Friedrichs, Heidi

[["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","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, Doerthe"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","Ribbe, Katja"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Radyushkin, Konstantin A."],["dc.contributor.author","Benseler, Fritz"],["dc.contributor.author","Reim, Kerstin"],["dc.contributor.author","Riggert, Joachim"],["dc.contributor.author","Falkai, Peter"],["dc.contributor.author","Bickeboeller, Heike"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Brose, Nils"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2018-11-07T08:44:54Z"],["dc.date.available","2018-11-07T08:44:54Z"],["dc.date.issued","2010"],["dc.identifier.isi","000276936800585"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/20301"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Florence, ITALY"],["dc.relation.issn","0920-9964"],["dc.title","Complexin2 Gene Polymorphisms Modify Cognitive Performance in Schizophrenia"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","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","573"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Best Practice and Research Clinical Anaesthesiology"],["dc.bibliographiccitation.lastpage","594"],["dc.contributor.author","Sargin, Derya"],["dc.contributor.author","Friedrichs, Heidi"],["dc.contributor.author","El-Kordi, Ahmed"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.date.accessioned","2017-09-07T11:46:19Z"],["dc.date.available","2017-09-07T11:46:19Z"],["dc.date.issued","2010"],["dc.description.abstract","Erythropoietin (EPO), originally discovered as hematopoietic growth factor, has direct effects on cells of the nervous system that make it a highly attractive candidate drug for neuroprotection/neuroregeneration. Hardly any other compound has led to so much preclinical work in the field of translational neuroscience than EPO. Almost all of the >180 preclinical studies performed by many independent research groups from all over the world in the last 12 years have yielded positive results on EPO as a neuroprotective drug. The fact that EPO was approved for the treatment of anemia >20 years ago and found to be well tolerated and safe, facilitated the first steps of translation from preclinical findings to the clinic. On the other hand, the same fact, naturally associated with loss of patent protection, hindered to develop EPO as a highly promising therapeutic strategy for application in human brain disease. Therefore, only few clinical neuroprotection studies have been concluded, all with essentially positive and stimulating results, but no further development towards the clinic has occurred thus far. This article reviews the preclinical and clinical work on EPO for the indications neuroprotection/neuroregeneration and cognition, and hopefully will stimulate new endeavours promoting development of EPO for the treatment of human brain diseases."],["dc.identifier.doi","10.1016/j.bpa.2010.10.005"],["dc.identifier.gro","3150484"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7254"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.title","Erythropoietin as neuroprotective and neuroregenerative treatment strategy: comprehensive overview of 12 years of preclinical and clinical research"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]