TY - JOUR A1 - Schmitt, Andrea A1 - Tatsch, Laura A1 - Vollhardt, Alisa A1 - Schneider-Axmann, Thomas A1 - Raabe, Florian J. A1 - Roell, Lukas A1 - Heinsen, Helmut A1 - Hof, Patrick R. A1 - Falkai, Peter A1 - Schmitz, Christoph T1 - Decreased oligodendrocyte number in hippocampal subfield CA4 in schizophrenia: a replication study JF - Cells N2 - Hippocampus-related cognitive deficits in working and verbal memory are frequent in schizophrenia, and hippocampal volume loss, particularly in the cornu ammonis (CA) subregions, was shown by magnetic resonance imaging studies. However, the underlying cellular alterations remain elusive. By using unbiased design-based stereology, we reported a reduction in oligodendrocyte number in CA4 in schizophrenia and of granular neurons in the dentate gyrus (DG). Here, we aimed to replicate these findings in an independent sample. We used a stereological approach to investigate the numbers and densities of neurons, oligodendrocytes, and astrocytes in CA4 and of granular neurons in the DG of left and right hemispheres in 11 brains from men with schizophrenia and 11 brains from age- and sex-matched healthy controls. In schizophrenia, a decreased number and density of oligodendrocytes was detected in the left and right CA4, whereas mean volumes of CA4 and the DG and the numbers and density of neurons, astrocytes, and granular neurons were not different in patients and controls, even after adjustment of variables because of positive correlations with postmortem interval and age. Our results replicate the previously described decrease in oligodendrocytes bilaterally in CA4 in schizophrenia and point to a deficit in oligodendrocyte maturation or a loss of mature oligodendrocytes. These changes result in impaired myelination and neuronal decoupling, both of which are linked to altered functional connectivity and subsequent cognitive dysfunction in schizophrenia. KW - schizophrenia KW - hippocampus KW - CA4 KW - dentate gyrus KW - postmortem KW - stereology KW - oligodendrocyte KW - neuron Y1 - 2022 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-290360 SN - 2073-4409 VL - 11 IS - 20 ER - TY - JOUR A1 - Taurines, R. A1 - Fekete, S. A1 - Preuss-Wiedenhoff, A. A1 - Warnke, A. A1 - Wewetzer, C. A1 - Plener, P. A1 - Burger, R. A1 - Gerlach, M. A1 - Romanos, M. A1 - Egberts, K. M. T1 - Therapeutic drug monitoring in children and adolescents with schizophrenia and other psychotic disorders using risperidone JF - Journal of Neural Transmission N2 - Risperidone is commonly used to treat different psychiatric disorders worldwide. Knowledge on dose–concentration relationships of risperidone treatment in children and adolescents with schizophrenia or other psychotic disorders is, however, scarce and no age-specific therapeutic ranges have been established yet. Multicenter data of a therapeutic drug monitoring service were analyzed to evaluate the relationship between risperidone dose and serum concentration of the active moiety (risperidone (RIS) plus its main metabolite 9-hydroxyrisperidone (9-OH-RIS)) in children and adolescents with psychotic disorders. Patient characteristics, doses, serum concentrations and therapeutic outcomes were assessed by standardized measures. The study also aimed to evaluate whether the therapeutic reference range for adults (20–60 ng/ml) is applicable for minors. In the 64 patients (aged 11–18 years) included, a positive correlation between daily dose and the active moiety (RIS\(_{am}\)) concentration was found (r\(_s\) = 0.49, p = 0.001) with variation in dose explaining 24% (r\(_s\)\(^2\) = 0.240) of the variability in serum concentrations. While the RIS\(_{am}\) concentration showed no difference, RIS as well 9-OH-RIS concentrations and the parent to metabolite ratio varied significantly in patients with co-medication of a CYP2D6 inhibitor. Patients with extrapyramidal symptoms (EPS) had on average higher RIS\(_{am}\) concentrations than patients without (p = 0.05). Considering EPS, the upper threshold of the therapeutic range of RIS\(_{am}\) was determined to be 33 ng/ml. A rough estimation method also indicated a possibly decreased lower limit of the preliminary therapeutic range in minors compared to adults. These preliminary data may contribute to the definition of a therapeutic window in children and adolescents with schizophrenic disorders treated with risperidone. TDM is recommended in this vulnerable population to prevent concentration-related adverse drug reactions. KW - risperidone KW - children KW - serum concentration KW - schizophrenia KW - therapeutic drug monitoring KW - pharmacovigilance Y1 - 2022 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-324833 VL - 129 IS - 5-6 ER - TY - THES A1 - Hägele, Sandra Elisabeth T1 - QTc-Zeit-Verlängerung in der Therapie schizophrener Psychosen unter Berücksichtigung genetischer Varianz in NOS1AP T1 - QTc time prolongation in the treatment of patients with schizophrenic psychosis considering genetic variation in NOS1AP N2 - QTc-Zeit Verlängerungen sind aufgrund potentieller Übergänge in lebensbedrohliche Tachyarrhythmien Gegenstand vieler Arbeiten. Einer der Häufigsten Risikofaktoren ist die Einnahme von typischen bzw. atypischen Antipsychotika. Mehrere Studien belegen darüber hinaus genetische Einflüsse und zeigen, dass das homozygote Vorhandensein von rs12143842(T) und rs10494366(G) in NOS1AP einen verlängernden Einfluss auf die QTc-Zeit hat. Zudem scheinen oben genannte Polymorphismen von NOS1AP bei der Entwicklung schizophrener Psychosen eine Rolle zu spielen. In bisherigen Studien wurde immer nur getrennte Analysen hinsichtlich der genannten Risikofaktoren vorgenommen. In dieser Arbeit soll erstmals der gemeinsame Einfluss von Psychopharmaka und den zwei beschriebenen Polymorphismen von NOS1AP bei Patienten mit Schizophrenie untersucht werden. N2 - The prolongation of the QTc-Time interval is a well examined phenomenon due to the risk of suffering a life threatening tachyarrhythmia. In patients with schizophrenia, several risk factors have been identified one of which is taking antipsychotic medication. Genetic variation in NOS1AP polymorphisms rs12143845 (T) and rs10494366 (G) are also found to be significant risk factors. Furthermore, NOS1AP is associated with a higher risk of developing schizophrenic psychosis. This study aims to detect the impact on QTc prolongation in an analysis of combined risk factors in patients with schizophrenia. KW - QTc-Zeit Verlängerung KW - Schizophrenie KW - NOS1AP KW - QTc-Zeit KW - Psychopharmaka KW - Polymorphismen KW - QTc prolongation KW - schizophrenia KW - antipsychotics KW - polymorphisms KW - pharmacology Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-206248 ER - TY - JOUR A1 - Meier, Sandra M. A1 - Kähler, Anna K. A1 - Bergen, Sarah E. A1 - Sullivan, Patrick F. A1 - Hultman, Christina M. A1 - Mattheisen, Manuel T1 - Chronicity and Sex Affect Genetic Risk Prediction in Schizophrenia JF - Frontiers in Psychiatry N2 - Schizophrenia (SCZ) is a severe mental disorder with immense personal and societal costs; identifying individuals at risk is therefore of utmost importance. Genomic risk profile scores (GRPS) have been shown to significantly predict cases-control status. Making use of a large-population based sample from Sweden, we replicate a previous finding demonstrating that the GRPS is strongly associated with admission frequency and chronicity of SCZ. Furthermore, we were able to show a substantial gap in prediction accuracy between males and females. In sum, our results indicate that prediction accuracy by GRPS depends on clinical and demographic characteristics. KW - schizophrenia KW - polygenic risk score KW - prediction KW - sex KW - course Y1 - 2020 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-205677 SN - 1664-0640 VL - 11 ER - TY - THES A1 - Wagner, Martin T1 - Assoziations- und Haplotypenanalyse genetischer Veränderungen der Pannexin-Gengruppe bei Patienten mit schizophrenen Psychosen nach ICD-10 und der Klassifikation von Karl Leonhard T1 - Association and haplotype analysis of genetic changes in the pannexin gene group in patients with schizophrenic psychosis according to ICD-10 and the classification of Karl Leonhard N2 - Bestimmung von genetischen Veränderungen auf PANX 1-3 anhand von Einzelnukleotid Polymorphismen (SNP). Test auf Assoziation von Allelen und Haplotypen mit den schizophrenen Psychosen nach ICD-10 und der Klassifikation von Karl Leonhard in Form einer Fall-Kontroll-Studie mit 1163 Patienten und 479 Kontrollen. N2 - Determination of genetic changes on PANX 1-3 using single nucleotide polymorphisms (SNP). Test for association of alleles and haplotypes with schizophrenic psychosis according to ICD-10 and the classification of Karl Leonhard in the form of a case-control study with 1163 patients and 479 controls. KW - panx1 KW - panx2 KW - panx3 KW - schizophrenia KW - Pannexin KW - Schizophrenie KW - Karl Leonhard Y1 - 2019 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-188512 ER - TY - THES A1 - Böhnlein, Stefan T1 - Assoziationsuntersuchungen zu schizophrenen und affektiven Psychosen im Bereich des EphA4 Gens T1 - Association studies on schizophrenic and affective psychoses in the region of the EphA4 gene N2 - Die Schizophrenie ist eine schwerwiegende Erkrankung, deren Gesamtlebenzeitprävalenz ca. 1% beträgt. Da bei schizophrenen Erkrankungen die genetische Komponente eine erhebliche Rolle spielt und es außerdem in bisherigen Studien Hinweise für einen Zusammenhang von EphA4 mit diversen neuronalen Krankheitsformen gibt, ist dieser mögliche Zusammenhang Gegenstand der durchgeführten Untersuchungen. In der vorliegenden Arbeit sollte die Rolle des Eph receptor A4 bei der Ätiopathogenese von schizophrenen und affektiven Psychosen untersucht werden, da besonders zur Rolle der Eph- und Ephrin A-Familie bei schizophrenen Erkrankungen derzeit noch grundlegendes Wissen fehlt. Dabei wurde ein Patientenkollektiv von mehr als 1000 Probanden sowohl nach der ICD-10-Klassifikation als auch der Klassifikation von Leonhard in Unterformen eingeteilt und diese getrennt untersucht und mit einer gesunden Kontrollgruppe verglichen. Es wurden sowohl SNP-Analysen als auch Haplotypanalysen durchgeführt. Das Kandidatengen EphA4 liegt beim Menschen auf dem Chromosom 2 (Basenpaar 221.418.027 bis 221.574.202), besteht aus insgesamt 156.176 Basenpaaren und dient vor allem der Steuerung der Zellform und -bewegung durch Veränderungen am Aktinoskelett. Insgesamt wurden 9 SNPs auf Assoziation mit schizophrenen Psychosen und zykloiden Psychosen untersucht, um einen möglichen Einfluss von EphA4 bei der Ätiopathogenese oder im Krankheitsverlauf zu diagnostizieren. Zum einen wurden 4 Single SNP-Analysen durchgeführt, um einzelne SNPs auf Assoziation mit dem erkrankten Phänotyp zu untersuchen. Weiterhin wurden Haplotypanalysen für 9 SNPs durchgeführt, um die Vererbung von gemeinsamen Polymorphismen miteinander auf benachbarten Bereichen der DNA zu untersuchen. Hierbei stellte sich als Hauptbefund der durchgeführten Studie ein Haplotyp rs2052940T – rs3087584T als möglicher Risikofaktor für die Entstehung schizophrener Erkrankungsformen heraus, welcher wahrscheinlich über einen Zufallsbefund hinausgeht und nach der Leonhard-Klassifikation vor allem Patienten mit dem Phänotyp affektvolle Paraphrenie betrifft. Für die Single-SNP-Analysen ergaben sich einige nominell positive Befunde, die jedoch einer Korrektur auf multiples Testen nach Bonferroni nicht standhalten konnten, womit folglich nicht klar ist, ob es sich hierbei möglicherweise um Zufallsbefunde handelt. Es ist nach Auswertung der vorliegenden Ergebnisse davon auszugehen, dass EphA4 zwar keinen gemeinsamen Risikofaktor für endogene Psychosen darstellt, jedoch einen Beitrag als spezifischer Risikofaktor für spezielle Unterformen schizophrener Psychosen leisten könnte. Dies konnte vor allem für die Unterform der affektvollen Paraphrenie nach Leonhard aufgezeigt werden. Um die Resultate dieser Studie zu verifizieren, wären weitere Untersuchungen wünschenswert, welche auf ein erweitertes Kollektiv mit einer höheren Anzahl von Fällen und Kontrollen zurückgreifen. N2 - Schizophrenia is a serious disease with an overall lifetime prevalence of approximately 1%. Since the genetic component plays a significant role in schizophrenic diseases and there is also evidence in previous studies for a connection of EphA4 with various neuronal forms of disease, this possible connection is the subject of the investigations carried out in this study. A group of more than 1000 volunteers was subdivided into subforms according to the ICD-10 classification as well as the Leonhard classification. The samples were compared with a healthy control group. SNP analyzes and haplotype analyzes were performed. The candidate gene EphA4 in humans is located on chromosome 2 (base pair 221.418.027 to 221.574.202), consists of a total of 156.176 base pairs and is primarily used to control cell shape and cell movement through changes in the actinoskeleton. A total of 9 SNPs were investigated for association with schizophrenic psychoses and cycloid psychoses in order to diagnose a possible effect of EphA4 in etiopathogenesis or disease progression. Firstly, single SNP analyzes were performed to examine individual SNPs for association with the diseased phenotype. Furthermore, haplotype analyzes were performed on 9 SNPs to study the inheritance of common polymorphisms with each other on adjacent regions of the DNA. The main finding of the study was a haplotype rs2052940T - rs3087584T as a possible risk factor for the development of schizophrenic forms, which - according to the Leonhard classification - mainly affects patients with the phenotype of affective paraphrenia. There were some nominally positive findings for the single-SNP analyzes, which, however, could not withstand a Bonferroni correction for multiple testing, so it is not clear whether these findings may be incidental. It is to be understood from the evaluation of the present results that although EphA4 is not a common risk factor for endogenous psychoses, it probably contributes as a specific risk factor for specific subtypes of schizophrenic psychoses. This could be shown especially for the subform of affective paraphrenia according to Leonhard. In order to verify the results of this study, it would be desirable to have further studies using an extended collective with a higher number of cases and controls. KW - EphA4 KW - Schizophrenie KW - schizophrenia Y1 - 2018 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-172481 ER - TY - JOUR A1 - Isles, Anthony R. A1 - Ingason, Andrés A1 - Lowther, Chelsea A1 - Walters, James A1 - Gawlick, Micha A1 - Stöber, Gerald A1 - Rees, Elliott A1 - Martin, Joanna A1 - Little, Rosie B. A1 - Potter, Harry A1 - Georgieva, Lyudmila A1 - Pizzo, Lucilla A1 - Ozaki, Norio A1 - Aleksic, Branko A1 - Kushima, Itaru A1 - Ikeda, Masashi A1 - Iwata, Nakao A1 - Levinson, Douglas F. A1 - Gejman, Pablo V. A1 - Shi, Jianxin A1 - Sanders, Alan R. A1 - Duan, Jubao A1 - Willis, Joseph A1 - Sisodiya, Sanjay A1 - Costain, Gregory A1 - Werge, Thomas M. A1 - Degenhardt, Franziska A1 - Giegling, Ina A1 - Rujescu, Dan A1 - Hreidarsson, Stefan J. A1 - Saemundsen, Evald A1 - Ahn, Joo Wook A1 - Ogilvie, Caroline A1 - Girirajan, Santhosh D. A1 - Stefansson, Hreinn A1 - Stefansson, Kari A1 - O'Donovan, Michael C. A1 - Owen, Michael J. A1 - Bassett, Anne A1 - Kirov, George T1 - Parental Origin of Interstitial Duplications at 15q11.2-q13.3 in Schizophrenia and Neurodevelopmental Disorders JF - PLoS Genetics N2 - Duplications at 15q11.2-q13.3 overlapping the Prader-Willi/Angelman syndrome (PWS/AS) region have been associated with developmental delay (DD), autism spectrum disorder (ASD) and schizophrenia (SZ). Due to presence of imprinted genes within the region, the parental origin of these duplications may be key to the pathogenicity. Duplications of maternal origin are associated with disease, whereas the pathogenicity of paternal ones is unclear. To clarify the role of maternal and paternal duplications, we conducted the largest and most detailed study to date of parental origin of 15q11.2-q13.3 interstitial duplications in DD, ASD and SZ cohorts. We show, for the first time, that paternal duplications lead to an increased risk of developing DD/ASD/multiple congenital anomalies (MCA), but do not appear to increase risk for SZ. The importance of the epigenetic status of 15q11.2-q13.3 duplications was further underlined by analysis of a number of families, in which the duplication was paternally derived in the mother, who was unaffected, whereas her offspring, who inherited a maternally derived duplication, suffered from psychotic illness. Interestingly, the most consistent clinical characteristics of SZ patients with 15q11.2-q13.3 duplications were learning or developmental problems, found in 76% of carriers. Despite their lower pathogenicity, paternal duplications are less frequent in the general population with a general population prevalence of 0.0033% compared to 0.0069% for maternal duplications. This may be due to lower fecundity of male carriers and differential survival of embryos, something echoed in the findings that both types of duplications are de novo in just over 50% of cases. Isodicentric chromosome 15 (idic15) or interstitial triplications were not observed in SZ patients or in controls. Overall, this study refines the distinct roles of maternal and paternal interstitial duplications at 15q11.2-q13.3, underlining the critical importance of maternally expressed imprinted genes in the contribution of Copy Number Variants (CNVs) at this interval to the incidence of psychotic illness. This work will have tangible benefits for patients with 15q11.2-q13.3 duplications by aiding genetic counseling. KW - interstitial duplications KW - schizophrenia KW - developmental delay KW - autism spectrum disorder KW - parental origin KW - genetics Y1 - 2016 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-166706 VL - 12 IS - 5 ER - TY - JOUR A1 - van de Kerkhof, Nora WA A1 - Fekkes, Durk A1 - van der Heijden, Frank MMA A1 - Hoogendijk, Witte JG A1 - Stöber, Gerald A1 - Egger, Jos IM A1 - Verhoeven, Willem MA T1 - Cycloid psychoses in the psychosis spectrum: evidence for biochemical differences with schizophrenia JF - Neuropsychiatric Disease and Treatment N2 - Cycloid psychoses (CP) differ from schizophrenia regarding symptom profile, course, and prognosis and over many decades they were thought to be a separate entity within the psychosis spectrum. As to schizophrenia, research into the pathophysiology has focused on dopamine, brain-derived neurotrophic factor, and glutamate signaling in which, concerning the latter, the N-methyl-d-aspartate receptor plays a crucial role. The present study aims to determine whether CP can biochemically be delineated from schizophrenia. Eighty patients referred for psychotic disorders were assessed with the Comprehensive Assessment of Symptoms and History, and (both at inclusion and after 6 weeks of antipsychotic treatment) with the Positive and Negative Syndrome Scale and Clinical Global Impression. From 58 completers, 33 patients were diagnosed with schizophrenia and ten with CP according to the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, and Leonhard criteria, respectively. Fifteen patients were diagnosed with other disorders within the psychosis spectrum. At both time points, blood levels of the dopamine metabolite homovanillic acid, brain-derived neurotrophic factor, and amino acids related to glutamate neurotransmission were measured and compared with a matched control sample. Patients with CP showed a significantly better response to antipsychotic treatment as compared to patients with schizophrenia. In CP, glycine levels were elevated and tryptophan levels were lowered as compared to schizophrenia. Glutamate levels were increased in both patient groups as compared to controls. These results, showing marked differences in both treatment outcome and glutamate-related variable parameters, may point at better neuroplasticity in CP, necessitating demarcation of this subgroup within the psychosis spectrum. KW - cycloid psychoses KW - schizophrenia KW - glutamate KW - glycine KW - tryptophan KW - neuroplasticity Y1 - 2016 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-166255 VL - 12 ER - TY - JOUR A1 - Stepniak, Beata A1 - Kästner, Anne A1 - Poggi, Giulia A1 - Mitjans, Marina A1 - Begemann, Martin A1 - Hartmann, Annette A1 - Van der Auwera, Sandra A1 - Sananbenesi, Farahnaz A1 - Krüger-Burg, Dilja A1 - Matuszko, Gabriela A1 - Brosi, Cornelia A1 - Homuth, Georg A1 - Völzke, Henry A1 - Benseler, Fritz A1 - Bagni, Claudia A1 - Fischer, Utz A1 - Dityatev, Alexander A1 - Grabe, Hans-Jörgen A1 - Rujescu, Dan A1 - Fischer, Andre A1 - Ehrenreich, Hannelore T1 - Accumulated common variants in the broader fragile X gene family modulate autistic phenotypes JF - EMBO Molecular Medicine N2 - Fragile X syndrome (FXS) is mostly caused by a CGG triplet expansion in the fragile X mental retardation 1 gene (FMR1). Up to 60% of affected males fulfill criteria for autism spectrum disorder (ASD), making FXS the most frequent monogenetic cause of syndromic ASD. It is unknown, however, whether normal variants (independent of mutations) in the fragile X gene family (FMR1, FXR1, FXR2) and in FMR2 modulate autistic features. Here, we report an accumulation model of 8 SNPs in these genes, associated with autistic traits in a discovery sample of male patients with schizophrenia (N = 692) and three independent replicate samples: patients with schizophrenia (N = 626), patients with other psychiatric diagnoses (N = 111) and a general population sample (N = 2005). For first mechanistic insight, we contrasted microRNA expression in peripheral blood mononuclear cells of selected extreme group subjects with high-versus low-risk constellation regarding the accumulation model. Thereby, the brain-expressed miR-181 species emerged as potential "umbrella regulator", with several seed matches across the fragile X gene family and FMR2. To conclude, normal variation in these genes contributes to the continuum of autistic phenotypes. KW - permutation KW - miR-181 KW - PGAS KW - FXR2 KW - FXR1 KW - FMR2 KW - FMR1 KW - identification KW - protein KW - fraxe mental retardation KW - CGG repeat KW - CPG Island KW - schizophrenia KW - expression KW - males Y1 - 2015 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-136893 VL - 7 IS - 12 ER - TY - THES A1 - Schölles, Kristina Joana T1 - Unterschiedliche Gehirnaktivierungsmuster bei psychiatrischen Patienten - eine Untersuchung mit funktioneller Nahinfrarotspektroskopie T1 - Different clusters of brain activation in psychiatric patients – an investigation with functional near-infrared spectroscopy N2 - Viele Patienten, die an Schizophrenie erkrankt sind, zeigen dauerhafte Einschränkungen in sozial-kommunikativen und sozial-kognitiven Kompetenzen. Dies führt oft zu sozialem Rückzug, erschwert alltägliche zwischenmenschliche Interaktion und mindert die Lebensqualität der Patienten deutlich. Jene Einschränkungen sind bei Patienten mit Negativsymptomatik oder chronischen Zuständen besonders ausgeprägt und könnten einer Minderaktivierung im Spiegelneuronensystem unterliegen. Ziel dieser Studie war es, Korrelate von Defiziten in der sozialen Interaktion bei schizophrenen Patienten mit überwiegender Negativsymptomatik im Gegensatz zu gesunden Kontrollpersonen auf verschiedenen Ebenen darzustellen. Hierfür wurde die Fähigkeit zur sozialen Kognition anhand zweier verschiedener psychologischer Testverfahren erhoben und zudem die Gehirnaktivierung während alltagsähnlicher sozialer Interaktion mittels funktioneller Nahinfrarotspektroskopie gemessen. Es konnte gezeigt werden, dass schizophrene Patienten mit vorherrschender Negativsymptomatik unter größeren Beeinträchtigungen zumindest in Teilaspekten von sozialer Kognition leiden als gesunde Kontrollpersonen. Hierbei steht Negativsymptomatik in Zusammenhang mit einer schlechteren Leistung im „Reading Mind in the Eyes Test“, was als „Undermentalizing“ angesehen werden kann. In Bezug auf die neurophysiologischen Messungen von Gehirnaktivität während alltagsähnlicher sozialer Interaktion konnte in der gesunden Kontrollgruppe eine fronto-temporo-parietale Aktivierung festgestellt werden. Hierbei steht insbesondere die Aktivität im Bereich des linken inferioren Parietallappens in Übereinstimmung mit den Ergebnissen zweier vorangegangener Studien (Egetemeir et al. 2011; Herrmann et al. 2015). In der Gruppe der schizophrenen Patienten dieser Studie jedoch zeigte sich keine während „Joint action“ spezifische Aktivität in temporo-parietalen Gehirnregionen. Ebenso war die Gehirnaktivität in den klassischen Spiegelneuronenarealen bei den Patienten im Vergleich zur Kontrollgruppe vermindert. Stattdessen kam es in der Patientengruppe zu einer erhöhten präfrontalen Gehirnaktivierung. Diese verschiedenartige Aktivierungsstrategie bei „Joint action“ kann als kompensatorische Gehirnaktivität interpretiert werden, die es den Patienten ermöglicht, soziale Interaktion erfolgreich zu bewältigen. Falls etwa die entscheidende Rolle während der Bewältigung der vorliegenden „Joint action“-Aufgabe in der Vermittlung visuell-räumlicher Aufmerksamkeitsprozesse durch den inferioren Parietallappen liegt (Herrmann et al. 2015), ist denkbar, dass diese Fähigkeit durch kompensatorische Vorgänge im präfrontalen Kortex übernommen werden kann. Da die Patienten dieser Studie zumeist seit längerer Zeit oder in chronisch residualem Zustand an Schizophrenie mit Negativsymptomatik litten, liegt es nahe, dass sich die kompensatorischen Strategien im Laufe der Zeit durch das alltägliche Leben ausreichend etablieren konnten. Die verminderte Aktivität in Spiegelneuronenarealen innerhalb der Patientengruppe untermauert das Konzept zur Krankheitsentstehung der Schizophrenie von Mehta und Kollegen, welches besagt, dass Gene und Umweltfaktoren ein möglicherweise angeboren defektes Spiegelneuronensystem beeinflussen, wobei erniedrigte Spiegelneuronenaktivität mit Defiziten in sozial kognitiven Einschränkungen und Negativsymptomatik einhergehe (Mehta et al. 2014a). Diese Zusammenhänge können jedoch im Rahmen dieser Studie lediglich vermutet und nicht objektiviert werden. Durch die vorliegende Untersuchung konnte festgestellt werden, dass schizophrene Patienten mit Negativsymptomatik andere neuronale Strategien während alltagsähnlicher sozialer Interaktion nutzen als gesunde Personen, was einen weiteren Einblick in die neurobiologischen Grundlagen der Erkrankung erlaubt. N2 - Many schizophrenic patients show impairments in social cognitive skills especially those with negative symptoms. Often this leads to social withdrawal, aggravates every day social interaction and reduces the quality of life of the patients. Several of these aspects could underlie a deficit in the mirror neuron system (MNS). In the present study different aspects of social interaction were investigated and compared between 16 schizophrenic patients and 17 healthy controls. Therefore, the ability of social cognition was tested by two different neuropsychological tests. In addition to that, functional brain activity including activation of the MNS was measured by functional near-infrared spectroscopy (fNIRS) during a real-life joint action task. This joint action paradigm was published before and led to a consistent activation of the left inferior parietal lobe (IPL) in healthy subjects (Egetemeir et al. 2011; Herrmann et al. 2015). The results show that schizophrenic patients with predominant negative symptoms use different clusters of neural activity during social interaction. By group contrast it could be shown that healthy participants had a significant higher activation in temporo-parietal regions than the patients who showed higher activation in prefrontal areas. Furthermore MNS activity was less in the patient than in the control group. Regarding social cognition patients performed worse in the “Reading the Mind in the Eyes Test”. But despite possible partial impairments in social cognition or dysfunctional brain regions it could be shown that schizophrenic patients are able to successfully manage social interaction through probably engaging compensatory brain strategies. KW - Schizophrenie KW - NIR-Spektroskopie KW - Interaktion KW - Spiegelneuron KW - NIRS KW - MNS KW - schizophrenia KW - joint-action KW - social interaction Y1 - 2015 U6 - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-138737 ER -