Kusch, Kathrin

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Nature Communications"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Moore, Sharlen"],["dc.contributor.author","Meschkat, Martin"],["dc.contributor.author","Ruhwedel, Torben"],["dc.contributor.author","Trevisiol, Andrea"],["dc.contributor.author","Tzvetanova, Iva D."],["dc.contributor.author","Battefeld, Arne"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Kole, Maarten H. P."],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","de Hoz, Livia"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2021-04-14T08:31:48Z"],["dc.date.available","2021-04-14T08:31:48Z"],["dc.date.issued","2020"],["dc.identifier.doi","10.1038/s41467-020-19152-7"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83719"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2041-1723"],["dc.title","A role of oligodendrocytes in information processing"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","e3000943"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PLoS Biology"],["dc.bibliographiccitation.volume","18"],["dc.contributor.author","Trevisiol, Andrea"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Steyer, Anna M."],["dc.contributor.author","Gregor, Ingo"],["dc.contributor.author","Nardis, Christos"],["dc.contributor.author","Winkler, Ulrike"],["dc.contributor.author","Köhler, Susanne"],["dc.contributor.author","Restrepo, Alejandro"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Nave, Klaus-Armin"],["dc.contributor.author","Hirrlinger, Johannes"],["dc.date.accessioned","2021-04-14T08:31:16Z"],["dc.date.available","2021-04-14T08:31:16Z"],["dc.date.issued","2020"],["dc.description.abstract","In several neurodegenerative disorders, axonal pathology may originate from impaired oligodendrocyte-to-axon support of energy substrates. We previously established transgenic mice that allow measuring axonal ATP levels in electrically active optic nerves. Here, we utilize this technique to explore axonal ATP dynamics in the Plpnull/y mouse model of spastic paraplegia. Optic nerves from Plpnull/y mice exhibited lower and more variable basal axonal ATP levels and reduced compound action potential (CAP) amplitudes, providing a missing link between axonal pathology and a role of oligodendrocytes in brain energy metabolism. Surprisingly, when Plpnull/y optic nerves are challenged with transient glucose deprivation, both ATP levels and CAP decline slower, but recover faster upon reperfusion of glucose. Structurally, myelin sheaths display an increased frequency of cytosolic channels comprising glucose and monocarboxylate transporters, possibly facilitating accessibility of energy substrates to the axon. These data imply that complex metabolic alterations of the axon–myelin unit contribute to the phenotype of Plpnull/y mice."],["dc.identifier.doi","10.1371/journal.pbio.3000943"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83539"],["dc.identifier.url","https://for2848.gwdguser.de/literature/publications/20"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation","FOR 2848: Architektur und Heterogenität der inneren mitochondrialen Membran auf der Nanoskala"],["dc.relation","FOR 2848 | P08: Strukturelle und funktionale Veränderungen der inneren mitochondrialen Membran axonaler Mitochondrien in vivo in einem dymyelinisierenden Mausmodell"],["dc.relation.eissn","1545-7885"],["dc.relation.workinggroup","RG Möbius"],["dc.rights","CC BY 4.0"],["dc.title","Structural myelin defects are associated with low axonal ATP levels but rapid recovery from energy deprivation in a mouse model of spastic paraplegia"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["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.journal","Frontiers in Molecular Neuroscience"],["dc.bibliographiccitation.volume","13"],["dc.contributor.author","Rankovic, Vladan"],["dc.contributor.author","Vogl, Christian"],["dc.contributor.author","Dörje, Nele M."],["dc.contributor.author","Bahader, Iman"],["dc.contributor.author","Duque-Afonso, Carlos J."],["dc.contributor.author","Thirumalai, Anupriya"],["dc.contributor.author","Weber, Thomas"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Strenzke, Nicola"],["dc.contributor.author","Moser, Tobias"],["dc.date.accessioned","2021-04-14T08:29:50Z"],["dc.date.available","2021-04-14T08:29:50Z"],["dc.date.issued","2021"],["dc.description.abstract","Hearing impairment is the most common sensory disorder in humans. So far, rehabilitation of profoundly deaf subjects relies on direct stimulation of the auditory nerve through cochlear implants. However, in some forms of genetic hearing impairment, the organ of Corti is structurally intact and therapeutic replacement of the mutated gene could potentially restore near natural hearing. In the case of defects of the otoferlin gene (OTOF), such gene therapy is hindered by the size of the coding sequence (~6 kb) exceeding the cargo capacity (\\u0026lt;5 kb) of the preferred viral vector, adeno-associated virus (AAV). Recently, a dual-AAV approach was used to partially restore hearing in deaf otoferlin knock-out (Otof-KO) mice. Here, we employed in vitro and in vivo approaches to assess the gene-therapeutic potential of naturally-occurring and newly-developed synthetic AAVs overloaded with the full-length Otof coding sequence. Upon early postnatal injection into the cochlea of Otof-KO mice, overloaded AAVs drove specific expression of otoferlin in ~30% of all IHCs, as demonstrated by immunofluorescence labeling and polymerase chain reaction. Recordings of auditory brainstem responses and a behavioral assay demonstrated partial restoration of hearing. Together, our results suggest that viral gene therapy of DFNB9—using a single overloaded AAV vector—is indeed feasible, reducing the complexity of gene transfer compared to dual-AAV approaches."],["dc.identifier.doi","10.3389/fnmol.2020.600051"],["dc.identifier.pmid","33488357"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83002"],["dc.identifier.url","https://mbexc.uni-goettingen.de/literature/publications/123"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.publisher","Frontiers Media S.A."],["dc.relation","EXC 2067: Multiscale Bioimaging"],["dc.relation.eissn","1662-5099"],["dc.relation.workinggroup","RG Moser (Molecular Anatomy, Physiology and Pathology of Sound Encoding)"],["dc.rights","http://creativecommons.org/licenses/by/4.0/"],["dc.title","Overloaded Adeno-Associated Virus as a Novel Gene Therapeutic Tool for Otoferlin-Related Deafness"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.subtype","original_ja"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Uecker, Martin"],["dc.contributor.author","Liepold, Thomas"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Werner, Hauke B."],["dc.contributor.author","Valerius, Oliver"],["dc.contributor.author","Jahn, Olaf"],["dc.contributor.author","Nave, Klaus-Armin"],["dc.date.accessioned","2018-11-07T10:23:03Z"],["dc.date.available","2018-11-07T10:23:03Z"],["dc.date.issued","2017"],["dc.identifier.isi","000403071700600"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/42387"],["dc.language.iso","en"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Wiley"],["dc.publisher.place","Hoboken"],["dc.relation.conference","13th European Meeting on Glial Cells in Health and Disease"],["dc.relation.eventlocation","Edinburgh, Scotland"],["dc.title","SIRT2 as a genetic modifier of axonal degeneration in white matter tracts"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","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","3518"],["dc.bibliographiccitation.issue","17"],["dc.bibliographiccitation.journal","Proteomics"],["dc.bibliographiccitation.lastpage","3530"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Winter, Theresa"],["dc.contributor.author","Winter, Jörn"],["dc.contributor.author","Polak, Martin"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Mäder, Ulrike"],["dc.contributor.author","Sietmann, Rabea"],["dc.contributor.author","Ehlbeck, Jörg"],["dc.contributor.author","van Hijum, Sacha"],["dc.contributor.author","Weltmann, Klaus-Dieter"],["dc.contributor.author","Hecker, Michael"],["dc.contributor.author","Kusch, Harald"],["dc.date.accessioned","2019-08-06T11:02:44Z"],["dc.date.available","2019-08-06T11:02:44Z"],["dc.date.issued","2011"],["dc.description.abstract","Plasma medicine and also decontamination of bacteria with physical plasmas is a promising new field of life science with huge interest especially for medical applications. Despite numerous successful applications of low temperature gas plasmas in medicine and decontamination, the fundamental nature of the interactions between plasma and microorganisms is to a large extent unknown. A detailed knowledge of these interactions is essential for the development of new as well as for the enhancement of established plasma-treatment procedures. In the present work we introduce for the first time a growth chamber system suitable for low temperature gas plasma treatment of bacteria in liquid medium. We have coupled the use of this apparatus to a combined proteomic and transcriptomic analyses to investigate the specific stress response of Bacillus subtilis 168 cells to treatment with argon plasma. The treatment with three different discharge voltages revealed not only effects on growth, but also clear evidence of cellular stress responses. B. subtilis suffered severe cell wall stress, which was made visible also by electron microscopy, DNA damages and oxidative stress as a result of exposure to plasma. These biological findings were supported by the detection of reactive plasma species by OES measurements."],["dc.identifier.doi","10.1002/pmic.201000637"],["dc.identifier.pmid","21751354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/62304"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1615-9861"],["dc.relation.issn","1615-9853"],["dc.title","Characterization of the global impact of low temperature gas plasma on vegetative microorganisms"],["dc.type","journal_article"],["dc.type.internalPublication","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1832"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","1847"],["dc.bibliographiccitation.volume","61"],["dc.contributor.author","de Monasterio-Schrader, Patricia"],["dc.contributor.author","Patzig, Julia"],["dc.contributor.author","Möbius, Wiebke"],["dc.contributor.author","Barrette, Benoit"],["dc.contributor.author","Wagner, Tadzio L."],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Edgar, Julia M."],["dc.contributor.author","Brophy, Peter J."],["dc.contributor.author","Werner, Hauke B."],["dc.date.accessioned","2022-03-01T11:45:36Z"],["dc.date.available","2022-03-01T11:45:36Z"],["dc.date.issued","2013"],["dc.identifier.doi","10.1002/glia.22561"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/103390"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-531"],["dc.relation.issn","0894-1491"],["dc.title","Uncoupling of neuroinflammation from axonal degeneration in mice lacking the myelin protein tetraspanin-2"],["dc.title.alternative","Tspan2-Deficient Myelin Induces Neuroinflammation"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","2080"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","Journal of Cerebral Blood Flow & Metabolism"],["dc.bibliographiccitation.lastpage","2088"],["dc.bibliographiccitation.volume","35"],["dc.contributor.author","Krey, Lea"],["dc.contributor.author","Luehder, Fred"],["dc.contributor.author","Kusch, Kathrin"],["dc.contributor.author","Czech-Zechmeister, Bozena"],["dc.contributor.author","Koennecke, Birte"],["dc.contributor.author","Outeiro, Tiago Fleming"],["dc.contributor.author","Trendelenburg, George"],["dc.date.accessioned","2018-11-07T09:48:30Z"],["dc.date.available","2018-11-07T09:48:30Z"],["dc.date.issued","2015"],["dc.description.abstract","Sirtuin-2 (Sirt2) is a member of the NAD+-dependent protein deacetylase family. Various members of the sirtuin class have been found to be involved in processes related to longevity, regulation of inflammation, and neuroprotection. Induction of Sirt2 mRNA was found in the whole hemisphere after experimental stroke in a recent screening approach. Moreover, Sirt2 protein is highly expressed in myelin-rich brain regions after stroke. To examine the effects of Sirt2 on ischemic stroke, we induced transient focal cerebral ischemia in adult male Sirt2-knockout and wild-type mice. Two stroke models with different occlusion times were applied: a severe ischemia (45 minutes of middle cerebral artery occlusion (MCAO)) and a mild one (15 minutes of MCAO), which was used to focus on subcortical infarcts. Neurological deficit was determined at 48 hours after 45 minutes of MCAO, and up to 7 days after induction of 15 minutes of cerebral ischemia. In contrast to recent data on Sirt1, Sirt2(-/-) mice showed less neurological deficits in both models of experimental stroke, with the strongest manifestation after 48 hours of reperfusion. However, we did not observe a significant difference of stroke volumes or inflammatory cell count between Sirt2-deficient and wild-type mice. Thus we postulate that Sirt2 mediates myelin-dependent neuronal dysfunction during the early phase after ischemic stroke."],["dc.identifier.doi","10.1038/jcbfm.2015.178"],["dc.identifier.isi","000365891300020"],["dc.identifier.pmid","26219598"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/35322"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Nature Publishing Group"],["dc.relation.issn","1559-7016"],["dc.relation.issn","0271-678X"],["dc.title","Knockout of silent information regulator 2 (SIRT2) preserves neurological function after experimental stroke in mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]