Nave, Klaus-Armin

[["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","673"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","674"],["dc.bibliographiccitation.volume","138"],["dc.contributor.author","Stumpf, Sina K."],["dc.contributor.author","Berghoff, Stefan A."],["dc.contributor.author","Trevisiol, Andrea"],["dc.contributor.author","Spieth, Lena"],["dc.contributor.author","Düking, Tim"],["dc.contributor.author","Schneider, Lennart V."],["dc.contributor.author","Schlaphoff, Lennart"],["dc.contributor.author","Dreha-Kulaczewski, Steffi"],["dc.contributor.author","Bley, Annette"],["dc.contributor.author","Burfeind, Dinah"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Mitkovski, Miso"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Guder, Philipp"],["dc.contributor.author","Röhse, Heiko"],["dc.contributor.author","Denecke, Jonas"],["dc.contributor.author","Gärtner, Jutta"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Saher, Gesine"],["dc.date.accessioned","2019-11-04T14:10:22Z"],["dc.date.accessioned","2021-10-27T13:21:24Z"],["dc.date.available","2019-11-04T14:10:22Z"],["dc.date.available","2021-10-27T13:21:24Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00401-019-02064-2"],["dc.identifier.pmid","31482207"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/16592"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/92019"],["dc.language.iso","en"],["dc.notes.intern","Migrated from goescholar"],["dc.relation.eissn","1432-0533"],["dc.relation.iserratumof","/handle/2/62293"],["dc.relation.issn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Correction to: Ketogenic diet ameliorates axonal defects and promotes myelination in Pelizaeus–Merzbacher disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","erratum_ja"],["dc.type.version","published_version"],["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.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","1"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","BMC Neuroscience"],["dc.bibliographiccitation.lastpage","9"],["dc.bibliographiccitation.volume","8"],["dc.contributor.author","Fünfschilling, Ursula"],["dc.contributor.author","Saher, Gesine"],["dc.contributor.author","Xiao, Le"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2019-07-09T11:41:50Z"],["dc.date.available","2019-07-09T11:41:50Z"],["dc.date.issued","2007"],["dc.description.abstract","Background: Cholesterol, an essential component of all mammalian plasma membranes, is highly enriched in the brain. Both during development and in the adult, brain cholesterol is derived from local cholesterol synthesis and not taken up from the circulation. However, the contribution of neurons and glial cells to total brain cholesterol metabolism is unknown.Results: Using conditional gene inactivation in the mouse, we disrupted the squalene synthase gene (fdft1), which is critical for cholesterol synthesis, in cerebellar granule cells and some precerebellar nuclei. Mutant mice showed no histological signs of neuronal degeneration, displayed ultrastructurally normal synapses, and exhibited normal motor coordination. This revealed that these adult neurons do not require cell-autonomous cholesterol synthesis for survival or function."],["dc.identifier.doi","10.1186/1471-2202-8-1"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?goescholar/1246"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/58528"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.subject.ddc","619"],["dc.title","Survival of adult neurons lacking cholesterol synthesis in vivo"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0209752"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","PlOS ONE"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Prukop, Thomas"],["dc.contributor.author","Stenzel, Jan"],["dc.contributor.author","Wernick, Stephanie"],["dc.contributor.author","Kungl, Theresa"],["dc.contributor.author","Mroczek, Magdalena"],["dc.contributor.author","Adam, Julia"],["dc.contributor.author","Ewers, David"],["dc.contributor.author","Nabirotchkin, Serguei"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Hajj, Rodolphe"],["dc.contributor.author","Cohen, Daniel"],["dc.contributor.author","Sereda, Michael W."],["dc.date.accessioned","2019-07-09T11:50:18Z"],["dc.date.available","2019-07-09T11:50:18Z"],["dc.date.issued","2019"],["dc.description.abstract","The most common type of Charcot-Marie-Tooth disease is caused by a duplication of PMP22 leading to dysmyelination, axonal loss and progressive muscle weakness (CMT1A). Currently, no approved therapy is available for CMT1A patients. A novel polytherapeutic proof-of-principle approach using PXT3003, a low-dose combination of baclofen, naltrexone and sorbitol, slowed disease progression after long-term dosing in adult Pmp22 transgenic rats, a known animal model of CMT1A. Here, we report an early postnatal, short-term treatment with PXT3003 in CMT1A rats that delays disease onset into adulthood. CMT1A rats were treated from postnatal day 6 to 18 with PXT3003. Behavioural, electrophysiological, histological and molecular analyses were performed until 12 weeks of age. Daily oral treatment for approximately 2 weeks ameliorated motor deficits of CMT1A rats reaching wildtype levels. Histologically, PXT3003 corrected the disturbed axon calibre distribution with a shift towards large motor axons. Despite dramatic clinical amelioration, only distal motor latencies were improved and correlated with phenotype performance. On the molecular level, PXT3003 reduced Pmp22 mRNA overexpression and improved the misbalanced downstream PI3K-AKT / MEK-ERK signalling pathway. The improved differentiation status of Schwann cells may have enabled better long-term axonal support function. We conclude that short-term treatment with PXT3003 during early development may partially prevent the clinical and molecular manifestations of CMT1A. Since PXT3003 has a strong safety profile and is currently undergoing a phase III trial in CMT1A patients, our results suggest that PXT3003 therapy may be a bona fide translatable therapy option for children and young adolescent patients suffering from CMT1A."],["dc.identifier.doi","10.1371/journal.pone.0209752"],["dc.identifier.pmid","30650121"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15906"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/59743"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.subject.ddc","610"],["dc.title","Early short-term PXT3003 combinational therapy delays disease onset in a transgenic rat model of Charcot-Marie-Tooth disease 1A (CMT1A)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]