Sereda, Michael Werner

[["dc.bibliographiccitation.journal","Annals of Clinical and Translational Neurology"],["dc.contributor.author","Epplen, Dirk B."],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Nientiedt, Tobias"],["dc.contributor.author","Albrecht, Philipp"],["dc.contributor.author","Arlt, Friederike A."],["dc.contributor.author","Stassart, Ruth M."],["dc.contributor.author","Kassmann, Celia M."],["dc.contributor.author","Methner, Axel"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2019-07-09T11:41:24Z"],["dc.date.available","2019-07-09T11:41:24Z"],["dc.date.issued","2015"],["dc.description.abstract","Objective: Pelizaeus–Merzbacher disease (PMD) is a progressive and lethal leukodystrophy caused by mutations affecting the proteolipid protein (PLP1) gene. The most common cause of PMD is a duplication of PLP1 and at present there is no curative therapy available. Methods: By using transgenic mice carrying additional copies of Plp1, we investigated whether curcumin diet ameliorates PMD symptoms. The diet of Plp1 transgenic mice was supplemented with curcumin for 10 consecutive weeks followed by phenotypical, histological and immunohistochemical analyses of the central nervous system. Plp1 transgenic and wild-type mice fed with normal chow served as controls. Results: Curcumin improved the motor phenotype performance of Plp1 transgenic mice by 50% toward wild-type level and preserved myelinated axons by 35% when compared to Plp1 transgenic controls. Furthermore, curcumin reduced astrocytosis, microgliosis and lymphocyte infiltration in Plp1 transgenic mice. Curcumin diet did not affect the pathologically increased Plp1 mRNA abundance. However, high glutathione levels indicating an oxidative misbalance in the white matter of Plp1 transgenic mice were restored by curcumin treatment. Interpretation: Curcumin may potentially serve as an antioxidant therapy of PMD caused by PLP1 gene duplication. ª"],["dc.identifier.doi","10.1002/acn3.219"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/12013"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58419"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation","info:eu-repo/grantAgreement/EC/FP7/201535/EU//NGIDD"],["dc.relation.euproject","Ngidd"],["dc.rights","CC BY-NC-ND 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by-nc-nd/4.0"],["dc.title","Curcumin therapy in a Plp1 transgenic mouse model of Pelizaeus-Merzbacher disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","282"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","282"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","Meyer zu Horste, Gerd"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2022-03-01T11:44:49Z"],["dc.date.available","2022-03-01T11:44:49Z"],["dc.date.issued","2007"],["dc.identifier.doi","10.1002/ana.21134"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103128"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.eissn","1531-8249"],["dc.relation.iserratumof","/handle/2/52190"],["dc.relation.issn","0364-5134"],["dc.title","Correction"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.subtype","erratum_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of the Peripheral Nervous System"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Milet, A."],["dc.contributor.author","Stenzel, J."],["dc.contributor.author","Cholet, N."],["dc.contributor.author","Nabirotchkin, S."],["dc.contributor.author","Hajj, R."],["dc.contributor.author","Nave, K-A"],["dc.contributor.author","Chumakov, I."],["dc.contributor.author","Cohen, Doron"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T09:56:13Z"],["dc.date.available","2018-11-07T09:56:13Z"],["dc.date.issued","2015"],["dc.format.extent","213"],["dc.identifier.isi","000360214600327"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/36911"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","Biennial Meeting of the Peripheral-Nerve-Society"],["dc.relation.eventlocation","Quebec, CANADA"],["dc.relation.issn","1529-8027"],["dc.relation.issn","1085-9489"],["dc.title","AN EXPERIMENTAL TRIAL OF AN EARLY ONSET TREATMENT WITH A COMBINATIONAL DRUG (PXT3003) CONSISTING OF BACLOFEN, NALTREXONE AND SORBITOL IN THE CMT1A RAT MODEL"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","77"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Molecular Neuroscience"],["dc.bibliographiccitation.lastpage","88"],["dc.bibliographiccitation.volume","28"],["dc.contributor.author","Horste, GMZ"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Nave, K. A."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T10:36:54Z"],["dc.date.available","2018-11-07T10:36:54Z"],["dc.date.issued","2006"],["dc.description.abstract","Charcot-Marie-Tooth (CMT) disease is a common hereditary neuropathy that causes progressive distally pronounced muscle weakness and can lead to life-long disability in patients. In most cases, the disorder has been associated with a partial duplication of human chromosome 17 (CMT1A), causing 1.5-fold overexpression of the peripheral myelin protein 22 kDa (PMP22). Increased PMP22 gene dosage results in demyelination, secondary axonal loss, and neurogenic muscle atrophy. Experimental therapeutic approaches based on the role of progesterone and ascorbic acid in myelin formation recently have reached preclinical proof-of-principle trials in rodents. It was shown that progesterone receptor antagonists can reduce PMP22 overexpression and clinical severity in a CMT1A rat model. Furthermore, ascorbic acid treatment reduced premature death and demyelination in a CMT1A mouse model. Thus, basic research has opened up new vistas for the understanding and treatment of hereditary neuropathies."],["dc.identifier.doi","10.1385/JMN:28:1:77"],["dc.identifier.isi","000236438000007"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/45435"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.relation.issn","0895-8696"],["dc.title","Myelin disorders causes and perspectives of Charcot-Marie-Tooth neuropathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["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","291"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of the Peripheral Nervous System"],["dc.bibliographiccitation.lastpage","292"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Stenzel, J."],["dc.contributor.author","Wernick, S."],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Mroczek, M."],["dc.contributor.author","Adam, J."],["dc.contributor.author","Boucard, A."],["dc.contributor.author","Cholet, N."],["dc.contributor.author","Kastberger, B."],["dc.contributor.author","Malderez, C."],["dc.contributor.author","Milet, A."],["dc.contributor.author","Murphy, N. P."],["dc.contributor.author","Nabirotchkin, S."],["dc.contributor.author","Chumakov, I."],["dc.contributor.author","Nave, K. A."],["dc.contributor.author","Hajj, R."],["dc.contributor.author","Cohen, Doron"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T10:09:32Z"],["dc.date.available","2018-11-07T10:09:32Z"],["dc.date.issued","2016"],["dc.identifier.isi","000383856200363"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39671"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","Inflammatory Neuropathy Consortium and GBS 100 Centenary Symposium and Ceilidh"],["dc.relation.eventlocation","Univ Glasgow, Glasgow, SCOTLAND"],["dc.relation.issn","1529-8027"],["dc.relation.issn","1085-9489"],["dc.title","AN EXPERIMENTAL TRIAL OF AN EARLY ONSET SHORT-TERM TREATMENT WITH A COMBINATIONAL DRUG (PXT3003) IN THE CHARCOT-MARIE-TOOTH 1A RAT MODEL"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","9"],["dc.contributor.author","Fledrich, R."],["dc.contributor.author","Abdelaal, T."],["dc.contributor.author","Rasch, L."],["dc.contributor.author","Bansal, V."],["dc.contributor.author","Schütza, V."],["dc.contributor.author","Brügger, B."],["dc.contributor.author","Lüchtenborg, C."],["dc.contributor.author","Prukop, T."],["dc.contributor.author","Stenzel, J."],["dc.contributor.author","Rahman, R. U."],["dc.contributor.author","Hermes, D."],["dc.contributor.author","Ewers, D."],["dc.contributor.author","Möbius, W."],["dc.contributor.author","Ruhwedel, T."],["dc.contributor.author","Katona, I."],["dc.contributor.author","Weis, J."],["dc.contributor.author","Klein, D."],["dc.contributor.author","Martini, R."],["dc.contributor.author","Brück, W."],["dc.contributor.author","Müller, W. C."],["dc.contributor.author","Bonn, S."],["dc.contributor.author","Bechmann, I."],["dc.contributor.author","Nave, K. A."],["dc.contributor.author","Stassart, R. M."],["dc.contributor.author","Sereda, M. W."],["dc.date.accessioned","2020-12-10T18:09:47Z"],["dc.date.available","2020-12-10T18:09:47Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1038/s41467-018-05420-0"],["dc.identifier.eissn","2041-1723"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15603"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/73759"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.notes.intern","Merged from goescholar"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Targeting myelin lipid metabolism as a potential therapeutic strategy in a model of CMT1A neuropathy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of the Peripheral Nervous System"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Weiss, B."],["dc.contributor.author","Yildiz, A. D."],["dc.contributor.author","Epplen, Dirk B."],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Nave, K. A."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T10:09:33Z"],["dc.date.available","2018-11-07T10:09:33Z"],["dc.date.issued","2016"],["dc.format.extent","292"],["dc.identifier.isi","000383856200364"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39673"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","Inflammatory Neuropathy Consortium and GBS 100 Centenary Symposium and Ceilidh"],["dc.relation.eventlocation","Univ Glasgow, Glasgow, SCOTLAND"],["dc.relation.issn","1529-8027"],["dc.relation.issn","1085-9489"],["dc.title","AN EXPERIMENTAL TRIAL OF A LATE ONSET LONG-TERM TREATMENT WITH TUMERIC AND MERIVA (R) CURCUMIN IN THE CHARCOT-MARIE-TOOTH 1A RAT MODEL"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","255"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of the Peripheral Nervous System"],["dc.bibliographiccitation.lastpage","256"],["dc.bibliographiccitation.volume","21"],["dc.contributor.author","Fledrich, Robert"],["dc.contributor.author","Abdelaal, Tamer A. M."],["dc.contributor.author","Rasch, Lennart M."],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Stassart, Ruth Martha"],["dc.contributor.author","Nave, K. A."],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2018-11-07T10:09:32Z"],["dc.date.available","2018-11-07T10:09:32Z"],["dc.date.issued","2016"],["dc.identifier.isi","000383856200270"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/39670"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Wiley-blackwell"],["dc.publisher.place","Hoboken"],["dc.relation.conference","Inflammatory Neuropathy Consortium and GBS 100 Centenary Symposium and Ceilidh"],["dc.relation.eventlocation","Univ Glasgow, Glasgow, SCOTLAND"],["dc.relation.issn","1529-8027"],["dc.relation.issn","1085-9489"],["dc.title","LECITHIN THERAPY IMPROVES DISEASE PROGRESSION IN A RAT MODEL OF 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"]]