Falkai, Peter Gaston

[["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","101"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","European Archives of Psychiatry and Clinical Neuroscience"],["dc.bibliographiccitation.lastpage","111"],["dc.bibliographiccitation.volume","260"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Koschel, Jiri"],["dc.contributor.author","Zink, Mathias"],["dc.contributor.author","Bauer, Manfred"],["dc.contributor.author","Sommer, Clemens"],["dc.contributor.author","Frank, Josef"],["dc.contributor.author","Treutlein, Jens"],["dc.contributor.author","Schulze, Thomas"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Parlapani, Eleni"],["dc.contributor.author","Rietschel, Marcella"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Henn, Fritz A."],["dc.date.accessioned","2018-11-07T08:45:24Z"],["dc.date.available","2018-11-07T08:45:24Z"],["dc.date.issued","2010"],["dc.description.abstract","To determine if NMDA receptor alterations are present in the cerebellum in schizophrenia, we measured NMDA receptor binding and gene expression of the NMDA receptor subunits in a post-mortem study of elderly patients with schizophrenia and non-affected subjects. Furthermore, we assessed influence of genetic variation in the candidate gene neuregulin-1 (NRG1) on the expression of the NMDA receptor in an exploratory study. Post-mortem samples from the cerebellar cortex of ten schizophrenic patients were compared with nine normal subjects. We investigated NMDA receptor binding by receptor autoradiography and gene expression of the NMDA receptor subunits NR1, NR2A, NR2B, NR2C and NR2D by in situ hybridization. For the genetic study, we genotyped the NRG1 polymorphism rs35753505 (SNP8NRG221533). Additionally, we treated rats with the antipsychotics haloperidol or clozapine and assessed cerebellar NMDA receptor binding and gene expression of subunits to examine the effects of antipsychotic treatment. Gene expression of the NR2D subunit was increased in the right cerebellum of schizophrenic patients compared to controls. Individuals carrying at least one C allele of rs35753505 (SNP8NRG221533) showed decreased expression of the NR2C subunit in the right cerebellum, compared to individuals homozygous for the T allele. Correlation with medication parameters and the animal model revealed no treatment effects. In conclusion, increased NR2D expression results in a hyperexcitable NMDA receptor suggesting an adaptive effect due to receptor hypofunction. The decreased NR2C expression in NRG1 risk variant may cause a deficit in NMDA receptor function. This supports the hypothesis of an abnormal glutamatergic neurotransmission in the right cerebellum in the pathophysiology of schizophrenia."],["dc.description.sponsorship","European Commission [LSHM-CT-2004-503039]"],["dc.identifier.doi","10.1007/s00406-009-0017-1"],["dc.identifier.isi","000275085300003"],["dc.identifier.pmid","19856012"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/4148"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20429"],["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","Gene expression of NMDA receptor subunits in the cerebellum of elderly patients with 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"]]

[["dc.bibliographiccitation.firstpage","395"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","407"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Steyskal, Corinna"],["dc.contributor.author","Bernstein, Hans-Gert"],["dc.contributor.author","Schneider-Axmann, Thomas"],["dc.contributor.author","Parlapani, Eleni"],["dc.contributor.author","Schaeffer, Evelin L."],["dc.contributor.author","Gattaz, Wagner F."],["dc.contributor.author","Bogerts, Bernhard"],["dc.contributor.author","Schmitz, Christoph"],["dc.contributor.author","Falkai, Peter"],["dc.date.accessioned","2018-11-07T08:30:49Z"],["dc.date.available","2018-11-07T08:30:49Z"],["dc.date.issued","2009"],["dc.description.abstract","Structural magnetic resonance imaging and postmortem studies showed volume loss in the hippocampus in schizophrenia. The noted tissue reduction in the posterior section suggests that some cellular subfractions within this structure might be reduced in schizophrenia. To address this, we investigated numbers and densities of neurons, oligodendrocytes and astrocytes in the posterior hippocampal subregions in postmortem brains from ten patients with schizophrenia and ten matched controls using design-based stereology performed on Nissl-stained sections. Compared to the controls, the patients with schizophrenia showed a significant decrease in the mean number of oligodendrocytes in the left and right CA4. This is the first finding of reduced numbers of oligodendrocytes in CA4 of the posterior part of the hippocampus in schizophrenia. Our results are in line with earlier findings in the literature concerning decreased numbers of oligodendrocytes in the prefrontal cortex in schizophrenia. Our results may indicate disturbed connectivity of the CA4 of the posterior part of the hippocampus in schizophrenia and, thus, contribute to the growing number of studies showing the involvement of posterior hippocampal pathology in the pathophysiology of schizophrenia."],["dc.description.sponsorship","European Commission [LSHM-CT-2004-503039]"],["dc.identifier.doi","10.1007/s00401-008-0430-y"],["dc.identifier.isi","000264174200005"],["dc.identifier.pmid","18777029"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/11220"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/16982"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Stereologic investigation of the posterior part of the hippocampus in 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"]]

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal für Neuologie, Neurochirurgie und Psychiatrie"],["dc.bibliographiccitation.lastpage","76"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Schmitt, Andrea"],["dc.contributor.author","Falkai, Peter Gaston"],["dc.contributor.author","Parlapani, Eleni"],["dc.date.accessioned","2019-07-10T08:13:30Z"],["dc.date.available","2019-07-10T08:13:30Z"],["dc.date.issued","2009"],["dc.description.abstract","Bei Schizophrenie finden sich Volumenverminderungen der grauen Substanz, besonders im Hippokampus und präfrontalen Kortex, sowie erweiterte Seitenventrikel. Die Diagnose dieser strukturellen Veränderungen sowie eine Hypergyrifizierung schon bei Ersterkrankung sprechen für das Vorliegen einer neuronalen Entwicklungsstörung, während andererseits die Volumenabnahme der grauen Substanz während der Erkrankungsdauer für einen zusätzlichen neurodegenerativen Prozess spricht. Klassische Anzeichen eines neurodegenerativen Prozesses wie die Abnahme der Neuronenzahl oder eine Astrogliose liegen bei der Erkrankung nicht gesichert vor. Dagegen gibt es Hinweise auf verminderte synaptische Proteine, die zu einer Konnektivitätsstörung in einem neuronalen Netzwerk führen können. Zusätzlich wurde in einer kürzlich veröffentlichten Postmortem- Studie eine verminderte Anzahl proliferierender Stammzellen im Gyrus dentatus des Hippokampus bei schizophrenen Patienten gefunden. Dies könnte eine zusätzliche Rolle bei der Bildung des Volumenverlusts des Hippokam- Aus der Abteilung für Psychiatrie und Psychotherapie, Universität Göttingen Korrespondenzadresse: Dr. med. Andrea Schmitt, Abteilung für Psychiatrie und Psychotherapie, Universität Göttingen, D-37075 Göttingen, von-Siebold-Straße 5; E-Mail: aschmit@gwdg.de pus spielen. Welche Wirkung dabei antipsychotisch wirksame Medikamente spielen, ist bislang unklar. Auch genetische Risikofaktoren können eine Rolle bei strukturellen Veränderungen im Gehirn spielen. Nachgewiesen wurde das für den Neuregulin-1-Risikohaplotyp (HAPICE), der bei schizophrenen Patienten und ihren gesunden Angehörigen mit einem kleineren Hippokampusvolumen assoziiert war. Weitere Erkenntnisse über Risikofaktoren der Schizophrenie könnten zukünftig spezifischere Therapieoptionen ermöglichen."],["dc.description.abstract","In schizophrenia, a reduced volume of gray matter, especially in the hippocampus and the prefrontal cortex, as well as enlarged lateral ventricles can be found. The diagnosis of these structural changes plus hypergyrification already in first-episode disease argues for the existence of a neuronal developmental disorder. On the other hand, the volume reduction of gray matter in the course of the illness additionally indicates progressing neurodegeneration. Indeed, classical signs of a neurodegenerative process such as reduction of neurons or astrogliosis cannot be securely identified for the disease, whereas there is evidence for reduced synaptic proteins which may lead to disturbed connectivity in a neuronal network. A recently published post-mortem study accessorily reports a reduced number of proliferating stem cells in the gyrus dentatus of the hippocampus in schizophrenic patients which might add to hippocampal volume loss. At present, the effects of antipsychotic medication remain unexplained. Genetic risk factors should also be considered as a possible cause for structural alterations in the brain. The neuregulin-1 risk haplotype (HAPICE), for example, has been proven to be associated with reduced hippocampus volume in schizophrenic patients and their healthy relatives. Further insights into schizophrenia risk factors could prospectively facilitate specific therapeutic options."],["dc.identifier.fs","535919"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6035"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61264"],["dc.language.iso","de"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1608-1587"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Ist die Schizophrenie eine Störung der Synapto- oder Neurogenese?"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]