Sargin, Derya

[["dc.bibliographiccitation.firstpage","546"],["dc.bibliographiccitation.issue","9-10"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","552"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","Rossner, Moritz J."],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Theis, Fabian"],["dc.contributor.author","Wichert, Sven P."],["dc.contributor.author","Stender, Nike"],["dc.contributor.author","Fischer, Benjamin"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Wiedl, Anne"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:37Z"],["dc.date.available","2017-09-07T11:46:37Z"],["dc.date.issued","2008"],["dc.description.abstract","Molecular mechanisms underlying bipolar affective disorders are unknown. Difficulties arise from genetic and phenotypic heterogeneity of patients and the lack of animal models. Thus, we focused on only one patient (n = 1) with an extreme form of rapid cycling, Ribonucleic acid (RNA) from peripheral blood mononuclear cells (PBMC) was analyzed in a three-tiered approach under widely standardized conditions. Firstly, RNA was extracted from PBMC of eight blood samples, obtained on two consecutive days within one particular episode, including two different consecutive depressive and two different consecutive manic episodes, and submitted to (1) screening by microarray hybridizations, followed by (2) detailed bioinformatic analysis, and (3) confirmation of episode-specific regulation of genes by quantitative real-time polymerase chain reaction (qRT-PCR). Secondly, results were validated in additional blood samples obtained one to two years later. Among gene transcripts elevated in depressed episodes were prostaglandin D synthetase (PTGDS) and prostaglandin D2 11-ketoreductase (AKR1C3), both involved in hibernation. We hypothesized them to account for some of the rapid cycling symptoms. A subsequent treatment approach over 5 months applying the cyclooxygenase inhibitor celecoxib (2 x 200 mg daily) resulted in reduced severity rating of both depressed and manic episodes. This case suggests that rapid cycling is a systemic disease, resembling hibernation, with prostaglandins playing a mediator role."],["dc.identifier.doi","10.2119/2008-00053.Begemann"],["dc.identifier.gro","3150556"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7331"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.subject","Bipolar Disorder; Inhibitor Celecoxib; Prostaglandin D-2; Major Depression; Double-Blind; Hibernation; Sleep; Indomethacin; Hippocampus; Neurons"],["dc.title","Episode-specific differential gene expression of peripheral blood mononuclear cells in rapid cycling supports novel treatment approaches"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1029"],["dc.bibliographiccitation.journal","Molecular Medicine"],["dc.bibliographiccitation.lastpage","1040"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Stepniak, Beata"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","Schwitulla, Judith"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Giegling, Ina"],["dc.contributor.author","Miskowiak, Kamilla W."],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Hannke, Kathrin"],["dc.contributor.author","Ramin, Anna"],["dc.contributor.author","Heinrich, Ralf"],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Rujescu, Dan"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:36Z"],["dc.date.available","2017-09-07T11:46:36Z"],["dc.date.issued","2012"],["dc.description.abstract","Erythropoietin (EPO) improves cognitive performance in clinical studies and rodent experiments. We hypothesized that an intrinsicrole of EPO for cognition exists, with particular relevance in situations of cognitive decline, which is reflected by associations ofEPO and EPO receptor (EPOR) genotypes with cognitive functions. To prove this hypothesis, schizophrenic patients (N > 1000) weregenotyped for 5′ upstream–located gene variants, EPO SNP rs1617640 (T/G) and EPOR STR(GA)n. Associations of these variants wereobtained for cognitive processing speed, fine motor skills and short-term memory readouts, with one particular combination ofgenotypes superior to all others (p < 0.0001). In an independent healthy control sample (N > 800), these associations were confirmed.A matching preclinical study with mice demonstrated cognitive processing speed and memory enhanced upon transgenicexpression of constitutively active EPOR in pyramidal neurons of cortex and hippocampus. We thus predicted that thehuman genotypes associated with better cognition would reflect gain-of-function effects. Indeed, reporter gene assays and quantitativetranscriptional analysis of peripheral blood mononuclear cells showed genotype-dependent EPO/EPOR expression differences.Together, these findings reveal a role of endogenous EPO/EPOR for cognition, at least in schizophrenic patients."],["dc.identifier.doi","10.2119/molmed.2012.00190"],["dc.identifier.gro","3150561"],["dc.identifier.pmid","22669473"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7335"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Common variants of the genes encoding erythropoietin and its receptor modulate cognitive performance in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","881"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Bipolar Disorders"],["dc.bibliographiccitation.lastpage","888"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Gurvich, Artem"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Dahm, Liane"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","Miskowiak, Kamilla W."],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:27Z"],["dc.date.available","2017-09-07T11:46:27Z"],["dc.date.issued","2014"],["dc.description.abstract","Objectives: Over 12% of patients with bipolar disorder exhibit rapid cycling. The underlying biological mechanisms of this extreme form of bipolar disease are still unknown. This study aimed at replicating and extending findings of our previously published case report, where an involvement of prostaglandin synthesis-related genes in rapid cycling was first proposed. Methods: Psychopathological follow-up of the reported case was performed under cessation of celecoxib treatment. In a prospective observational study, patients with bipolar disorder (n = 47; of these, four had rapid cycling) or with monopolar depression (n = 97) were recruited over a period of three years. Repeated psychopathology measurements were conducted using standard instruments. Peripheral blood mononuclear cells (PBMC) were obtained during as many consecutive episodes as possible and processed for mRNA isolation and quantitative real-time reverse transcriptase polymerase chain reaction for prostaglandin D2 synthase (PTGDS), aldo-ketoreductase family 1, member C3 (AKR1C3), cyclooxygenase-2 (PAN means all splice variants) (COX2PAN), prostaglandin-endoperoxide synthase 2 (PTGS2), and purinergic receptor P2X, ligand-gated ion channel 7 (P2RX7). Results: The follow-up of our original case of a patient with rapid cycling who had shown impressive psychopathological improvement under celecoxib revealed complete loss of this effect upon discontinuation of the COX2 inhibitor. Episode-specific gene expression measurements in PBMC of four newly recruited rapid cycling patients confirmed the higher expression of PTGDS in depressive compared to manic phases. Additionally, higher relative expression of PTGS2/COX2PAN was found. No comparable alterations were observable in samples available from the remaining 43 patients with bipolar disorder and the 97 monopolar depressed patients, emphasizing the advantages of the rapid cycling condition with its rapid and frequent shifts for identification of gene expression changes.Conclusions: This study supports a role for prostaglandins in rapid cycling and advocates the cyclooxygenase cascade as a treatment target in this condition."],["dc.identifier.doi","10.1111/bdi.12223"],["dc.identifier.gro","3150518"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7291"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","A role for prostaglandins in rapid cycling suggested by episode-specific gene expression shifts in peripheral blood mononuclear cells: a preliminary report"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]