Fledrich, Robert

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","87"],["dc.bibliographiccitation.volume","135"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Schlotter-Weigel, Beate"],["dc.contributor.author","Schnizer, Tuuli J."],["dc.contributor.author","Wichert, Sven P."],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Hoerste, Gerd Meyer Zu"],["dc.contributor.author","Klink, Axel"],["dc.contributor.author","Weiss, Bernhard G."],["dc.contributor.author","Haag, Uwe"],["dc.contributor.author","Walter, Maggie C."],["dc.contributor.author","Rautenstrauss, Bernd"],["dc.contributor.author","Paulus, Walter J."],["dc.contributor.author","Rossner, Moritz J."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:15:45Z"],["dc.date.available","2018-11-07T09:15:45Z"],["dc.date.issued","2012"],["dc.description.abstract","Charcot-Marie-Tooth disease is the most common inherited neuropathy and a duplication of the peripheral myelin protein 22 gene causes the most frequent subform Charcot-Marie-Tooth 1A. Patients develop a slowly progressive dysmyelinating and demyelinating peripheral neuropathy and distally pronounced muscle atrophy. The amount of axonal loss determines disease severity. Although patients share an identical monogenetic defect, the disease progression is strikingly variable and the impending disease course can not be predicted in individual patients. Despite promising experimental data, recent therapy trials have failed. Established clinical outcome measures are thought to be too insensitive to detect amelioration within trials. Surrogate biomarkers of disease severity in Charcot-Marie-Tooth 1A are thus urgently needed. Peripheral myelin protein 22 transgenic rats harbouring additional copies of the peripheral myelin protein 22 gene ('Charcot-Marie-Tooth rats'), which were kept on an outbred background mimic disease hallmarks and phenocopy the variable disease severity of patients with Charcot-Marie-Tooth 1A. Hence, we used the Charcot-Marie-Tooth rat to dissect prospective and surrogate markers of disease severity derived from sciatic nerve and skin tissue messenger RNA extracts. Gene set enrichment analysis of sciatic nerve transcriptomes revealed that dysregulation of lipid metabolism associated genes such as peroxisome proliferator-activated receptor gamma constitutes a modifier of present and future disease severity. Importantly, we directly validated disease severity markers from the Charcot-Marie-Tooth rats in 46 patients with Charcot-Marie-Tooth 1A. Our data suggest that the combination of age and cutaneous messenger RNA levels of glutathione S-transferase theta 2 and cathepsin A composes a strong indicator of disease severity in patients with Charcot-Marie-Tooth 1A, as quantified by the Charcot-Marie-Tooth Neuropathy Score. This translational approach, utilizing a transgenic animal model, demonstrates that transcriptional analysis of skin biopsy is suitable to identify biomarkers of Charcot-Marie-Tooth 1A."],["dc.identifier.doi","10.1093/brain/awr322"],["dc.identifier.isi","000300044400016"],["dc.identifier.pmid","22189569"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13524"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/27771"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0006-8950"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","A rat model of Charcot-Marie-Tooth disease 1A recapitulates disease variability and supplies biomarkers of axonal loss in patients"],["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","3973"],["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA"],["dc.bibliographiccitation.lastpage","3978"],["dc.bibliographiccitation.volume","109"],["dc.contributor.author","Makoukji, Joelle"],["dc.contributor.author","Belle, Martin"],["dc.contributor.author","Meffre, Delphine"],["dc.contributor.author","Stassart, Ruth"],["dc.contributor.author","Grenier, Julien"],["dc.contributor.author","Shackleford, Ghjuvan'Ghjacumu"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Fonte, Cosima"],["dc.contributor.author","Branchu, Julien"],["dc.contributor.author","Goulard, Marie"],["dc.contributor.author","de Waele, Catherine"],["dc.contributor.author","Charbonnier, Frederic"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Baulieu, Etienne-Emile"],["dc.contributor.author","Schumacher, Michael"],["dc.contributor.author","Bernard, Sophie"],["dc.contributor.author","Massaad, Charbel"],["dc.date.accessioned","2018-11-07T09:12:24Z"],["dc.date.available","2018-11-07T09:12:24Z"],["dc.date.issued","2012"],["dc.description.abstract","Glycogen synthase kinase 3 beta (GSK3 beta) inhibitors, especially the mood stabilizer lithium chloride, are also used as neuroprotective or anti-inflammatory agents. We studied the influence of LiCl on the remyelination of peripheral nerves. We showed that the treatment of adult mice with LiCl after facial nerve crush injury stimulated the expression of myelin genes, restored the myelin structure, and accelerated the recovery of whisker movements. LiCl treatment also promoted remyelination of the sciatic nerve after crush. We also demonstrated that peripheral myelin gene MPZ and PMP22 promoter activities, transcripts, and protein levels are stimulated by GSK3 beta inhibitors (LiCl and SB216763) in Schwann cells as well as in sciatic and facial nerves. LiCl exerts its action in Schwann cells by increasing the amount of beta-catenin and provoking its nuclear localization. We showed by ChIP experiments that LiCl treatment drives beta-catenin to bind to T-cell factor/lymphoid-enhancer factor response elements identified in myelin genes. Taken together, our findings open perspectives in the treatment of nerve demyelination by administering GSK3 beta inhibitors such as lithium."],["dc.identifier.doi","10.1073/pnas.1121367109"],["dc.identifier.isi","000301117700073"],["dc.identifier.pmid","22355115"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26939"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Natl Acad Sciences"],["dc.relation.issn","0027-8424"],["dc.title","Lithium enhances remyelination of peripheral nerves"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1840"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Akkermann, Dagmar"],["dc.contributor.author","Schütza, Vlad"],["dc.contributor.author","Abdelaal, Tamer A."],["dc.contributor.author","Hermes, Doris"],["dc.contributor.author","Schäffner, Erik"],["dc.contributor.author","Soto-Bernardini, M. Clara"],["dc.contributor.author","Götze, Tilmann"],["dc.contributor.author","Klink, Axel"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Krueger, Martin"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Frydrychowicz, Clara"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Mueller, Wolf C."],["dc.contributor.author","Bechmann, Ingo"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Schwab, Markus H."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Stassart, Ruth M."],["dc.date.accessioned","2019-07-09T11:51:38Z"],["dc.date.available","2019-07-09T11:51:38Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1038/s41467-019-09886-4"],["dc.identifier.pmid","30992451"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16160"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59979"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Publisher Correction: NRG1 type I dependent autoparacrine stimulation of Schwann cells in onion bulbs of peripheral neuropathies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","533"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The American Journal of Human Genetics"],["dc.bibliographiccitation.lastpage","546"],["dc.bibliographiccitation.volume","94"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Epplen, Dirk B."],["dc.contributor.author","Nientiedt, Tobias"],["dc.contributor.author","Wichert, Sven P."],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Rossner, Moritz J."],["dc.contributor.author","Edgar, Julia M."],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:41:24Z"],["dc.date.available","2018-11-07T09:41:24Z"],["dc.date.issued","2014"],["dc.description.abstract","Pelizaeus-Merzbacher disease (PMD) is a severe hypomyelinating disease, characterized by ataxia, intellectual disability, epilepsy, and premature death. In the majority of cases, PMD is caused by duplication of PLP1 that is expressed in myelinating oligodendrocytes. Despite detailed knowledge of PLP1, there is presently no curative therapy for PMD. We used a Plp1 transgenic PMD mouse model to test the therapeutic effect of Lonaprisan, an antagonist of the nuclear progesterone receptor, in lowering Plp1 mRNA overexpression. We applied placebo-controlled Lonaprisan therapy to PMD mice for 10 weeks and performed the grid slip analysis to assess the clinical phenotype. Additionally, mRNA expression and protein accumulation as well as histological analysis of the central nervous system were performed. Although Plp1 mRNA levels are increased 1.8-fold in PMD mice compared to wild-type controls, daily Lonaprisan treatment reduced overexpression at the RNA level to about 1.5-fold, which was sufficient to significantly improve the poor motor phenotype. Electron microscopy confirmed a 25% increase in the number of myelinated axons in the corticospinal tract when compared to untreated PMD mice. Microarray analysis revealed the upregulation of proapoptotic genes in PMD mice that could be partially rescued by Lonaprisan treatment, which also reduced microgliosis, astrogliosis, and lymphocyte infiltration."],["dc.identifier.doi","10.1016/j.ajhg.2014.03.001"],["dc.identifier.isi","000333765300005"],["dc.identifier.pmid","24680886"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/33720"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Cell Press"],["dc.relation.issn","1537-6605"],["dc.relation.issn","0002-9297"],["dc.title","Progesterone Antagonist Therapy in a Pelizaeus-Merzbacher Mouse Model"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","89"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","British Medical Bulletin"],["dc.bibliographiccitation.lastpage","113"],["dc.bibliographiccitation.volume","102"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:09:45Z"],["dc.date.available","2018-11-07T09:09:45Z"],["dc.date.issued","2012"],["dc.description.abstract","Charcot-Marie-Tooth (CMT) disease represents a broad group of inherited motor and sensory neuropathies which can originate from various genetic aberrations, e.g. mutations, deletions and duplications. We performed a literature review on murine animal models of CMT disease with regard to experimental therapeutic approaches. Hereby, we focussed on the demyelinating subforms of CMT (CMT1). PubMed items were CMT, animal model, demyelination and therapy. Patients affected by CMT suffer from slowly progressive, distally pronounced muscle atrophy caused by an axonal loss. The disease severity is highly variable and impairments may result in wheelchair boundness. No therapy is available yet. Numerous rodent models for the various CMT subtypes are available today. The selection of the correct animal model for the specific CMT subtype provides an important prerequisite for the successful translation of experimental findings in patients. Despite more than 20 years of remarkable progress in CMT research, the disease is still left untreatable. There is a growing number of experimental therapeutic strategies that may be translated into future clinical trials in patients with CMT. The slow disease progression and insensitive outcome measures hamper clinical therapy trials in CMT. Biomarkers may provide powerful tools to monitor therapeutic efficacy. Recently, we have shown that transcriptional profiling can be utilized to assess and predict the disease severity in a transgenic rat model and in affected humans."],["dc.identifier.doi","10.1093/bmb/lds010"],["dc.identifier.isi","000304831300007"],["dc.identifier.pmid","22551516"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/26332"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Oxford Univ Press"],["dc.relation.issn","0007-1420"],["dc.title","Murine therapeutic models for Charcot-Marie-Tooth (CMT) disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","1467"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Akkermann, Dagmar"],["dc.contributor.author","Schütza, Vlad"],["dc.contributor.author","Abdelaal, Tamer A."],["dc.contributor.author","Hermes, Doris"],["dc.contributor.author","Schäffner, Erik"],["dc.contributor.author","Soto-Bernardini, M. Clara"],["dc.contributor.author","Götze, Tilmann"],["dc.contributor.author","Klink, Axel"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Krueger, Martin"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Frydrychowicz, Clara"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Mueller, Wolf C."],["dc.contributor.author","Bechmann, Ingo"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Schwab, Markus H."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Stassart, Ruth M."],["dc.date.accessioned","2019-07-09T11:50:53Z"],["dc.date.available","2019-07-09T11:50:53Z"],["dc.date.issued","2019"],["dc.description.abstract","In contrast to acute peripheral nerve injury, the molecular response of Schwann cells in chronic neuropathies remains poorly understood. Onion bulb structures are a pathological hallmark of demyelinating neuropathies, but the nature of these formations is unknown. Here, we show that Schwann cells induce the expression of Neuregulin-1 type I (NRG1-I), a paracrine growth factor, in various chronic demyelinating diseases. Genetic disruption of Schwann cell-derived NRG1 signalling in a mouse model of Charcot-Marie-Tooth Disease 1A (CMT1A), suppresses hypermyelination and the formation of onion bulbs. Transgenic overexpression of NRG1-I in Schwann cells on a wildtype background is sufficient to mediate an interaction between Schwann cells via an ErbB2 receptor-MEK/ERK signaling axis, which causes onion bulb formations and results in a peripheral neuropathy reminiscent of CMT1A. We suggest that diseased Schwann cells mount a regeneration program that is beneficial in acute nerve injury, but that overstimulation of Schwann cells in chronic neuropathies is detrimental."],["dc.identifier.doi","10.1038/s41467-019-09385-6"],["dc.identifier.pmid","30931926"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16018"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59847"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","NRG1 type I dependent autoparacrine stimulation of Schwann cells in onion bulbs of peripheral neuropathies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","48"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Neuroscience"],["dc.bibliographiccitation.lastpage","U76"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Velanac, Viktorija"],["dc.contributor.author","Brinkmann, Bastian G."],["dc.contributor.author","Schwab, Markus H."],["dc.contributor.author","Meijer, Dies"],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2018-11-07T09:30:54Z"],["dc.date.available","2018-11-07T09:30:54Z"],["dc.date.issued","2013"],["dc.description.abstract","After peripheral nerve injury, axons regenerate and become remyelinated by resident Schwann cells. However, myelin repair never results in the original myelin thickness, suggesting insufficient stimulation by neuronal growth factors. Upon testing this hypothesis, we found that axonal neuregulin-1 NRG1) type III and, unexpectedly, also NRG1 type I restored normal myelination when overexpressed in transgenic mice. This led to the observation that Wallerian degeneration induced de novo NRG1 type I expression in Schwann cells themselves. Mutant mice lacking a functional Nrg1 gene in Schwann cells are fully myelinated but exhibit impaired remyelination in adult life. We suggest a model in which loss of axonal contact triggers denervated Schwann cells to transiently express NRG1 as an autocrine/paracrine signal that promotes Schwann cell differentiation and remyelination."],["dc.identifier.doi","10.1038/nn.3281"],["dc.identifier.isi","000312633900012"],["dc.identifier.pmid","23222914"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/31418"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1097-6256"],["dc.title","A role for Schwann cell-derived neuregulin-1 in remyelination"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Haag, Lea-Maxie"],["dc.contributor.author","Veselcic, P."],["dc.contributor.author","Czesnik, D."],["dc.contributor.author","Nave, K.-A."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:23:22Z"],["dc.date.available","2018-11-07T09:23:22Z"],["dc.date.issued","2013"],["dc.format.extent","S198"],["dc.identifier.isi","000320408400638"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29560"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","11th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","0894-1491"],["dc.title","NEUREGULIN-1 TYPE I ENHANCES FUNCTIONAL RECOVERY AFTER ACUTE PERIPHERAL NERVE INJURY AND RESCUES AXONAL LOSS IN A MOUSE MODEL FOR CHARCOT MARIE TOOTH DISEASE 1A"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1055"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Nature Medicine"],["dc.bibliographiccitation.lastpage","1061"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Klink, Axel"],["dc.contributor.author","Rasch, Lennart M."],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Haag, Lauren"],["dc.contributor.author","Czesnik, Dirk"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Abdelaal, Tamer A. M."],["dc.contributor.author","Keric, Naureen"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Brueck, Wolfgang"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:36:01Z"],["dc.date.available","2018-11-07T09:36:01Z"],["dc.date.issued","2014"],["dc.description.abstract","Duplication of the gene encoding the peripheral myelin protein of 22 kDa (PMP22) underlies the most common inherited neuropathy, Charcot-Marie-Tooth 1A (CMT1A)(1-3), a disease without a known cure(4-6). Although demyelination represents a characteristic feature, the clinical phenotype of CMT1A is determined by the degree of axonal loss, and patients suffer from progressive muscle weakness and impaired sensation(4,7). CMT1A disease manifests within the first two decades of life(8,9), and walking disabilities, foot deformities and electrophysiological abnormalities are already present in childhood(7-11). Here, we show in Pmp22-transgenic rodent models of CMT1A that Schwann cells acquire a persistent differentiation defect during early postnatal development, caused by imbalanced activity of the PI3K-Akt and the Mek-Erk signaling pathways. We demonstrate that enhanced PI3K-Akt signaling by axonally overexpressed neuregulin-1 (NRG1) type I drives diseased Schwann cells toward differentiation and preserves peripheral nerve axons. Notably, in a preclinical experimental therapy using a CMT1A rat model, when treatment is restricted to early postnatal development, soluble NRG1 effectively overcomes impaired peripheral nerve development and restores axon survival into adulthood. Our findings suggest a model in which Schwann cell differentiation within a limited time window is crucial for the long-term maintenance of axonal support."],["dc.identifier.doi","10.1038/nm.3664"],["dc.identifier.isi","000341404000019"],["dc.identifier.pmid","25150498"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/32517"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1546-170X"],["dc.relation.issn","1078-8956"],["dc.title","Soluble neuregulin-1 modulates disease pathogenesis in rodent models of Charcot-Marie-Tooth disease 1A"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","S140"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","S141"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Velanac, Viktorija"],["dc.contributor.author","Meijer, Dies"],["dc.contributor.author","Schwab, M."],["dc.contributor.author","Sereda, Michael W."],["dc.contributor.author","Nave, K.-A"],["dc.date.accessioned","2018-11-07T09:23:24Z"],["dc.date.available","2018-11-07T09:23:24Z"],["dc.date.issued","2013"],["dc.identifier.isi","000320408400449"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29571"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","11th European Meeting on Glial Cell Function in Health and Disease"],["dc.relation.eventlocation","Berlin, GERMANY"],["dc.relation.issn","0894-1491"],["dc.title","SCHWANN CELL NEUREGULIN-1 CONSTITUTES AN ENDOGENEOUS FACTOR OF MYELIN REPAIR"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]