Ribbe, Katja

[["dc.bibliographiccitation.firstpage","879"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Archives of General Psychiatry"],["dc.bibliographiccitation.lastpage","888"],["dc.bibliographiccitation.volume","67"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Malzahn, Dörte"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Hannke, Kathrin"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Schwerdtfeger, Dayana"],["dc.contributor.author","Thanhäuser, Ivonne"],["dc.contributor.author","Gerchen, Martin Fungisai"],["dc.contributor.author","Ghorbani, Mohammed"],["dc.contributor.author","Gutwinski, Stefan"],["dc.contributor.author","Hilmes, Constanze"],["dc.contributor.author","Leppert, Richard"],["dc.contributor.author","Ronnenberg, Anja"],["dc.contributor.author","Sowislo, Julia"],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Stödtke, Maren"],["dc.contributor.author","Szuszies, Christoph"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Eckstein, Fritz"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:57Z"],["dc.date.available","2017-09-07T11:46:57Z"],["dc.date.issued","2010"],["dc.description.abstract","Context: Schizophrenia is the collective term for a heterogeneous group of mental disorders with a still obscure biological basis. In particular, the specific contribution of risk or candidate gene variants to the complex schizophrenic phenotype is largely unknown. Objective: To prepare the ground for a novel “phenomics” approach, a unique schizophrenia patient database was established by GRAS (Göttingen Research Association for Schizophrenia), designed to allow association of genetic information with quantifiable phenotypes. Because synaptic dysfunction plays a key role in schizophrenia, the complexin 2 gene (CPLX2) was examined in the first phenotype-based genetic association study (PGAS) of GRAS. Design: Subsequent to a classic case-control approach, we analyzed the contribution of CPLX2 polymorphisms to discrete cognitive domains within the schizophrenic population. To gain mechanistic insight into how certain CPLX2 variants influence gene expression and function, peripheral blood mononuclear cells of patients, Cplxnull mutantmice, and transfected cells were investigated.Setting: Coordinating research center (Max Planck Institute of Experimental Medicine) and 23 collaboratingpsychiatric centers all over Germany.Participants: One thousand seventy-one patients with schizophrenia (DSM-IV) examined by an invariant investigator team, resulting in the GRAS database with more than 3000 phenotypic data points per patient, and 1079 healthy control subjects of comparable ethnicity.Main Outcome Measure: Cognitive performance including executive functioning, reasoning, and verbal learning/memory. Results: Six single-nucleotide polymorphisms, distributed over the whole CPLX2 gene, were found to be highly associated with current cognition of schizophrenic subjects but only marginally with premorbid intelligence. Correspondingly, in Cplx2-null mutant mice, prominent cognitive loss of function was obtained only in combination with a minor brain lesion applied during puberty, modeling a clinically relevant environmental risk (“second hit”) for schizophrenia. In the human CPLX2 gene, 1 of the identified 6 cognition-relevant single-nucleotide polymorphisms, rs3822674 in the 3´ untranslated region, was detected to influence microRNA-498 binding and gene expression. The same marker was associated with differential expression of CPLX2 in peripheral blood mononuclear cells. Conclusions: The PGAS allows identification of markerassociated clinical/biological traits. Current cognitive performance in schizophrenic patients is modified by CPLX2 variants modulating posttranscriptional gene expression"],["dc.identifier.doi","10.1001/archgenpsychiatry.2010.107"],["dc.identifier.fs","577608"],["dc.identifier.gro","3150567"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6097"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7343"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.notes.status","final"],["dc.rights.access","closedAccess"],["dc.subject","Schizophrenia"],["dc.subject.ddc","610"],["dc.title","Modification of cognitive performance in schizophrenia by complexin 2 gene polymorphisms"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","27"],["dc.bibliographiccitation.journal","Der Neurologe und Psychiater"],["dc.bibliographiccitation.lastpage","32"],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Niehaus, Silja"],["dc.contributor.author","Wagner, Thilo"],["dc.date.accessioned","2017-09-07T11:46:31Z"],["dc.date.available","2017-09-07T11:46:31Z"],["dc.date.issued","2007"],["dc.identifier.gro","3150527"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7300"],["dc.language.iso","de"],["dc.notes.status","zu prüfen"],["dc.title","Ambulante Langzeit - Intensivtherapie für Alkoholkranke (ALITA)"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","340"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","American Journal of Medical Genetics Part B: Neuropsychiatric Genetics"],["dc.bibliographiccitation.lastpage","345"],["dc.bibliographiccitation.volume","156B"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Rosenberger, Albert"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Schwab, Markus H."],["dc.contributor.author","Jahn, Henriette"],["dc.contributor.author","Gunkel, Stefan"],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:36Z"],["dc.date.available","2017-09-07T11:46:36Z"],["dc.date.issued","2011"],["dc.description.abstract","By pure endpoint diagnosis of the disease, the risk of developing schizophrenia has been repeatedly associated with specific variants of the neuregulin1 (NRG1) gene. However, the role of NRG1 in the etiology of schizophrenia has remained unclear. Since Nrg1 serves vital functions in early brain development of mice, we hypothesized that human NRG1 alleles codetermine developmentally influenced readouts of the disease: age of onset and positive symptom severity. We analyzed 1,071 comprehensively phenotyped schizophrenic/schizoaffective patients, diagnosed according to DSM-IV-TR, from the GRAS (Göttingen Research Association for Schizophrenia) Data Collection for genetic variability in the Icelandic region of risk in the NRG1 gene. For the case-control analysis part of the study, we included 1,056 healthy individuals with comparable ethnicity. The phenotype-based genetic association study (PGAS) was performed on the GRAS sample. Instead of a risk constellation, we detected that several haplotypic variants of NRG1 were, unexpectedly, less frequent in the schizophrenic than in the control sample (mean OR=0.78, range between 0.68 and 0.85). In the PGAS we found that these \"protective\" NRG1 variants are specifically underrepresented in subgroups of schizophrenic subjects with early age of onset and high positive symptom load. The GRAS Data Collection as a prerequisite for PGAS has enabled us to associate protective NRG1 genotypes with later onset and milder course of schizophrenia."],["dc.identifier.doi","10.1002/ajmg.b.31168"],["dc.identifier.gro","3150547"],["dc.identifier.pmid","21234898"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7321"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","A phenotype-based genetic association study reveals the contribution of neuregulin1 gene variants to age of onset and positive symptom severity in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","309"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","EMBO Molecular Medicine"],["dc.bibliographiccitation.lastpage","319"],["dc.bibliographiccitation.volume","3"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Gerchen, Martin F."],["dc.contributor.author","Adamcio, Bartosz"],["dc.contributor.author","Pardo, Luis A."],["dc.contributor.author","Martin, Sabine"],["dc.contributor.author","Malzahn, Dörthe"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Radyushkin, Konstantin A."],["dc.contributor.author","Müller, Michael"],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Bickeböller, Heike"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:44:13Z"],["dc.date.available","2017-09-07T11:44:13Z"],["dc.date.issued","2011"],["dc.description.abstract","KCNN3, encoding the small conductance calcium-activated potassium channel SK3, harbours a polymorphic CAG repeat in the amino-terminal coding region with yet unproven function. Hypothesizing that KCNN3 genotypes do not influence susceptibility to schizophrenia but modify its phenotype, we explored their contribution to specific schizophrenic symptoms. Using the Gottingen Research Association for Schizophrenia (GRAS) data collection of schizophrenic patients (n=1074), we performed a phenotype-based genetic association study (PGAS) of KCNN3. We show that long CAG repeats in the schizophrenic sample are specifically associated with better performance in higher cognitive tasks, comprising the capacity to discriminate, select and execute (p<0.0001). Long repeats reduce SK3 channel function, as we demonstrate by patch-clamping of transfected HEK293 cells. In contrast, modelling the opposite in mice, i.e. KCNN3 overexpression/channel hyperfunction, leads to selective deficits in higher brain functions comparable to those influenced by SK3 conductance in humans. To conclude, KCNN3 genotypes modify cognitive performance, shown here in a large sample of schizophrenic patients. Reduction of SK3 function may constitute a pharmacological target to improve cognition in schizophrenia and other conditions with cognitive impairment."],["dc.identifier.doi","10.1002/emmm.201100135"],["dc.identifier.gro","3142723"],["dc.identifier.isi","000292277600003"],["dc.identifier.pmid","21433290"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/8179"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/159"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1757-4676"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A CAG repeat polymorphism of KCNN3 predicts SK3 channel function and cognitive performance in schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Pharmacopsychiatry"],["dc.bibliographiccitation.volume","40"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Niehaus, S."],["dc.contributor.author","Ribbe, K."],["dc.contributor.author","Wagner, T."],["dc.contributor.author","Bartels, C."],["dc.contributor.author","Kroener-Herwig, Birgit"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T10:59:23Z"],["dc.date.available","2018-11-07T10:59:23Z"],["dc.date.issued","2007"],["dc.format.extent","235"],["dc.identifier.isi","000249873600151"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/50685"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.publisher.place","Stuttgart"],["dc.relation.conference","25th Symposium of the Arbeitsgemeinschaft-Neuropsychopharmakologie-und-Pharmakopsychiatrie"],["dc.relation.eventlocation","Munich, GERMANY"],["dc.relation.issn","0176-3679"],["dc.title","Prediction of outcome by multimodal monitoring of treatment processes in alcoholism therapy"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","91"],["dc.bibliographiccitation.journal","BMC Psychiatry"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Kästner, Anne"],["dc.contributor.author","Gerchen, Martin Fungisai"],["dc.contributor.author","Ackermann, Verena"],["dc.contributor.author","Tarami, Asieh"],["dc.contributor.author","Treitz, Annika"],["dc.contributor.author","Flögel, Marlene"],["dc.contributor.author","Adler, Lothar"],["dc.contributor.author","Aldenhoff, Josef B."],["dc.contributor.author","Becker-Emner, Marianne"],["dc.contributor.author","Becker, Thomas"],["dc.contributor.author","Czernik, Adelheid"],["dc.contributor.author","Dose, Matthias"],["dc.contributor.author","Folkerts, Here"],["dc.contributor.author","Freese, Roland"],["dc.contributor.author","Guenther, Rolf"],["dc.contributor.author","Herpertz, Sabine"],["dc.contributor.author","Hesse, Dirk"],["dc.contributor.author","Kruse, Gunther"],["dc.contributor.author","Kunze, Heinrich"],["dc.contributor.author","Franz, Michael"],["dc.contributor.author","Lohrer, Frank"],["dc.contributor.author","Maier, Wolfgang"],["dc.contributor.author","Mielke, Andreas"],["dc.contributor.author","Müller-Isberner, Rüdiger"],["dc.contributor.author","Oestereich, Cornelia"],["dc.contributor.author","Pajonk, Frank-Gerald"],["dc.contributor.author","Pollmächer, Thomas"],["dc.contributor.author","Schneider, Udo"],["dc.contributor.author","Schwarz, Hans-Joachim"],["dc.contributor.author","Kröner-Herwig, Birgit"],["dc.contributor.author","Havemann-Reinecke, Ursula"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Stühmer, Walter"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Brose, Nils"],["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","2010"],["dc.description.abstract","Background: Schizophrenia is the collective term for an exclusively clinically diagnosed, heterogeneous group of mental disorders with still obscure biological roots. Based on the assumption that valuable information about relevant genetic and environmental disease mechanisms can be obtained by association studies on patient cohorts of ≥ 1000 patients, if performed on detailed clinical datasets and quantifiable biological readouts, we generated a new schizophrenia data base, the GRAS (Göttingen Research Association for Schizophrenia) data collection. GRAS is the necessary ground to study genetic causes of the schizophrenic phenotype in a 'phenotype-based genetic association study' (PGAS). This approach is different from and complementary to the genome-wide association studies (GWAS) on schizophrenia. Methods: For this purpose, 1085 patients were recruited between 2005 and 2010 by an invariable team of traveling investigators in a cross-sectional field study that comprised 23 German psychiatric hospitals. Additionally, chart records and discharge letters of all patients were collected. Results: The corresponding dataset extracted and presented in form of an overview here, comprises biographic information, disease history, medication including side effects, and results of comprehensive cross-sectional psychopathological, neuropsychological, and neurological examinations. With >3000 data points per schizophrenic subject, this data base of living patients, who are also accessible for follow-up studies, provides a wide-ranging and standardized phenotype characterization of as yet unprecedented detail. Conclusions: The GRAS data base will serve as prerequisite for PGAS, a novel approach to better understanding 'the schizophrenias' through exploring the contribution of genetic variation to the schizophrenic phenotypes."],["dc.format.extent","20"],["dc.identifier.doi","10.1186/1471-244X-10-91"],["dc.identifier.gro","3150558"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5803"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7333"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","The cross-sectional GRAS sample: a comprehensive phenotypical data collection of schizophrenic patients"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","27"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Suchtmedizin in Forschung und Praxis"],["dc.bibliographiccitation.lastpage","47"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Niehaus, Silja"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Wagner, Thilo"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Kröner-Herwig, Birgit"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:31Z"],["dc.date.available","2017-09-07T11:46:31Z"],["dc.date.issued","2007"],["dc.description.abstract","Background: Research on addiction treatment lacks prospectivelongitudinal studies that analyze with observational instrumentsbehavior of alcohol dependent patients during therapy sessions.With the \"Video-Assisted Monitoring of Psychotherapeutic pro-cesses in chronic psychiatric disease (VAMP)\" this study investi-gates 64 chronic alcohol dependent patients at three time-points,t1 (week 3), t2 (month 6), and t3 (month 12) during the first year ofthe Outpatient Longterm Intensive Therapy for Alcoholics (OLITA).Aims: Change of therapeutic processes between t1, t2, and t3,prediction of cumulative abstinence probability during a follow-up of up to 4 years, construction of the TOPPS ( Therapy Orientationby Process Prediction Score).Methods: 175 video recordings of therapy sessions were analyzedwith the VAMP. After each video recording, patients and therapistsrated their experience of the therapeutic alliance. Change oftherapeutic processes over time were tested with repeatedmeasures ANOVA, and prediction of cumulative abstinence pro-bability by therapy processes was determined with Cox Regressi-on Analysis.Results: Most of the processes changed only marginally betweent1, t2 and t3. The TOPPS predicts cumulative abstinence probabilityat all of the three time-points (p < 0,001) by integrating eightprocess variables with the highest predictive validity: Experienceof ressources, abstinence self-efficacy, implicit craving, relapsealertness, relapse risk, disease concept, dysfunctional therapeuticengagement, dysfunctional problem solving of current problems.Patients who relapsed after 12 months showed continuously lowTOPPS from t1 to t3. However, patients who maintained long-termabstinence had high TOPPS at t1 which increased slightly betweent2 and t3 (p < 0,015).Conclusions: The eight TOPPS processes are determined from thecurrent behavior of a patient during a specific therapy session andindicate to which extent his common behavior predicts probabi-lity of longterm abstinence or relapse risk. The results suggest toemploy the TOPPS in addiction therapy as a guideline of indivi-dual relapse prevention strategies."],["dc.identifier.gro","3150528"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7301"],["dc.language.iso","de"],["dc.notes.status","final"],["dc.subject","Behavior observation; HAQ; Helping Alliance Question- naire; processes of change; psychotherapy of alcohol dependence; therapy process and outcome research"],["dc.subject","Psychotherapie der Alkoholabhängigkeit; HAQ; Helping Alliance Questionnaire; Therapieprozess-Forschung; Ver- änderungsprozesse; Verhaltensbeobachtung"],["dc.title","Multimodales Monitoring psychotherapeutischer Prozesse in der Behandlung alkoholkranker Patienten"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","337"],["dc.bibliographiccitation.issue","2-3"],["dc.bibliographiccitation.journal","Schizophrenia Research"],["dc.bibliographiccitation.lastpage","338"],["dc.bibliographiccitation.volume","117"],["dc.contributor.author","Klaus, Sabrina"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Malzahn, Dörthe"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Radyushkin, Konstantin"],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2022-03-01T11:45:23Z"],["dc.date.available","2022-03-01T11:45:23Z"],["dc.date.issued","2010"],["dc.identifier.doi","10.1016/j.schres.2010.02.583"],["dc.identifier.pii","S0920996410006687"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103308"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0920-9964"],["dc.title","Complexin2 Gene Polymorphisms Modify Cognitive Performance in Schizophrenia"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1247"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Archives of General Psychiatry"],["dc.bibliographiccitation.lastpage","1256"],["dc.bibliographiccitation.volume","68"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Ackermann, Verena"],["dc.contributor.author","Schwitulla, Judith"],["dc.contributor.author","Begemann, Martin"],["dc.contributor.author","Papiol, Sergi"],["dc.contributor.author","Grube, Sabrina"],["dc.contributor.author","Sperling, Swetlana"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Sillaber, I."],["dc.contributor.author","Gefeller, Olaf"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:35Z"],["dc.date.available","2017-09-07T11:46:35Z"],["dc.date.issued","2011"],["dc.description.abstract","Context Stress plays a major role in the development of comorbid alcohol use disorder (AUD). In turn, AUD worsens the outcome of psychiatric patients with respect to global disease severity, social situation, and socioeconomic burden. Prediction of persons at risk for AUD is crucial for future preventive and therapeutic strategies.Objective To investigate whether genetic variants of the corticotropin-releasing factor system or their interaction influence the risk of developing AUD in chronic disease populations.Design Genotype analysis comprising selected single-nucleotide polymorphisms within the CRHR1 and CRHBP genes in patients with schizophrenia and in a nonschizophrenic psychiatric disease control sample should allow the extraction of predictors of comorbid AUD. Gene expression (messenger RNA) analysis in peripheral blood mononuclear cells was performed to gain the first mechanistic insight.Setting An ideal setup for this study was the Göttingen Research Association for Schizophrenia Data Collection of schizophrenic patients, specifically intended to enable association of genetic information with quantifiable phenotypes in a phenotype-based genetic association study.Patients A total of 1037 schizophrenic patients (Göttingen Research Association for Schizophrenia sample), 80 nonschizophrenic psychiatric disease controls as a small replicate sample, and a case-control study including 1141 healthy subjects.Main Outcome Measures Association of CRHR1 and CRHBP genotypes with the following: (1) AUD; (2) a newly developed alcoholism severity score comprising 5 AUD-relevant variables; and (3) quantitative CRHR1 and CRHBP messenger RNA expression.Results An interaction of CRHR1 rs110402 and CRHBP rs3811939 predicts high risk of comorbid AUD in schizophrenic patients (odds ratio = 2.27; 95% confidence interval, 1.56-3.30; P < .001) as well as psychiatric disease controls (odds ratio = 4.02; 95% confidence interval, 0.95-17.05; P = .06) and leads to the highest CRHR1/CRHBP messenger RNA ratio (P = .02; dysbalanced stress axis).Conclusions The high predictive value of a genetic interaction within the stress axis for the risk of comorbid AUD may be used for novel preventive and individualized therapeutic approaches."],["dc.identifier.doi","10.1001/archgenpsychiatry.2011.100"],["dc.identifier.gro","3150549"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7323"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.title","Prediction of the risk of comorbid alcoholism in schizophrenia by interaction of common genetic variants in the corticotropin-releasing factor system"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","30"],["dc.bibliographiccitation.journal","Journal of Psychiatric Research"],["dc.bibliographiccitation.lastpage","47"],["dc.contributor.author","Krampe, Henning"],["dc.contributor.author","Stawicki, Sabina"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","Wagner, Thilo"],["dc.contributor.author","Bartels, Claudia"],["dc.contributor.author","Kroener-Herwig, Birgit"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:32Z"],["dc.date.available","2017-09-07T11:46:32Z"],["dc.date.issued","2008"],["dc.description.abstract","Outcome prediction in alcoholism therapy is of major sociopolitical and economic significance. Instruments based on psychotherapeutic processes are lacking. Therefore, treatment processes of 64 chronic alcohol dependent patients have been investigated at three time-points, t1 (week 3), t2 (month 6), and t3 (month 12) during the first year of a comprehensive outpatient treatment program, guaranteeing strictly controlled alcohol abstinence. Main focus of the study was the prediction of cumulative abstinence probability over a follow-up period of up to 4 years based on these treatment processes. One hundred and seventy-five video recordings of therapy sessions were analyzed with the behavior observational system VAMP (Video-Assisted Monitoring of Psychotherapeutic Processes in Chronic Psychiatric Disease). Patients’ self-rating of treatment processes was measured with questionnaires for self-efficacy, abstinence confidence, self-consciousness and stress coping. Prediction of cumulative abstinence probability was determined with Cox regression analysis. By integrating the observer rated process variables with the highest predictive validity, the composite score TOPPS (Therapy Orientation by Process Prediction Score) was constructed. It includes the process variables experience of resources, abstinence self-efficacy, implicit craving, relapse alertness, relapse risk, disease concept, dysfunctional therapeutic engagement, and dysfunctional problem solving of current problems. Whereas patients’ self-rating of treatment processes was insufficiently predictive, the TOPPS strongly predicted four-year abstinence probability at any of the 3 time-points (p < 0.001). The results suggest to validate the item combination described in the TOPPS in addiction therapy as a treatment guideline of individual relapse prevention strategies."],["dc.identifier.doi","10.1016/j.jpsychires.2008.01.007"],["dc.identifier.gro","3150530"],["dc.identifier.pmid","18342335"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7302"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.title","Development of an outcome prediction measure for alcoholism therapy by multimodal monitoring of treatment processes"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]