Sättler, Muriel B.

[["dc.bibliographiccitation.firstpage","1770"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","The American Journal of Pathology"],["dc.bibliographiccitation.lastpage","1781"],["dc.bibliographiccitation.volume","178"],["dc.contributor.author","Rau, C. R."],["dc.contributor.author","Hein, K."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Kretzschmar, B."],["dc.contributor.author","Hillgruber, C."],["dc.contributor.author","Mcrae, B. L."],["dc.contributor.author","Diem, R."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:44:17Z"],["dc.date.available","2017-09-07T11:44:17Z"],["dc.date.issued","2011"],["dc.description.abstract","In multiple sclerosis, long-term disability is caused by axonal and neuronal damage. Established therapies target primarily the inflammatory component of the disease, but fail to prevent neurodegeneration. Fingolimod (codenamed FTY720) is an oral sphingosine 1-phosphate (S1P) receptor modulator with promising results in phase II trials in multiple sclerosis patients and is under further development as a novel treatment for multiple sclerosis. To evaluate whether FTY720 has neuroprotective properties, we tested this drug in a rat model of myelin oligodendrocyte glycoprotein-induced optic neuritis. FTY720 exerted significant anti-inflammatory effects during optic neuritis and reduced inflammation, demyelination, and axonal damage; however, FTY720 treatment did not prevent apoptosis of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve. Consistent with this lack of effect on RGC survival, FTY720 treatment did not improve visual function, nor did it prevent apoptosis of RGCs in vitro. We observed a persistent activation of apoptotic signaling pathways in RGCs under FTY720 treatment, a possible underlying mechanism for the lack of neuroprotection in the presence of strong anti-inflammatory effects, Furthermore, FTY720 shifted the remaining inflammation in the optic nerve toward neurotoxicity by modest up-regulation of potential neurotoxic cytokines. We conclude that FTY720-induced anti-inflammation and axon protection did not of itself protect neurons from apoptotic cell death. (Am J Pathol 2011, 178:1770-1781; DOI: 10.1016/j.ajpath.2011.01.003)"],["dc.identifier.doi","10.1016/j.ajpath.2011.01.003"],["dc.identifier.gro","3142743"],["dc.identifier.isi","000298306700034"],["dc.identifier.pmid","21406175"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/181"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: European Union [LSHM-CT-2005-018637]; Abbott USA"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0002-9440"],["dc.title","Anti-Inflammatory Effects of FTY720 Do Not Prevent Neuronal Cell Loss in a Rat Model of Optic Neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.volume","228"],["dc.contributor.author","Hein, Katharina"],["dc.contributor.author","Gadjanski, Ivana"],["dc.contributor.author","Saettler, Muriel B."],["dc.contributor.author","Kretzschmar, Benedikt"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Baehr, Mathias"],["dc.date.accessioned","2018-11-07T08:36:54Z"],["dc.date.available","2018-11-07T08:36:54Z"],["dc.date.issued","2010"],["dc.identifier.isi","000283694400499"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/18417"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Elsevier Science Bv"],["dc.publisher.place","Amsterdam"],["dc.relation.eventlocation","Sitges, SPAIN"],["dc.title","Monitoring of degeneration of the retinal nerve fiber layer by optical coherence tomography in rats with autoimmune optic neuritis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","199"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","210"],["dc.bibliographiccitation.volume","72"],["dc.contributor.author","Sühs, K.-W."],["dc.contributor.author","Hein, K."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Görlitz, A."],["dc.contributor.author","Ciupka, C."],["dc.contributor.author","Scholz, K."],["dc.contributor.author","Käsmann-Kellner, B."],["dc.contributor.author","Papanagiotou, P."],["dc.contributor.author","Schäffler, N."],["dc.contributor.author","Restemeyer, C."],["dc.contributor.author","Bittersohl, D."],["dc.contributor.author","Hassenstein, A."],["dc.contributor.author","Seitz, B."],["dc.contributor.author","Reith, W."],["dc.contributor.author","Fassbender, K."],["dc.contributor.author","Hilgers, R."],["dc.contributor.author","Heesen, C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Diem, R."],["dc.date.accessioned","2017-09-07T11:48:29Z"],["dc.date.available","2017-09-07T11:48:29Z"],["dc.date.issued","2012"],["dc.description.abstract","Objective: Based on findings in animal models of autoimmune optic nerve inflammation, we have assessed the safety and efficacy of erythropoietin in patients presenting with a first episode of optic neuritis. Methods: Patients with optic neuritis who attended the University Hospitals of Homburg/Saar, Gottingen, or Hamburg (Germany) were included in this double-blind, placebo-controlled, phase 2 study (ClinicalTrials.gov, NCT00355095). They were randomly assigned to groups receiving either 33,000IU recombinant human erythropoietin intravenously daily for 3 days or placebo as an add-on therapy to methylprednisolone. The primary outcome parameter was change in retinal nerve fiber layer (RNFL) thickness after 16 weeks. Secondary outcome parameters included optic nerve atrophy as assessed by magnetic resonance imaging, and changes in visual acuity, visual field, and visual evoked potentials (VEPs). Results: Forty patients were assigned to the treatment groups (21/19 erythropoietin/placebo). Safety monitoring revealed no relevant issues. Thirty-seven patients (20/17 erythropoietin/placebo) were analyzed for the primary endpoint according to the intention-to-treat protocol. RNFL thinning was less apparent after erythropoietin treatment. Thickness of the RNFL decreased by a median of 7.5 mu m by week 16 (mean +/- standard deviation, 10.55 +/- 17.54 mu m) compared to a median of 16.0 mu m (22.65 +/- 29.18 mu m) in the placebo group (p = 0.0357). Decrease in retrobulbar diameter of the optic nerve was smaller in the erythropoietin group (p = 0.0112). VEP latencies at week 16 were shorter in erythropoietin-treated patients than in the placebo group (p = 0.0011). Testing of visual functions revealed trends toward an improved outcome after erythropoietin treatment. Interpretation: These results give the first indications that erythropoietin might be neuroprotective in optic neuritis. ANN NEUROL 2012;72:199210."],["dc.identifier.doi","10.1002/ana.23573"],["dc.identifier.gro","3142489"],["dc.identifier.isi","000307946000010"],["dc.identifier.pmid","22926853"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/8846"],["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","0364-5134"],["dc.title","A randomized, double-blind, phase 2 study of erythropoietin in optic neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","81"],["dc.bibliographiccitation.journal","Annals of Neurology"],["dc.bibliographiccitation.lastpage","93"],["dc.bibliographiccitation.volume","66"],["dc.contributor.author","Gadjanski, Ivana"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Williams, Sarah K."],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Knöferle, Johanna"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Fairless, Richard"],["dc.contributor.author","Hochmeister, Sonja"],["dc.contributor.author","Sühs, Kurt-Wolfram"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Storch, Maria K."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2019-07-09T11:52:52Z"],["dc.date.available","2019-07-09T11:52:52Z"],["dc.date.issued","2009"],["dc.description.abstract","Objective: The aim of this study was to investigate the role of voltage-dependent calcium channels (VDCCs) in axon degeneration during autoimmune optic neuritis. Methods: Calcium ion (Ca2 ) influx into the optic nerve (ON) through VDCCs was investigated in a rat model of optic neuritis using manganese-enhanced magnetic resonance imaging and in vivo calcium imaging. After having identified the most relevant channel subtype (N-type VDCCs), we correlated immunohistochemistry of channel expression with ON histopathology. In the confirmatory part of this work, we performed a treatment study using -conotoxin GVIA, an N-type specific blocker. Results: We observed that pathological Ca2 influx into ONs during optic neuritis is mediated via N-type VDCCs. By analyzing the expression of VDCCs in the inflamed ONs, we detected an upregulation of 1B, the pore-forming subunit of N-type VDCCs, in demyelinated axons. However, high expression levels were also found on macrophages/activated microglia, and lower levels were detected on astrocytes. The relevance of N-type VDCCs for inflammation-induced axonal degeneration and the severity of optic neuritis was corroborated by treatment with -conotoxin GVIA. This blocker led to decreased axon and myelin degeneration in the ONs together with a reduced number of macrophages/activated microglia. These protective effects were confirmed by analyzing the spinal cords of the same animals. Interpretation: We conclude that N-type VDCCs play an important role in inflammation-induced axon degeneration via two mechanisms: First, they directly mediate toxic Ca2 influx into the axons; and second, they contribute to macrophage/microglia function, thereby promoting secondary axonal damage."],["dc.identifier.doi","10.1002/ ana.21668"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/6088"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/60296"],["dc.language.iso","en"],["dc.subject.ddc","610"],["dc.title","Role of N-Type Voltage-Dependent Calcium Channels in Autoimmune Optic Neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","27"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","36"],["dc.bibliographiccitation.volume","184"],["dc.contributor.author","Diem, R."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:49:51Z"],["dc.date.available","2017-09-07T11:49:51Z"],["dc.date.issued","2007"],["dc.description.abstract","Neurodegeneration in multiple sclerosis (MS) is the structural correlate of permanent neurological disability in patients. The histopathological features of neurodegeneration include destruction of axons as well as apoptotic cell death of neuronal cell bodies. Therapeutic efforts to control these clinically important aspects of MS pathology showed limited success so far. In this review article, we give an overview about the current knowledge concerning the molecular mechanisms of neurodegeneration in autoimmune inflammation that is mainly derived from animal models. Further, we critically discuss experimental neuroprotective strategies with respect to their functional relevance and differentiate between anti-apoptotic and axon protective treatment approaches. (c) 2006 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2006.11.025"],["dc.identifier.gro","3143529"],["dc.identifier.isi","000245727400004"],["dc.identifier.pmid","17188756"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1053"],["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","0165-5728"],["dc.title","Neurodegeneration and -protection in autoimmune CNS inflammation"],["dc.type","review"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","375"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Brain"],["dc.bibliographiccitation.lastpage","385"],["dc.bibliographiccitation.volume","128"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:45:35Z"],["dc.date.available","2017-09-07T11:45:35Z"],["dc.date.issued","2005"],["dc.description.abstract","Neurodegenerative processes determine the clinical disease course of multiple sclerosis, an inflammatory autoimmune CNS disease that frequently manifests with acute optic neuritis. None of the established multiple sclerosis therapies has been shown to clearly reduce neurodegeneration. In a rat model of experimental autoimmune encephalomyelitis, we recently demonstrated increased neuronal apoptosis under methylprednisolone therapy, although CNS inflammation was effectively controlled. In the present study, we combined steroid treatment with application of erythropoietin to target inflammatory as well as neurodegenerative aspects. After immunization with myelin oligodendrocyte glycoprotein (MOG), animals were randomly assigned to six treatment groups receiving different combinations of erythropoietin and methylprednisolone, or respective monotherapies. After MOG-induced experimental autoimmune encephalomyelitis became clinically manifest, optic neuritis was monitored by recording visual evoked potentials. The function of retinal ganglion cells, the neurons that form the axons of the optic nerve, was measured by electroretinograms. Functional and histo pathological data of retinal ganglion cells and optic nerves revealed that neuron and axon protection was most effective when erythropoietin treatment that was started at immunization was combined with high-dose methylprednisolone therapy given from days 1 to 3 of MOG-induced experimental autoimmune encephalomyelitis. In contrast, isolated neuronal or axonal protection without clinical benefit was achieved under monotherapy with erythropoietin or methylprednisolone, respectively."],["dc.identifier.doi","10.1093/brain/awh365"],["dc.identifier.gro","3150407"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7168"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.doi","10.1093/brain/awh365"],["dc.relation.issn","0006-8950"],["dc.title","Combined therapy with methylprednisolone and erythropoietin in a model of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","47"],["dc.bibliographiccitation.journal","Experimental Eye Research"],["dc.bibliographiccitation.lastpage","56"],["dc.bibliographiccitation.volume","115"],["dc.contributor.author","Sandalon, S."],["dc.contributor.author","Könnecke, B."],["dc.contributor.author","Levkovitch-Verbin, H."],["dc.contributor.author","Simons, Mikael"],["dc.contributor.author","Hein, K."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Ofri, R."],["dc.date.accessioned","2017-09-07T11:47:07Z"],["dc.date.available","2017-09-07T11:47:07Z"],["dc.date.issued","2013"],["dc.description.abstract","Voltage gated sodium channels (Nag), are proposed mediators of neuronal damage in ischemic and excitotoxicity disease models. We evaluated the neuroprotective effects of lamotrigine, a Na-v, blocker, in the acute and chronic rat ocular hypertension models. Additionally, expression of the main Nav subtypes in the optic nerve (ON) was assessed to test whether their upregulation plays a role in the pathogenesis of ocular hypertension induced optic neuropathy. Unilateral intraocular pressure (IOP) elevation was induced for 60 min (80 mmHg) and 14-21 days (670-859 mmHg day) in the acute and chronic models, respectively. Lamotrigine was administered at dosages of 10 mg/kg twice daily and 12.5 mg/kg once daily in the acute (n = 9) and chronic (n = 11) trials, respectively. Treatment began 2 days prior to IOP elevation until sacrifice. Outer and inner retinal function was evaluated with dark- and light-adapted flash electroretinography and pattern electroretinography, respectively, 6 and 14 days post acute IOP elevation and 13, 28 and 48 days post chronic IOP elevation. Retinal ganglion cell and axon densities and inflammatory reaction were evaluated through Fluorogold, Bielschowsky's silver impregnation and ED1 labeling respectively. Immunohistochemistry for Na(v)1.1, 1.2 and 1.6 was performed in ONs of untreated rats 7 and 15 days post IOP elevation in the acute model and after 7, 28 and 50 days in the chronic model. In the acute model, no differences were found in the a-wave amplitudes between lamotrigine-treated and vehicle-treated rats. B-wave amplitudes decreased by 40-66% in both treatment groups 6 days post IOP elevation, with no significant difference between groups (p = 0.38). However, a partial recovery of b-wave amplitudes was found in lamotrigine-treated rats between day 6 and day 14 post procedure (p < 0.05). No differences were found in any other parameter tested in this model. Similarly, lamotrigine treatment did not result in any beneficial effect in structural parameters of the chronic model. Functional evaluation of this model was inconclusive due to super-normal values in the hypertensive eyes. Upregulation of Na(v)1.1 and 1.2 expression was found in both models, beginning by day 7; an increase of the former continued in a time-dependent manner in the chronic model. Na(v)1.6 labeling was inconclusive. In conclusion we found lamotrigine treatment to be mostly ineffective in both acute and chronic ocular hypertension models. (C) 2013 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.exer.2013.06.018"],["dc.identifier.gro","3142275"],["dc.identifier.isi","000326060600007"],["dc.identifier.pmid","23810807"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/6476"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1096-0007"],["dc.relation.issn","0014-4835"],["dc.title","Functional and structural evaluation of lamotrigine treatment in rat models of acute and chronic ocular hypertension"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","378"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Brain pathology"],["dc.bibliographiccitation.lastpage","387"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Rau, Christian R."],["dc.contributor.author","Storch, Maria K."],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Weissert, Robert"],["dc.contributor.author","Taheri, Naimeh"],["dc.contributor.author","Kuhnert, Antje V."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2017-09-07T11:43:14Z"],["dc.date.available","2017-09-07T11:43:14Z"],["dc.date.issued","2004"],["dc.description.abstract","Multiple sclerosis (MS) is a chronic inflammatory disease of the CNS which leads to demyelination, axonal destruction and neuronal loss in the early stages. Available therapies mainly target the inflammatory component of the disease but fail to prevent neurodegeneration. To investigate the effect of ciliary neurotrophic factor (CNTF) on the survival of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve, we used a rat model of myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis. Optic neuritis in this model was diagnosed by recording visual evoked potentials, and RGC function was monitored by measuring electroretinograms. This study demonstrates that CNTF has a neuroprotective effect on affected RGCs during acute optic neuritis. Furthermore, we demonstrate that CNTF exerts its neuroprotective effect through activation of the Janus kinase/signal transducer and activator of transcription pathway, mitogen activated protein kinases and a shift in the Bcl-2 family of proteins towards the anti-apoptotic side. In summary, our results demonstrate that CNTF can serve as an effective neuroprotective treatment in a rat model of MS that especially reflects the neurodegenerative aspects of this disease."],["dc.identifier.doi","10.1111/j.1750-3639.2004.tb00081.x"],["dc.identifier.isi","000225174100006"],["dc.identifier.pmid","15605985"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1508"],["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","1015-6305"],["dc.relation.issn","1015-6305"],["dc.title","Ciliary neurotrophic factor protects retinal ganglion cells from secondary cell death during acute autoimmune optic neuritis in rats"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.artnumber","e0162583"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","PLoS ONE"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Obert, D."],["dc.contributor.author","Helms, G."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Jung, K."],["dc.contributor.author","Kretzschmar, B."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Dechent, P."],["dc.contributor.author","Diem, R."],["dc.contributor.author","Hein, K."],["dc.date.accessioned","2017-09-07T11:44:38Z"],["dc.date.available","2017-09-07T11:44:38Z"],["dc.date.issued","2016"],["dc.description.abstract","Magnetic resonance spectroscopy (MRS) provides the unique ability to monitor several disease-related pathological processes via their characteristic metabolic markers in vivo. In the present study metabolic compositions were assessed every six months over the period of two years in 36 patients with Multiple Sclerosis (MS) including 21 relapsing-remitting (RR), 15 secondary progressive (SP) patients and 12 normal subjects. The concentrations of the main MRS-detectable metabolites N-acetylaspartate and N-acetylaspartylglutamate (tNAA), creatine and phosphocreatine (tCr), choline containing compounds (Cho), myo-Inositol (Ins), glutamine and glutamate (Glx) and their ratios were calculated in the normal appearing white matter (NAWM) and in selected non-enhancing white matter (WM) lesions. Association between metabolic concentrations in the NAWM and disability were investigated. Concentration of tNAA, a marker for neuroaxonal integrity, did not show any difference between the investigated groups. However, the patients with SPMS showed significant reduction of tNAA in the NAWM over the investigation period of two years indicating diffuse neuroaxonal loss during the disease course. Furthermore, we found a significant increase of Ins, Ins/tCr and Ins/tNAA in WM lesions independently from the course of the disease suggesting ongoing astrogliosis in silent-appearing WM lesions. Analyzing correlations between MRS metabolites in the NAWM and patients clinical status we found the positive correlation of Ins/tNAA with disability in patients with RRMS. In SPMS positive correlation of Cho with disability was found."],["dc.description.sponsorship","Open-Access-Publikationsfonds 2016"],["dc.format.extent","15"],["dc.identifier.doi","10.1371/journal.pone.0162583"],["dc.identifier.gro","3141620"],["dc.identifier.isi","000383723700009"],["dc.identifier.pmid","27636543"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/13693"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/2011"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10 / Funder: Bayer Vital GmbH, Leverkusen, Germany; Merck Serono GmbH, Darmstadt"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","1932-6203"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","Brain Metabolite Changes in Patients with Relapsing-Remitting and Secondary Progressive Multiple Sclerosis: A Two-Year Follow-Up Study"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","172"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","181"],["dc.bibliographiccitation.volume","201"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Williams, Sarah K."],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Gadjanski, Ivana"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2017-09-07T11:52:35Z"],["dc.date.available","2017-09-07T11:52:35Z"],["dc.date.issued","2006"],["dc.description.abstract","lntcrferon-beta-1a (IFN-beta-1a) is an approved treatment for multiple sclerosis (MS). It improves the disease course by reducing the relapse rate as well as the persistent neurological deficits. Recent MRI and post-mortem studies revealed that neuronal and axonal damage are most relevant for chronic disability in MS patients. We have characterized previously time course and mechanisms of neuronal apoptosis in a rat model of myelin oligodendrocyte glycoprotein (MOG)-induced optic neuritis. In this animal model, application of IFN-beta-1a three times per week slightly decreases the loss of retinal ganglion cells (RGCs), the neurons that form the axons within the optic nerve. In contrast to neurotrophic factors, this cytokine does not directly protect cultured RGCs from apoptosis. We conclude that IFN-beta-1a is a suitable candidate to be combined with a directly neuroprotective agent in order to further decrease axonal and neuronal degeneration in MS patients. (c) 2006 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.expneurol.2006.04.015"],["dc.identifier.gro","3143633"],["dc.identifier.isi","000240152100019"],["dc.identifier.pmid","16764858"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1169"],["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","0014-4886"],["dc.subject","EAE; interferon-beta; Neuronal apoptosis; Retinal ganglion cells; Mitogen-activated protein kinase; Axonal damage"],["dc.title","Effects of interferon-beta-1a on neuronal survival under autoimmune inflammatory conditions"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]