Now showing 1 - 10 of 40
  • 2017Journal Article
    [["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Molecular Neurobiology"],["dc.bibliographiccitation.lastpage","86"],["dc.bibliographiccitation.volume","54"],["dc.contributor.author","Ribas, Vinicius Toledo"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Michel, Uwe"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2018-01-09T11:14:21Z"],["dc.date.available","2018-01-09T11:14:21Z"],["dc.date.issued","2017"],["dc.description.abstract","Axonal degeneration is one of the initial steps in many traumatic and neurodegenerative central nervous system (CNS) disorders and thus a promising therapeutic target. A focal axonal lesion is followed by acute axonal degeneration (AAD) of both adjacent axon parts, before proximal and distal parts follow different degenerative fates at later time points. Blocking calcium influx by calcium channel inhibitors was previously shown to attenuate AAD after optic nerve crush (ONC). However, it remains unclear whether the attenuation of AAD also promotes consecutive axonal regeneration. Here, we used a rat ONC model to study the effects of calcium channel inhibitors on axonal degeneration, retinal ganglion cell (RGC) survival, and axonal regeneration, as well as the molecular mechanisms involved. Application of calcium channel inhibitors attenuated AAD after ONC and preserved axonal integrity as visualized by live imaging of optic nerve axons. Consecutively, this resulted in improved survival of RGCs and improved axonal regeneration at 28 days after ONC. We show further that calcium channel inhibition attenuated lesion-induced calpain activation in the proximity of the crush and inhibited the activation of the c-Jun N-terminal kinase pathway. Pro-survival signaling via Akt in the retina was also increased. Our data thus show that attenuation of AAD improves consecutive neuronal survival and axonal regeneration and that calcium channel inhibitors could be valuable tools for therapeutic interventions in traumatic and degenerative CNS disorders."],["dc.identifier.doi","10.1007/s12035-015-9676-2"],["dc.identifier.pmid","26732591"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11580"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1559-1182"],["dc.title","Attenuation of Axonal Degeneration by Calcium Channel Inhibitors Improves Retinal Ganglion Cell Survival and Regeneration After Optic Nerve Crush"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]
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  • 2011Journal Article Research Paper
    [["dc.bibliographiccitation.firstpage","3472"],["dc.bibliographiccitation.issue","18"],["dc.bibliographiccitation.journal","FEBS Journal"],["dc.bibliographiccitation.lastpage","3483"],["dc.bibliographiccitation.volume","278"],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Barski, E."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Michel, U."],["dc.date.accessioned","2017-09-07T11:43:25Z"],["dc.date.available","2017-09-07T11:43:25Z"],["dc.date.issued","2011"],["dc.description.abstract","Repressor element-1 silencing transcription factor (REST) is a transcriptional repressor of neuron-specific genes that binds to a conserved DNA element, the neuron restrictive silencer element (NRSE/RE1). Interestingly, increased REST activity is found in several neurological diseases like Huntington's disease and cerebral ischemia. Recently, it was shown that NRSE dsRNA, a double-stranded non-coding RNA can bind to REST during a defined period of neuronal differentiation, and thereby changes REST from a transcriptional repressor to an activator of neuron-specific genes. Here, we analyzed the effects of NRSE dsRNA expression in primary retinal ganglion cells. We found that NRSE dsRNA expression vectors significantly enhance neurite outgrowth even when axonal degeneration is induced by neurotrophin deprivation. Transfection of HEK cells with NRSE dsRNA-expressing vectors altered their morphology leading to the formation of thin processes and induced the expression of neurofilament-68. Surprisingly, control vectors containing REST-binding sites, but not expressing NRSE dsRNA, resulted in the same effects, also in the retinal ganglion cell model. Reporter assays and retention of REST in the cytoplasm with a labeled NRSE/RE1-containing plasmid incapable of entering the nucleus suggest that sequestration of REST in the cytoplasm is the reason for the observed effects. No evidence for a biological function of NRSE dsRNA could be found in these models. We conclude that sequestration of REST leads to enhanced neurite outgrowth in retinal ganglion cells and that an increased activity of REST, as it is found in several neurodegenerative diseases, can be effectively modulated by sequestration of REST with plasmids containing NRSE/RE1 sites."],["dc.identifier.doi","10.1111/j.1742-4658.2011.08269.x"],["dc.identifier.gro","3142674"],["dc.identifier.isi","000294810600024"],["dc.identifier.pmid","21790997"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/104"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1742-464X"],["dc.title","Plasmids containing NRSE/RE1 sites enhance neurite outgrowth of retinal ganglion cells via sequestration of REST independent of NRSE dsRNA expression"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2019Journal Article
    [["dc.bibliographiccitation.firstpage","1516"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","1525"],["dc.bibliographiccitation.volume","266"],["dc.contributor.author","Dorst, Johannes"],["dc.contributor.author","Chen, Lu"],["dc.contributor.author","Rosenbohm, Angela"],["dc.contributor.author","Dreyhaupt, Jens"],["dc.contributor.author","Hübers, Annemarie"],["dc.contributor.author","Schuster, Joachim"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Gess, Burkhard"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Weyen, Ute"],["dc.contributor.author","Hermann, Andreas"],["dc.contributor.author","Winkler, Jürgen"],["dc.contributor.author","Grehl, Torsten"],["dc.contributor.author","Hagenacker, Tim"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Sperfeld, Anne"],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Großkreutz, Julian"],["dc.contributor.author","Metelmann, Moritz"],["dc.contributor.author","Wolf, Joachim"],["dc.contributor.author","Winkler, Andrea S."],["dc.contributor.author","Klopstock, Thomas"],["dc.contributor.author","Boentert, Matthias"],["dc.contributor.author","Johannesen, Siw"],["dc.contributor.author","Storch, Alexander"],["dc.contributor.author","Schrank, Bertold"],["dc.contributor.author","Zeller, Daniel"],["dc.contributor.author","Liu, Xiao-lu"],["dc.contributor.author","Tang, Lu"],["dc.contributor.author","Fan, Dong-Sheng"],["dc.contributor.author","Ludolph, Albert C."],["dc.date.accessioned","2020-12-10T14:10:33Z"],["dc.date.available","2020-12-10T14:10:33Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00415-019-09290-4"],["dc.identifier.eissn","1432-1459"],["dc.identifier.issn","0340-5354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70799"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Prognostic factors in ALS: a comparison between Germany and China"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2021Journal Article
    [["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration"],["dc.bibliographiccitation.lastpage","7"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Statland, Jeffrey M."],["dc.contributor.author","Hussain, Sumaira"],["dc.contributor.author","Hennecke, Christiane"],["dc.contributor.author","Wuu, Joanne"],["dc.contributor.author","Langbein, Thomas"],["dc.contributor.author","Ahmed, Raees"],["dc.contributor.author","Günther, René"],["dc.contributor.author","Ilse, Benjamin"],["dc.contributor.author","Kassubek, Jan"],["dc.contributor.author","Kollewe, Katja"],["dc.contributor.author","Kuttler, Josua"],["dc.contributor.author","Leha, Andreas"],["dc.contributor.author","Lengenfeld, Teresa"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Neuwirth, Christoph"],["dc.contributor.author","Tostmann, Ralf"],["dc.contributor.author","Benatar, Michael"],["dc.date.accessioned","2021-04-14T08:30:11Z"],["dc.date.available","2021-04-14T08:30:11Z"],["dc.date.issued","2021"],["dc.identifier.doi","10.1080/21678421.2021.1879866"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/83141"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-399"],["dc.relation.eissn","2167-9223"],["dc.relation.issn","2167-8421"],["dc.title","Challenges and opportunities for Multi-National Investigator-Initiated clinical trials for ALS: European and United States collaborations"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2018Journal Article
    [["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Pharmacology & Therapeutics"],["dc.bibliographiccitation.lastpage","21"],["dc.bibliographiccitation.volume","189"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Tatenhorst, Lars"],["dc.contributor.author","Roser, Anna-Elisa"],["dc.contributor.author","Saal, Kim-Ann"],["dc.contributor.author","Tönges, Lars"],["dc.contributor.author","Lingor, Paul"],["dc.date.accessioned","2020-12-10T15:20:44Z"],["dc.date.available","2020-12-10T15:20:44Z"],["dc.date.issued","2018"],["dc.identifier.doi","10.1016/j.pharmthera.2018.03.008"],["dc.identifier.issn","0163-7258"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/72778"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","ROCK inhibition in models of neurodegeneration and its potential for clinical translation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2019Journal Article
    [["dc.bibliographiccitation.firstpage","36"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Neurology"],["dc.bibliographiccitation.lastpage","44"],["dc.bibliographiccitation.volume","267"],["dc.contributor.author","Wurster, Claudia D."],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Günther, René"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Uzelac, Zeljko"],["dc.contributor.author","Witzel, Simon"],["dc.contributor.author","Wollinsky, Kurt"],["dc.contributor.author","Winter, Benedikt"],["dc.contributor.author","Osmanovic, Alma"],["dc.contributor.author","Schreiber-Katz, Olivia"],["dc.contributor.author","Al Shweiki, Rami"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Hermann, Andreas"],["dc.contributor.author","Otto, Markus"],["dc.date.accessioned","2020-12-10T14:10:34Z"],["dc.date.available","2020-12-10T14:10:34Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1007/s00415-019-09547-y"],["dc.identifier.eissn","1432-1459"],["dc.identifier.issn","0340-5354"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/70801"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Neurofilament light chain in serum of adolescent and adult SMA patients under treatment with nusinersen"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2019Journal Article
    [["dc.bibliographiccitation.firstpage","315"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Clinical Neurophysiology"],["dc.bibliographiccitation.lastpage","319"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Günther, René"],["dc.contributor.author","Neuwirth, Christoph"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Braun, Nathalie"],["dc.contributor.author","Untucht, Robert"],["dc.contributor.author","Petzold, Daniel"],["dc.contributor.author","Weber, Markus"],["dc.contributor.author","Hermann, Andreas"],["dc.date.accessioned","2020-12-10T14:23:09Z"],["dc.date.available","2020-12-10T14:23:09Z"],["dc.date.issued","2019"],["dc.identifier.doi","10.1016/j.clinph.2018.11.009"],["dc.identifier.issn","1388-2457"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/71849"],["dc.language.iso","en"],["dc.notes.intern","DOI Import GROB-354"],["dc.title","Motor Unit Number Index (MUNIX) of hand muscles is a disease biomarker for adult spinal muscular atrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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  • 2002Journal Article
    [["dc.bibliographiccitation.artnumber","115327"],["dc.bibliographiccitation.issue","11"],["dc.bibliographiccitation.journal","PHYSICAL REVIEW B"],["dc.bibliographiccitation.volume","65"],["dc.contributor.author","Habenicht, S."],["dc.contributor.author","Lieb, Klaus-Peter"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Wieck, Andreas D."],["dc.date.accessioned","2018-11-07T10:31:08Z"],["dc.date.available","2018-11-07T10:31:08Z"],["dc.date.issued","2002"],["dc.description.abstract","The propagation of surface ripples during Ga ion beam erosion of Si was measured in real time by combining focused ion beam technology with scanning electron microscopy. By detecting the secondary electrons emitted during implantation the surface was monitored in situ during the erosion. The ripple wavelength increases with the erosion time as lambdaproportional tot(0.50(4)). The value of the ripple velocity was observed to agree qualitatively with the results of Monte-Carlo simulations of the erosion process, and was found to decrease with the ripple dimension like nuproportional tolambda(x)(-1.5(1))."],["dc.identifier.doi","10.1103/PhysRevB.65.115327"],["dc.identifier.isi","000174548400096"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/44032"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","American Physical Soc"],["dc.relation.issn","1098-0121"],["dc.title","Ripple propagation and velocity dispersion on ion-beam-eroded silicon surfaces"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]
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  • 2012Journal Article Research Paper
    [["dc.bibliographiccitation.artnumber","e3936"],["dc.bibliographiccitation.issue","61"],["dc.bibliographiccitation.journal","Journal of Visualized Experiments"],["dc.contributor.author","Günther, R."],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Koch, J. C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Tönges, L."],["dc.date.accessioned","2017-09-07T11:48:58Z"],["dc.date.available","2017-09-07T11:48:58Z"],["dc.date.issued","2012"],["dc.description.abstract","Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder resulting in progressive degeneration of motoneurons. Peak of onset is around 60 years for the sporadic disease and around 50 years for the familial disease. Due to its progressive course, 50% of the patients die within 30 months of symptom onset. In order to evaluate novel treatment options for this disease, genetic mouse models of ALS have been generated based on human familial mutations in the SOD gene, such as the SOD1 (G93A) mutation. Most important aspects that have to be evaluated in the model are overall survival, clinical course and motor function. Here, we demonstrate the clinical evaluation, show the conduction of two behavioural motor tests and provide quantitative scoring systems for all parameters. Because an in depth analysis of the ALS mouse model usually requires an immunohistochemical examination of the spinal cord, we demonstrate its preparation in detail applying the dorsal laminectomy method. Exemplary histological findings are demonstrated. The comprehensive application of the depicted examination methods in studies on the mouse model of ALS will enable the researcher to reliably test future therapeutic options which can provide a basis for later human clinical trials."],["dc.identifier.doi","10.3791/3936"],["dc.identifier.gro","3142575"],["dc.identifier.isi","000209222800054"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8941"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1940-087X"],["dc.title","Clinical Testing and Spinal Cord Removal in a Mouse Model for Amyotrophic Lateral Sclerosis (ALS)"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]
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  • 2022Journal Article
    [["dc.bibliographiccitation.artnumber","acn3.51645"],["dc.bibliographiccitation.journal","Annals of Clinical and Translational Neurology"],["dc.contributor.author","Freigang, Maren"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Wurster, Claudia D."],["dc.contributor.author","Schreiber‐Katz, Olivia"],["dc.contributor.author","Osmanovic, Alma"],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Rostásy, Kevin"],["dc.contributor.author","Huss, André"],["dc.contributor.author","Tumani, Hayrettin"],["dc.contributor.author","Günther, René"],["dc.date.accessioned","2022-09-01T09:51:18Z"],["dc.date.available","2022-09-01T09:51:18Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1002/acn3.51645"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113929"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","2328-9503"],["dc.relation.issn","2328-9503"],["dc.title","Glial fibrillary acidic protein in cerebrospinal fluid of patients with spinal muscular atrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]
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