Maier, Katharina

[["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","514"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","525"],["dc.bibliographiccitation.volume","25"],["dc.contributor.author","Maier, K."],["dc.contributor.author","Merkler, D."],["dc.contributor.author","Gerber, Joachim"],["dc.contributor.author","Taheri, N."],["dc.contributor.author","Kuhnert, A. V."],["dc.contributor.author","Williams, S. K."],["dc.contributor.author","Neusch, C."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Diem, R."],["dc.date.accessioned","2017-09-07T11:49:51Z"],["dc.date.available","2017-09-07T11:49:51Z"],["dc.date.issued","2007"],["dc.description.abstract","Axonal destruction and neuronal loss occur early during multiple sclerosis, an autoimmune inflammatory CNS disease that frequently manifests with acute optic neuritis. Available therapies mainly target the inflammatory component of the disease but fail to prevent neurodegeneration. To investigate the effect of minocycline 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 (MOG)-induced experimental autoimmune encephalomyelitis. Optic neuritis in this model was diagnosed by recording visual evoked potentials and RGC function was monitored by measuring electroretinograms. Functional and histopathological data of RGCs and optic nerves revealed neuronal and axonal protection when minocycline treatment was started on the day of immunization. Furthermore, we demonstrate that minocycline-induced neuroprotection is related to a direct antagonism of multiple mechanisms leading to neuronal cell death such as the induction of anti-apoptotic intracellular signalling pathways and a decrease in glutamate excitotoxicity. From these observations, we conclude that minocycline exerts neuroprotective effects independent of its anti-inflammatory properties. This hypothesis was confirmed in a non-inflammatory disease model leading to degeneration of RGCs, the surgical transection of the optic nerve. (c) 2007 Published by Elsevier Inc."],["dc.identifier.doi","10.1016/j.nbd.2006.10.022"],["dc.identifier.gro","3143534"],["dc.identifier.isi","000244872200007"],["dc.identifier.pmid","17239606"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1059"],["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","0969-9961"],["dc.title","Multiple neuroprotective mechanisms of minocycline in autoimmune CNS inflammation"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["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","S181"],["dc.bibliographiccitation.issue","Suppl. 2"],["dc.bibliographiccitation.journal","Cell Death and Differentiation"],["dc.bibliographiccitation.lastpage","S192"],["dc.bibliographiccitation.volume","11"],["dc.contributor.author","Sättler, Muriel B."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Ehrenreich, Hannelore"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2017-09-07T11:45:34Z"],["dc.date.available","2017-09-07T11:45:34Z"],["dc.date.issued","2004"],["dc.description.abstract","In multiple sclerosis (MS), long-term disability is primarily caused by axonal and neuronal damage. We demonstrated in a previous study that neuronal apoptosis occurs early during experimental autoimmune encephalomyelitis, a common animal model of MS. In the present study, we show that, in rats suffering from myelin oligodendrocyte glycoprotein (MOG)-induced optic neuritis, systemic application of erythropoietin (Epo) significantly increased survival and function of retinal ganglion cells (RGCs), the neurons that form the axons of the optic nerve. We identified three independent intracellular signaling pathways involved in Epo-induced neuroprotection in vivo: Protein levels of phospho-Akt, phospho-MAPK 1 and 2, and Bcl-2 were increased under Epo application. Using a combined treatment of Epo together with a selective inhibitor of phosphatidylinositol 3-kinase (PI3-K) prevented upregulation of phospho-Akt and consecutive RGC rescue. We conclude that in MOG-EAE the PI3-K/Akt pathway has an important influence on RGC survival under systemic treatment with Epo."],["dc.identifier.doi","10.1038/sj.cdd.4401504"],["dc.identifier.gro","3150406"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7167"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.issn","1350-9047"],["dc.subject","optic neuritis; erythropoietin; retinal ganglion cells; Bcl-2 family; phosphatidylinositol 3-kinase"],["dc.title","Neuroprotective effects and intracellular signaling pathways of erythropoietin in a rat model of multiple sclerosis"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.peerReviewed","no"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","218"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Neurobiology of Disease"],["dc.bibliographiccitation.lastpage","226"],["dc.bibliographiccitation.volume","20"],["dc.contributor.author","Diem, Ricarda"],["dc.contributor.author","Taheri, Naimeh"],["dc.contributor.author","Dietz, Gunnar P. H."],["dc.contributor.author","Kuhnert, Antje V."],["dc.contributor.author","Maier, Katharina"],["dc.contributor.author","Sattler, Michael"],["dc.contributor.author","Gadjanski, L."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:54:11Z"],["dc.date.available","2017-09-07T11:54:11Z"],["dc.date.issued","2005"],["dc.description.abstract","In multiple sclerosis (MS), post-mortem studies of human brain tissue as well as data from animal models have shown that apoptosis of neurons occurs to a significant extent during this disease. As neurodegeneration in MS correlates with permanent neurological deficits in patients, understanding the mechanisms would be an important precondition for designing appropriate neuroprotective therapies. Myelin oligodendrocyte glycoprotein-induced experimental autoimmune encephalomyelitis often affects the optic nerve and leads to consecutive apoptosis of retinal ganglion cells (RGCs), the neurons that form its axons. In this study, we fused Bcl-X-L to the protein transduction domain of the HIV-transactivator of transcription. Thereby, this antiapoptotic member of the Bcl-2 family was delivered into RGCs of rats with electrophysiologically diagnosed optic neuritis. Transduction of Bel-XI, in our study led to significant rescue of RGCs indicating the relevance of this pathway for neuronal survival under autoimmune inflammatory conditions. (c) 2005 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.nbd.2005.03.003"],["dc.identifier.gro","3143794"],["dc.identifier.isi","000233096700005"],["dc.identifier.pmid","16242630"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1348"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0969-9961"],["dc.title","HIV-tat-mediated BCl-X-L delivery protects retinal ganglion cells during experimental autoimmune optic neuritis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]