Günther, René

[["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"]]

[["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"]]

[["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"]]

[["dc.bibliographiccitation.firstpage","1"],["dc.bibliographiccitation.journal","Amyotrophic Lateral Sclerosis and Frontotemporal Degeneration"],["dc.bibliographiccitation.lastpage","10"],["dc.contributor.author","Meyer, Thomas"],["dc.contributor.author","Spittel, Susanne"],["dc.contributor.author","Grehl, Torsten"],["dc.contributor.author","Weyen, Ute"],["dc.contributor.author","Steinbach, Robert"],["dc.contributor.author","Kettemann, Dagmar"],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Weydt, Patrick"],["dc.contributor.author","Günther, René"],["dc.contributor.author","Baum, Petra"],["dc.contributor.author","Maier, André"],["dc.date.accessioned","2022-09-01T09:50:25Z"],["dc.date.available","2022-09-01T09:50:25Z"],["dc.date.issued","2022"],["dc.description.sponsorship","Boris Canessa ALS Stiftung"],["dc.description.sponsorship","Bremer ALS Stiftung"],["dc.description.sponsorship","BMBF"],["dc.identifier.doi","10.1080/21678421.2022.2104649"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/113709"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-597"],["dc.relation.eissn","2167-9223"],["dc.relation.issn","2167-8421"],["dc.rights.uri","http://creativecommons.org/licenses/by-nc-nd/4.0/"],["dc.title","Remote digital assessment of amyotrophic lateral sclerosis functional rating scale – a multicenter observational study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","1011"],["dc.bibliographiccitation.issue","12"],["dc.bibliographiccitation.journal","ROFO-FORTSCHRITTE AUF DEM GEBIET DER RONTGENSTRAHLEN UND DER BILDGEBENDEN VERFAHREN"],["dc.bibliographiccitation.lastpage","1015"],["dc.bibliographiccitation.volume","172"],["dc.contributor.author","Mahnken, A. H."],["dc.contributor.author","Wildberger, J. E."],["dc.contributor.author","Bergmann, F."],["dc.contributor.author","Fuzesi, Laszlo"],["dc.contributor.author","Adam, Gerhard"],["dc.contributor.author","Gunther, R."],["dc.date.accessioned","2018-11-07T10:15:31Z"],["dc.date.available","2018-11-07T10:15:31Z"],["dc.date.issued","2000"],["dc.description.abstract","Objective: To analyze the CT appearance of papillary renal cell tumor (pRCT) under consideration of gross pathology. Material and Methods: Preoperative CT-scans of 10 patients suffering from pRCT were re-evaluated by two experienced radiologists. CT appearance was correlated to gross morphology. Results: On CT, 9/10 tumors were depicted as rounded, well circumscribed and sharply delineated masses. These tumors presented a hypodense central area correlating to necrosis in gross pathology. The central area of necrosis was surrounded by vital tumor tissue, presenting as a serpiginous, contrast-enhancing margin on CT. One tumor was polycyclic due to multiple tumor nodules, but sharply demarcated towards the surrounding renal tissue. Conclusions: pRCT presents a quite unique CT appearance similar to its gross pathology."],["dc.identifier.doi","10.1055/s-2000-9221"],["dc.identifier.isi","000166208200011"],["dc.identifier.pmid","11199428"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/40824"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Georg Thieme Verlag Kg"],["dc.relation.issn","1438-9029"],["dc.title","Papillary renal cell tumor: Comparison of CT and gross morphology"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["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"]]

[["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"]]

[["dc.bibliographiccitation.journal","JAMA Neurology"],["dc.contributor.author","Witzel, Simon"],["dc.contributor.author","Maier, André"],["dc.contributor.author","Steinbach, Robert"],["dc.contributor.author","Grosskreutz, Julian"],["dc.contributor.author","Koch, Jan C."],["dc.contributor.author","Sarikidi, Anastasia"],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Günther, René"],["dc.contributor.author","Wolf, Joachim"],["dc.contributor.author","Hermann, Andreas"],["dc.contributor.author","Ludolph, Albert C."],["dc.contributor.authorgroup","German Motor Neuron Disease Network (MND-NET)"],["dc.date.accessioned","2022-02-01T10:31:06Z"],["dc.date.available","2022-02-01T10:31:06Z"],["dc.date.issued","2022"],["dc.identifier.doi","10.1001/jamaneurol.2021.4893"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/98785"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-517"],["dc.relation.issn","2168-6149"],["dc.title","Safety and Effectiveness of Long-term Intravenous Administration of Edaravone for Treatment of Patients With Amyotrophic Lateral Sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","217"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Glia"],["dc.bibliographiccitation.lastpage","232"],["dc.bibliographiccitation.volume","62"],["dc.contributor.author","Tönges, L."],["dc.contributor.author","Günther, R."],["dc.contributor.author","Suhr, M."],["dc.contributor.author","Jansen, J."],["dc.contributor.author","Balck, A."],["dc.contributor.author","Saal, K.-A."],["dc.contributor.author","Barski, E."],["dc.contributor.author","Nientied, T."],["dc.contributor.author","Götz, A. A."],["dc.contributor.author","Koch, J.-C."],["dc.contributor.author","Mueller, B. K."],["dc.contributor.author","Weishaupt, J. H."],["dc.contributor.author","Sereda, M. W."],["dc.contributor.author","Hanisch, U.-K."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Lingor, P."],["dc.date.accessioned","2017-09-07T11:46:53Z"],["dc.date.available","2017-09-07T11:46:53Z"],["dc.date.issued","2014"],["dc.description.abstract","Disease progression in amyotrophic lateral sclerosis (ALS) is characterized by degeneration of motoneurons (MN) and their axons, but is also influenced by neighboring cells such as astrocytes and microglial cells. The role of microglia in ALS is complex as it switches from an anti-inflammatory and neuroprotective phenotype in early disease to a proinflammatory and neurotoxic phenotype in later stages. Our previous studies in models of neurodegeneration identified rho kinase (ROCK) as a target, which can be manipulated to beneficially influence disease progression. Here, we examined the neuroprotective potential of the ROCK inhibitor Fasudil to target the central pathogenic features of ALS. Application of Fasudil to kainic acid-lesioned primary MN in vitro resulted in a strong prosurvival effect. In vivo, SOD1(G93A) mice benefited from oral treatment with Fasudil showing prolonged survival and improved motor function. These findings were correlated to an improved survival of motor neurons and a pronounced alteration of astroglial and microglial cell infiltration of the spinal cord under Fasudil treatment. Modeling a proinflammatory microglial phenotype by stimulation with LPS in vitro, Fasudil decreased the release of proinflammatory cytokines and chemokines TNF, Il6, CCL2, CCL3, and CCL5 while CXCL1 release was only transiently suppressed. In sciatic nerve motor axons, neuromuscular junction remodeling processes were increased. In conclusion, we provide preclinical and neurobiological evidence that inhibition of ROCK by the clinically approved small molecule inhibitor Fasudil may be a novel therapeutic approach in ALS combining both neuroprotection and immunomodulation for the cure of this devastating disease. GLIA 2014;62:217-232"],["dc.identifier.doi","10.1002/glia.22601"],["dc.identifier.gro","3142195"],["dc.identifier.isi","000328209300005"],["dc.identifier.pmid","24311453"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/5588"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1098-1136"],["dc.relation.issn","0894-1491"],["dc.title","Rho Kinase Inhibition Modulates Microglia Activation and Improves Survival in a Model of Amyotrophic Lateral Sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","330"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Orphanet Journal of Rare Diseases"],["dc.bibliographiccitation.volume","16"],["dc.contributor.author","Freigang, Maren"],["dc.contributor.author","Steinacker, Petra"],["dc.contributor.author","Wurster, Claudia Diana"],["dc.contributor.author","Schreiber-Katz, Olivia"],["dc.contributor.author","Osmanovic, Alma"],["dc.contributor.author","Petri, Susanne"],["dc.contributor.author","Koch, Jan Christoph"],["dc.contributor.author","Rostásy, Kevin"],["dc.contributor.author","Falkenburger, Björn"],["dc.contributor.author","Ludolph, Albert Christian"],["dc.contributor.author","Günther, René"],["dc.date.accessioned","2021-09-01T06:38:26Z"],["dc.date.available","2021-09-01T06:38:26Z"],["dc.date.issued","2021"],["dc.description.abstract","Abstract Background Studies regarding the impact of (neuro)inflammation and inflammatory response following repetitive, intrathecally administered antisense oligonucleotides (ASO) in 5q-associated spinal muscular atrophy (SMA) are sparse. Increased risk of hydrocephalus in untreated SMA patients and a marginal but significant increase of the serum/CSF albumin ratio (Qalb) with rare cases of communicating hydrocephalus during nusinersen treatment were reported, which confirms the unmet need of an inflammatory biomarker in SMA. The aim of this study was to investigate the (neuro)inflammatory marker chitotriosidase 1 (CHIT1) in SMA patients before and following the treatment with the ASO nusinersen. Methods In this prospective, multicenter observational study, we studied CSF CHIT1 concentrations in 58 adult and 21 pediatric patients with SMA type 1, 2 or 3 before treatment initiation in comparison to age- and sex-matched controls and investigated its dynamics during nusinersen treatment. Concurrently, motor performance and disease severity were assessed. Results CHIT1 concentrations were elevated in treatment-naïve SMA patients as compared to controls, but less pronounced than described for other neurodegenerative diseases such as amyotrophic lateral sclerosis. CHIT1 concentration did not correlate with disease severity and did not distinguish between clinical subtypes. CHIT1 concentration did show a significant increase during nusinersen treatment that was unrelated to the clinical response to nusinersen therapy. Conclusions CHIT1 elevation in treatment-naïve SMA patients indicates the involvement of (neuro)inflammation in SMA. The lacking correlation of CHIT1 concentration with disease severity argues against its use as a marker of disease progression. The observed CHIT1 increase during nusinersen treatment may indicate an immune response-like, off-target reaction. Since antisense oligonucleotides are an establishing approach in the treatment of neurodegenerative diseases, this observation needs to be further evaluated."],["dc.description.abstract","Abstract Background Studies regarding the impact of (neuro)inflammation and inflammatory response following repetitive, intrathecally administered antisense oligonucleotides (ASO) in 5q-associated spinal muscular atrophy (SMA) are sparse. Increased risk of hydrocephalus in untreated SMA patients and a marginal but significant increase of the serum/CSF albumin ratio (Qalb) with rare cases of communicating hydrocephalus during nusinersen treatment were reported, which confirms the unmet need of an inflammatory biomarker in SMA. The aim of this study was to investigate the (neuro)inflammatory marker chitotriosidase 1 (CHIT1) in SMA patients before and following the treatment with the ASO nusinersen. Methods In this prospective, multicenter observational study, we studied CSF CHIT1 concentrations in 58 adult and 21 pediatric patients with SMA type 1, 2 or 3 before treatment initiation in comparison to age- and sex-matched controls and investigated its dynamics during nusinersen treatment. Concurrently, motor performance and disease severity were assessed. Results CHIT1 concentrations were elevated in treatment-naïve SMA patients as compared to controls, but less pronounced than described for other neurodegenerative diseases such as amyotrophic lateral sclerosis. CHIT1 concentration did not correlate with disease severity and did not distinguish between clinical subtypes. CHIT1 concentration did show a significant increase during nusinersen treatment that was unrelated to the clinical response to nusinersen therapy. Conclusions CHIT1 elevation in treatment-naïve SMA patients indicates the involvement of (neuro)inflammation in SMA. The lacking correlation of CHIT1 concentration with disease severity argues against its use as a marker of disease progression. The observed CHIT1 increase during nusinersen treatment may indicate an immune response-like, off-target reaction. Since antisense oligonucleotides are an establishing approach in the treatment of neurodegenerative diseases, this observation needs to be further evaluated."],["dc.identifier.doi","10.1186/s13023-021-01961-8"],["dc.identifier.pii","1961"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/88933"],["dc.language.iso","en"],["dc.notes.intern","DOI-Import GROB-455"],["dc.relation.eissn","1750-1172"],["dc.title","Increased chitotriosidase 1 concentration following nusinersen treatment in spinal muscular atrophy"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]