Demmer, Iris

[["dc.bibliographiccitation.firstpage","163"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","171"],["dc.bibliographiccitation.volume","193"],["dc.contributor.author","Sattler, Michael"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Boger, I."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:54:30Z"],["dc.date.available","2017-09-07T11:54:30Z"],["dc.date.issued","2005"],["dc.description.abstract","In patients with multiple sclerosis (MS), non-remitting deficits are mainly caused by axonal and neuronal damage. We demonstrated previously that myelin oligodendrocyte glycoprotein (MOG)-induced experimental autoimmune encephalomyelitis in rats provokes severe axonal and neuronal injury even before clinical manifestation of the disease. In our present study, we investigated effects of simvastatin treatment on degeneration of retinal ganglion cell (RGC) bodies as well as their axons during MOG-induced optic neuritis. Electrophysiological functions of optic nerves and RGCs were analyzed in vivo. Although neuroprotective effects of simvastatin have been demonstrated before in other experimental settings, we did not observe an increase in RGC survival nor an improvement of visual functions. As we could not reproduce the anti-inflammatory effects that were observed under statin therapy in other EAE models, we hypothesize that patients suffering from optic neuritis might not take advantage of simvastatin applications. (c) 2004 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.expneurol.2004.12.010"],["dc.identifier.gro","3143859"],["dc.identifier.isi","000228413300016"],["dc.identifier.pmid","15817275"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1419"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","final"],["dc.notes.submitter","PUB_WoS_Import"],["dc.publisher","Academic Press Inc Elsevier Science"],["dc.relation.issn","0014-4886"],["dc.title","Simvastatin treatment does not protect retinal ganglion cells from degeneration in a rat model of autoimmune 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","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","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.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"]]

[["dc.bibliographiccitation.firstpage","3707"],["dc.bibliographiccitation.issue","8"],["dc.bibliographiccitation.journal","Investigative Opthalmology & Visual Science"],["dc.bibliographiccitation.lastpage","3714"],["dc.bibliographiccitation.volume","49"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Schmelting, Barthel"],["dc.contributor.author","Williams, Sarah K."],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Brück, Wolfgang"],["dc.contributor.author","Fuchs, Eberhard"],["dc.date.accessioned","2017-09-07T11:45:29Z"],["dc.date.available","2017-09-07T11:45:29Z"],["dc.date.issued","2008"],["dc.description.abstract","purpose. To assess the use of visual evoked potentials (VEPs) for the in vivo detection of impaired visual function in a marmoset model of multiple sclerosis. The sensitivity of the VEP recordings was determined by comparison with magnetic resonance imaging (MRI) and histopathology.methods. Baseline VEPs were recorded in six healthy marmoset monkeys in response to light-flash stimulation. Experimental autoimmune encephalomyelitis (EAE) was induced in four of the six monkeys. Clinical scores were assessed daily, and VEPs were recorded every second week. In vivo MRI and subsequent histopathology of the brains and optic nerves were performed at the end of the study.results. After induction of EAE, all four marmosets exhibited clinical signs between day 26 and 38 after immunization. VEPs were normal during the induction phase of the disease, but deteriorated in amplitude with the occurrence of clinical symptoms in all animals. MRI revealed bilateral optic neuritis and signal alterations in the optic tracts and occipital subcortical white matter in two of the animals. In the remaining two animals, MRI detected signal alterations in the occipital subcortical white matter. Histopathologic results were concordant with the MRI findings.conclusions. VEPs are an easily accessible noninvasive tool for measuring visual function and diagnosing impairment of the visual pathway in a marmoset EAE model."],["dc.identifier.doi","10.1167/iovs.08-1896"],["dc.identifier.gro","3150371"],["dc.identifier.pmid","18450589"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7128"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1552-5783"],["dc.title","Autoimmune Optic Neuritis in the Common Marmoset Monkey: Comparison of Visual Evoked Potentials with MRI and Histopathology"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","72"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Neuroscience Letters"],["dc.bibliographiccitation.lastpage","76"],["dc.bibliographiccitation.volume","436"],["dc.contributor.author","Hein (née Maier), K."],["dc.contributor.author","Köhler, A."],["dc.contributor.author","Diem, R."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Lange, P."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Otto, M."],["dc.date.accessioned","2017-09-07T11:48:43Z"],["dc.date.available","2017-09-07T11:48:43Z"],["dc.date.issued","2008"],["dc.description.abstract","Axonal degeneration is now recognized as an important pathological feature of multiple sclerosis (MS). Acute axonal damage happens early in the disease course, and therefore early changes might occur in markers in body fluids, such as cerebrospinal fluid (CSF) and blood. In our study we investigated the relevance of serum and CSF markers for axonal damage in patients with clinically isolated syndrome indicative for MS. We measured the concentration of tau, phospho-tau, S100B, Amyloid beta and neuron specific enolase (NSE) in CSF and serum. Interestingly, the NSE concentration in CSF and serum was decreased in clinically isolated syndrome (CIS)-patients in comparison to the control group indicating reduced neuronal metabolic activity in the early stage of the disease. Concerning other biomarkers, we did not observe any changes in the concentrations between groups. Moreover, we did not detect any correlation between Expanded Disability Status Scale (EDSS) and the concentration of investigated proteins. (C) 2008 Elsevier Ireland Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.neulet.2008.02.064"],["dc.identifier.gro","3143299"],["dc.identifier.isi","000255696400016"],["dc.identifier.pmid","18359164"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/798"],["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.issn","0304-3940"],["dc.title","Biological markers for axonal degeneration in CSF and blood of patients with the first event indicative for multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","323"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","NeuroImage"],["dc.bibliographiccitation.lastpage","334"],["dc.bibliographiccitation.volume","41"],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Gadjanski, Ivana"],["dc.contributor.author","Demmer, Iris"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Frahm, Jens"],["dc.date.accessioned","2017-09-07T11:45:31Z"],["dc.date.available","2017-09-07T11:45:31Z"],["dc.date.issued","2008"],["dc.description.abstract","Neuritis of the optic nerve is one of the most frequent early symptoms ofmultiple sclerosis. There are only scarce data correlating magneticresonance imaging (MRI) contrast alterations with the underlyingpathology, that is inflammation, demyelination, and axonal damage.Here we studied optic neuritis in a rat model of experimental autoimmuneencephalomyelitis by comparingin vivoMRI findings from multipletechniques (T1, T2, proton density, magnetization transfer) to histo-pathology. We further assessed a breakdown of the blood–brain barrierby using Gd-DTPA and indirectly estimated the intracellular accumula-tion of calcium as a consequence of axonal damage by using manganese-enhanced MRI. Hyperintensity on T2-weighted images and signalenhancement after Gd-DTPA were highly sensitive to lesions of the opticnerve but did not differentiate between mild, moderate, and severedamage. Signal reduction on T1-weighted images was less sensitive butcorrelated well with the severity of tissue damage. No significant changesin magnetization transfer ratio were observed. Manganese ions tended toaccumulate in the central parts of the inflamed optic nerve. The resultingsignal enhancement at 24 h after administration positively correlated withthe severity of axonal loss. Thus, manganese might be an indicator ofintracellular calcium accumulation that is known to be associated withaxon damage. Although none of the methods alone distinguished betweeninflammation, demyelination, and reduced axon density, their specificcapabilities should prove useful for futurein vivoMRI studies of opticneuritis in both animal models and humans."],["dc.identifier.doi","10.1016/j.neuroimage.2008.02.021"],["dc.identifier.gro","3150382"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7140"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1053-8119"],["dc.subject","Optic neuritis; EAE; MRI; Manganese-enhanced MRI"],["dc.title","MRI of optic neuritis in a rat model"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]