elderly healthy controls. Nine schizophrenia patients had been medicated with clozapine and 9 had been receiving typical neuroleptics over decades. In addition to assessments with psychopathological and neuropsychological rating scales we used an acoustic and visual stimulation paradigm in a 1.5 Tesla MRI scanner to investigate BOLD-response in different brain areas. Results: Compared to healthy controls schizophrenia patients showed decreased brain activation in the prefrontal and parietal cortex as well as medial anterior cingulate gyrus compared to healthy controls. In these regions, patients medicated with clozapine showed increased BOLD-response compared to patients treated with typical neuroleptics. Discussion: Our study confirmed prefronto-parietal network disturbances in elderly schizophrenia patients thus pointing to the preservation of brain activation deficits and the influence of neurodevelopmental disturbances in chronic schizophrenia until old-age. Conclusion: The atypical antipsychotic clozapine seems to facilitate brain activation even in elderly, chronic schizophrenia patients."],["dc.identifier.doi","10.1590/S0101-60832009000300002"],["dc.identifier.fs","548703"],["dc.identifier.isi","000269276800002"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5793"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18078"],["dc.language.iso","es"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Univ Sao Paulo, Inst Psiquiatria"],["dc.relation.issn","0101-6083"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.access","openAccess"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Parieto-prefrontal dysfunction during visuo-auditory information processing in elderly, chronic schizophrenic patients and medication effects"],["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","182"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Schizophrenia Research"],["dc.bibliographiccitation.lastpage","191"],["dc.bibliographiccitation.volume","173"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Keeser, Daniel"],["dc.contributor.author","Keller, Katriona"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Rauchmann, Boris-Stephan"],["dc.contributor.author","Kimura, Hiroshi"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Dechent, Peter"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Ertl-Wagner, Birgit"],["dc.contributor.author","Honer, William G."],["dc.contributor.author","Hillmer-Vogel, Ursula"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Niklas, Andree"],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T10:13:58Z"],["dc.date.available","2018-11-07T10:13:58Z"],["dc.date.issued","2016"],["dc.description.abstract","The objective of this longitudinal magnetic resonance (MR) imaging study was to examine the effects of endurance training on hippocampal and grey matter volumes in schizophrenia patients and healthy controls. 20 chronic schizophrenia patients and 21 age- and gender-matched healthy controls underwent 3months of endurance training (30 min, 3 times per week). 19 additionally recruited schizophrenia patients played table soccer (\"foosball\" in the USA) over the same period. MR imaging with 3D-volumetric T1-weighted sequences was performed on a 3 T MR scanner at baseline, after 6 weeks and after the 3-month intervention and 3 additional training-free months. In addition to voxel-based morphometry (VBM), we performed manual and automatic delineation of the hippocampus and its substructures. Endurance capacity and psychopathological symptoms were measured as secondary endpoints. No significant increases in the volumes of the hippocampus or hippocampal substructures were observed in schizophrenia patients or healthy controls. However, VBM analyses displayed an increased volume of the left superior, middle and inferior anterior temporal gyri compared to baseline in schizophrenia patients after the endurance training, whereas patients playing table soccer showed increased volumes in the motor and anterior cingulate cortices. After the additional training-free period, the differences were no longer present. While endurance capacity improved in exercising patients and healthy controls, psychopathological symptoms did not significantly change. The subtle changes in the left temporal cortex indicate an impact of exercise on brain volumes in schizophrenia. Subsequent studies in larger cohorts are warranted to address the question of response variability of endurance training. (C) 2015 Elsevier B.V. All rights reserved."],["dc.description.sponsorship","Dorothea Schlozer Programme at the Georg-August-Universitat Gottingen"],["dc.identifier.doi","10.1016/j.schres.2015.01.005"],["dc.identifier.isi","000375847400010"],["dc.identifier.pmid","25623601"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40533"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.relation.issn","1573-2509"],["dc.relation.issn","0920-9964"],["dc.title","Effects of endurance training on brain structures in chronic schizophrenia patients and healthy controls"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S155"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","S168"],["dc.bibliographiccitation.volume","263"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Hasan, Alkomiet"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Jatzko, Alexander"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Wobrock, Thomas"],["dc.date.accessioned","2018-11-07T09:18:17Z"],["dc.date.available","2018-11-07T09:18:17Z"],["dc.date.issued","2013"],["dc.description.abstract","Schizophrenia is a severe neuropsychiatric disorder with familial loading as heritable risk factor and cannabis abuse as the most relevant environmental risk factor up to date. Cannabis abuse has been related to an earlier onset of the disease and persisting cannabis consumption is associated with reduced symptom improvement. However, the underlying morphological and biochemical brain alterations due to these risk factors as well as the effects of gene-environmental interaction are still unclear. In this magnetic resonance imaging (MRI) study in 47 first-episode schizophrenia patients and 30 healthy control subjects, we investigated effects of previous cannabis abuse and increased familial risk on subcortical brain regions such as hippocampus, amygdala, caudate nucleus, putamen, thalamus and subsegments of the corpus callosum (CC). In a subsequent single-volume H-1-magnetic resonance spectroscopy study, we investigated spectra in the left hippocampus and putamen to detect metabolic alterations. Compared to healthy controls, schizophrenia patients displayed decreased volumes of the left hippocampus, bilateral amygdala and caudate nucleus as well as an increased area of the midsagittal CC1 segment of the corpus callosum. Patients fulfilling the criteria for cannabis abuse at admission showed an increased area of the CC2 segment compared to those who did not fulfill the criteria. Patients with a family history of schizophrenia combined with previous cannabis abuse showed lower volumes of the bilateral caudate nucleus compared to all other patients, implicating an interaction between the genetic background and cannabis abuse as environmental factor. Patients with cannabis abuse also had higher ratios of N-acetyl aspartate/choline in the left putamen, suggesting a possible neuroprotective effect in this area. However, antipsychotic medication prior to MRI acquisition and gender effects may have influenced our results. Future longitudinal studies in first-episode patients with quantification of cannabis abuse and assessment of schizophrenia risk genes are warranted."],["dc.identifier.doi","10.1007/s00406-013-0451-y"],["dc.identifier.isi","000325944100005"],["dc.identifier.pmid","24085610"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28375"],["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","Effects of cannabis and familial loading on subcortical brain volumes in first-episode schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","201"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","215"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Leonardi-Essmann, Fernando"],["dc.contributor.author","Durrenberger, Pascal F."],["dc.contributor.author","Parlapani, Eleni"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Spanagel, Rainer"],["dc.contributor.author","Arzberger, Thomas"],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Herrera-Marschitz, Mario"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Reynolds, Richard"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Gebicke-Haerter, Peter J."],["dc.date.accessioned","2018-11-07T08:57:28Z"],["dc.date.available","2018-11-07T08:57:28Z"],["dc.date.issued","2011"],["dc.description.abstract","Objectives. The role of neuroinflammation in schizophrenia has been an issue for long time. There are reports supporting the hypothesis of ongoing inflammation and others denying it. This may be partly ascribed to the origin of the materials (CSF, blood, brain tissue) or to the genes selected for the respective studies. Moreover, in some locations, inflammatory genes may be up-regulated, others may be down-regulated. Methods. Genome-wide microarrays have been used for expression profiling in post-mortem brains of schizophrenia patients. Array data have been analyzed by gene set enrichment analysis (GSEA) and further confirmed with selected genes by real-time PCR. Results. In Brodman Area 22 of left superior temporal cortex, at least 70 genes (19%) out of 369 down-regulated genes (P < 0.05) belonged to the immune system. 23 from those 70 genes were randomly selected for real-time PCR. Six reached significance level at P < 0.05. Conclusions. The present data support a brain-specific view of the role immune-modulatory genes may play in the left superior temporal cortex in schizophrenia, because immune functions in the patients are not disturbed. In keeping with comparable, previous studies supporting the notion that schizophrenia is a disease of the synapse, we hypothesize that dysregulation of immune-related genes modifies synaptic functions and stability in this region."],["dc.identifier.doi","10.3109/15622975.2010.530690"],["dc.identifier.isi","000289439200004"],["dc.identifier.pmid","21091092"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23409"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1562-2975"],["dc.title","Regulation of immune-modulatory genes in left superior temporal cortex of schizophrenia patients: a genome-wide microarray study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","469"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","473"],["dc.bibliographiccitation.volume","263"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Malchow, Berend"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Honer, William G."],["dc.contributor.author","Pajonk, Frank-Gerald B."],["dc.contributor.author","Sun, Frank"],["dc.contributor.author","Cannon, Tyrone D."],["dc.date.accessioned","2018-11-07T09:20:46Z"],["dc.date.available","2018-11-07T09:20:46Z"],["dc.date.issued","2013"],["dc.description.abstract","Via influencing brain plasticity, aerobic exercise could contribute to the treatment of schizophrenia patients. As previously shown, physical exercise increases hippocampus volume and improves short-term memory. We now investigated gray matter density and brain surface expansion in this sample using MRI-based cortical pattern matching methods. Comparing schizophrenia patients to healthy controls before and after 3 months of aerobic exercise training (cycling) plus patients playing table football yielded gray matter density increases in the right frontal and occipital cortex merely in healthy controls. However, respective exercise effects might be attenuated in chronic schizophrenia, which should be verified in a larger sample."],["dc.identifier.doi","10.1007/s00406-012-0383-y"],["dc.identifier.isi","000323513800003"],["dc.identifier.pmid","23161338"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28954"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Heidelberg"],["dc.relation.issn","0940-1334"],["dc.title","The effect of aerobic exercise on cortical architecture in patients with chronic schizophrenia: a randomized controlled MRI study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","187"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","195"],["dc.bibliographiccitation.volume","120"],["dc.contributor.author","Schaeffer, Evelin L."],["dc.contributor.author","Kuehn, Franziska"],["dc.contributor.author","Schmitt, Angelika"],["dc.contributor.author","Gattaz, Wagner F."],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Schmitt, Andrea"],["dc.date.accessioned","2018-11-07T09:30:47Z"],["dc.date.available","2018-11-07T09:30:47Z"],["dc.date.issued","2013"],["dc.description.abstract","As a consequence of obstetric complications, neonatal hypoxia has been discussed as an environmental factor in the pathophysiology of schizophrenia. However, the biological consequences of hypoxia are unclear. The neurodevelopmental hypothesis of schizophrenia suggests that the onset of abnormal brain development and neuropathology occurs perinatally, whereas symptoms of the disease appear in early adulthood. In our animal model of chronic neonatal hypoxia, we have detected behavioral alterations resembling those known from schizophrenia. Disturbances in cell proliferation possibly contribute to the pathophysiology of this disease. In the present study, we used postnatal rats to investigate cell proliferation in several brain areas following neonatal hypoxia. Rats were repeatedly exposed to hypoxia (89 % N-2, 11 % O-2) from postnatal day (PD) 4-8. We then evaluated cell proliferation on PD 13 and 39, respectively. These investigations were performed in the anterior cingulate cortex (ACC), caudate-putamen (CPU), dentate gyrus, and subventricular zone. Rats exposed to hypoxia exhibited increased cell proliferation in the ACC at PD 13, normalizing at PD 39. In other brain regions, no alterations have been detected. Additionally, hypoxia-treated rats showed decreased CPU volume at PD 13. The results of the present study on the one hand support the assumption of chronic hypoxia influencing transient cell proliferation in the ACC, and on the other hand reveal normalization during ageing."],["dc.identifier.doi","10.1007/s00702-012-0859-y"],["dc.identifier.isi","000313043900020"],["dc.identifier.pmid","22806004"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31393"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.issn","0300-9564"],["dc.title","Increased cell proliferation in the rat anterior cingulate cortex following neonatal hypoxia: relevance to schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","35"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","39"],["dc.bibliographiccitation.volume","258"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Parlapani, Eleni"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Wobrock, Thomas"],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T11:09:24Z"],["dc.date.available","2018-11-07T11:09:24Z"],["dc.date.issued","2008"],["dc.description.abstract","To a large extend schizophrenia has been shown to be heritable, with neuregulin-1 (NRG1) one of the candidate genes considered to play a role in the pathophysiology of the disorder. While several polymorphisms within this gene have been reported to be associated with schizophrenia, the impact of NRG1 risk genotypes on disturbed brain function and symptoms of the disease is unknown and might be elucidated using post-mortem studies. Neuregulins are signalling proteins and the NRG1 family encodes at least 15 different splice variants, classified into four isoforms. They play an important role in cell differentiation, migration, myelination and proliferation of oligodendrocytes and neurons. Dysfunction in these processes may be related to neurodevelopmental disturbances in schizophrenia. NRG1 isoforms are differentially expressed in relevant brain regions of schizophrenia patients such as the prefrontal cortex and hippocampus and may contribute to pathophysiological processes. Different NRG1 genotypes have been shown to influence gene expression of isoforms and the risk-associated variants are in primarily noncoding and promoter regions, probably operating by altering gene expression or splicing. In addition, NRG1 regulates the expression of the nicotinic acetylcholine receptor, and expression of the 7-aminobutyric acid (GABA(A)) and N-methyl-D-aspartate receptor in the brain. However, the contribution of NRG1 risk genotypes to expression of isoforms and cognitive or psychotic symptoms in patients remain to be investigated in prospective post-mortem studies."],["dc.identifier.doi","10.1007/s00406-008-5019-x"],["dc.identifier.isi","000262752900007"],["dc.identifier.pmid","18985292"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/53001"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Dr Dietrich Steinkopff Verlag"],["dc.relation.issn","0940-1334"],["dc.title","Impact of neuregulin-1 on the pathophysiology of schizophrenia in human post-mortem studies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","490"],["dc.bibliographiccitation.issue","7"],["dc.bibliographiccitation.journal","The World Journal of Biological Psychiatry"],["dc.bibliographiccitation.lastpage","499"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","von Wilmsdorff, Martina"],["dc.contributor.author","Blaich, Carolin"],["dc.contributor.author","Zink, Mathias"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Bauer, Manfred"],["dc.contributor.author","Schulze, Thomas"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Gruber, Oliver"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T09:20:40Z"],["dc.date.available","2018-11-07T09:20:40Z"],["dc.date.issued","2013"],["dc.description.abstract","Objectives. The glutamatergic hypothesis of schizophrenia proposes alterations of excitatory amino acid transporters (solute carrier family, SLCs) expression and cerebellar dysfunctions. The influence of the neuregulin-1 (NRG1) risk genotype or effects of antipsychotics on expression of EAATs are unknown. Methods. We compared post-mortem samples from the cerebellar hemispheres and vermis of 10 schizophrenia patients with nine normal subjects by investigating gene expression of SLC1A3, SLC1A1 and SLC1A6 by in-situ hybridization. We further assessed the allelic composition regarding the polymorphism rs35753505 (SNP8NRG221533) near the NRG1 gene. To control for effects due to antipsychotic treatment, we chronically treated rats with the antipsychotics haloperidol or clozapine and assessed gene expression of SLCs. Results. Schizophrenia patients showed increased expression of SLC1A3 in the molecular layer of the vermis. Individuals carrying at least one C allele of rs35753505 (SNP8NRG221533) showed decreased expression of SLC1A6 in the molecular layer of both hemispheres, compared to individuals homozygous for the T allele. The animal model revealed suppression of SLC1A6 by clozapine. Conclusions. Increased SLC1A3 expression indicates facilitated transport and may result in reduced glutamate neurotransmission. Decreased SLC1A6 expression in NRG1 risk variant may be an adaptive effect to restore glutamate signalling, but treatment effects cannot be excluded."],["dc.description.sponsorship","European Commission [LSHM-CT-2004-503039]"],["dc.identifier.doi","10.3109/15622975.2011.645877"],["dc.identifier.isi","000324403800003"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/28933"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Informa Healthcare"],["dc.relation.issn","1562-2975"],["dc.title","Gene expression of glutamate transporters SLC1A1, SLC1A3 and SLC1A6 in the cerebellar subregions of elderly schizophrenia patients and effects of antipsychotic treatment"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]