Gadjanski, Ivana

[["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","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.issue","9"],["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","15"],["dc.contributor.author","Suehs, Kurt-Wolfram"],["dc.contributor.author","Fairless, Richard"],["dc.contributor.author","Williams, S. K."],["dc.contributor.author","Gadjanski, I."],["dc.contributor.author","Saettler, M. B."],["dc.contributor.author","Meyer, N."],["dc.contributor.author","Cavalie, A."],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2018-11-07T11:25:15Z"],["dc.date.available","2018-11-07T11:25:15Z"],["dc.date.issued","2009"],["dc.format.extent","S64"],["dc.identifier.isi","000269652500182"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/56584"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.conference","25th Congress of the European-Committee-for-Treatment-and-Research-in-Multiple-Sclerosis"],["dc.relation.eventlocation","Dusseldorf, GERMANY"],["dc.relation.issn","1352-4585"],["dc.title","NMDA receptor blockade is benefical in experimental autoimmune optic neuritis"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Gadjanski, I."],["dc.contributor.author","Boretius, Susann"],["dc.contributor.author","Michaelis, Thomas"],["dc.contributor.author","Frahm, Jens"],["dc.contributor.author","Baehr, M."],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2018-11-07T09:22:33Z"],["dc.date.available","2018-11-07T09:22:33Z"],["dc.date.issued","2006"],["dc.format.extent","S9"],["dc.identifier.isi","000241921400028"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29368"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","Madrid, SPAIN"],["dc.relation.issn","1352-4585"],["dc.title","Upregulated expression of N-type voltage dependent calcium channels (Cav2.2) in autoimmune optic neuritis detected by magnetic resonance imaging and immunochemistry"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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","82"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Eye Research"],["dc.bibliographiccitation.lastpage","90"],["dc.bibliographiccitation.volume","93"],["dc.contributor.author","Gadjanski, I."],["dc.contributor.author","Williams, S. K."],["dc.contributor.author","Hein, K."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Diem, R."],["dc.date.accessioned","2017-09-07T11:44:06Z"],["dc.date.available","2017-09-07T11:44:06Z"],["dc.date.issued","2011"],["dc.description.abstract","Optical coherence tomography (OCT) is becoming the state-of-the-art method for the non-invasive imaging of a variety of ocular diseases. The aim of this study was to assess the application of OCT for the in vivo monitoring and follow-up of pathological changes during experimental autoimmune uveoretinitis (EAU) in rats. Initially we established OCT imaging in healthy brown Norway rats and correlated it with retinal histology. Subsequently, we induced EAU and imaged animals by OCT throughout the pre-peak, peak, and post-peak phases of the disease. The sensitivity of OCT imaging was determined by comparison with clinical EAU and histopathology scores obtained ex vivo at several time points throughout the disease course. Our data demonstrate that OCT imaging of the healthy rat retina closely correlates with histological observations and allows the clear visualization of all retinal layers. After induction of EAU, the first pathological changes could be detected by OCT at day (d) 8 post-immunization (p.i.) which corresponded to the time point of clinical disease onset. An increase in retinal thickness (RI) was detected from d10 p.i. onwards which peaked at d16 p.i. and decreased again to near control levels by d20 p.i. We introduce a novel semi-quantitative OCT scoring which correlates with histopathological findings and complements the clinical scores. Therefore, we conclude that OCT is an easily accessible, non-invasive tool for detection and follow-up of histopathological changes during EAU in rats. Indeed, significant differences in RI between different stages of EAU suggest that this OCT parameter is a sensitive marker for distinguishing disease phases in vivo. (C) 2011 Elsevier Ltd. All rights reserved."],["dc.identifier.doi","10.1016/j.exer.2011.04.012"],["dc.identifier.gro","3142703"],["dc.identifier.isi","000293042200010"],["dc.identifier.pmid","21586286"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/137"],["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","0014-4835"],["dc.title","Correlation of optical coherence tomography with clinical and histopathological findings in experimental autoimmune uveoretinitis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","77"],["dc.bibliographiccitation.issue","1-2"],["dc.bibliographiccitation.journal","Journal of Neuroimmunology"],["dc.bibliographiccitation.lastpage","86"],["dc.bibliographiccitation.volume","193"],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Togni, M."],["dc.contributor.author","Gadjanski, I."],["dc.contributor.author","Sühs, K.-W."],["dc.contributor.author","Meyer, N."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Diem, R."],["dc.date.accessioned","2017-09-07T11:48:49Z"],["dc.date.available","2017-09-07T11:48:49Z"],["dc.date.issued","2008"],["dc.description.abstract","Heterogeneity in clinical disease course and histopathology complicates the treatment of multiple sclerosis. We detected important differences in neurodegeneration in various subtypes of myelin oligodendrocyte glycoprotein (MOG)-induced optic neuritis. Dark Agouti (DA) rats showed a significantly higher survival of retinal ganglion cells in comparison to Brown Norway rats. After surgical transection of the optic nerve neuronal loss was similar in both rat strains. We identified an increased expression of interleukin I and glial cell line-derived neurotrophic factor in DA rats as the possible mechanism of the observed endogenous neuroprotection in MOG-induced optic neuritis. (C) 2007 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.jneuroim.2007.10.021"],["dc.identifier.gro","3143382"],["dc.identifier.isi","000253217400009"],["dc.identifier.pmid","18037506"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/889"],["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.subject","Experimental autoimmune encephalomyelitis; Optic neuritis; NeurodegenerationInterleukin 1β; Glial cell line-derived neurotrophic factor"],["dc.title","Strain-specific susceptibility for neurodegeneration 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","157"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Investigative Ophthalmology & Visual Science"],["dc.bibliographiccitation.lastpage","163"],["dc.bibliographiccitation.volume","53"],["dc.contributor.author","Hein, K."],["dc.contributor.author","Gadjanski, I."],["dc.contributor.author","Kretzschmar, B."],["dc.contributor.author","Lange, K."],["dc.contributor.author","Diem, R."],["dc.contributor.author","Sättler, M. B."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:43:10Z"],["dc.date.available","2017-09-07T11:43:10Z"],["dc.date.issued","2012"],["dc.description.abstract","The aim of the present study was to evaluate the ability and accuracy of spectral domain optical coherence tomography (OCT) for in vivo monitoring of retinal ganglion cell degeneration in a rat model of myelin oligodendrocyte glycoprotein-induced optic neuritis. METHODS. First, OCT imaging was established for imaging of all retinal layers in Brown Norway rats. Second, thickness measurements of retinal nerve fiber layer (RNFL) were performed by periodically imaging during the development and progression of autoimmune optic neuritis. Third, the reproducibility of OCT measurements was determined by comparing RNFL measurements of two independent investigators. Fourth, OCT data were correlated with histopathology obtained ex vivo after the final imaging session. RESULTS. Results showed that RNFL thickness declined significantly before clinical manifestation of the disease and decline progresses continuously during the disease course. RNFL thickness measured by OCT had good repeatability and also corresponded with histomorphometric measurements. The reproducibility was limited because of the post-processing analyses performed by manual measurements. CONCLUSIONS. In summary, it is shown here for the first time that OCT can reliably monitor neurodegeneration in an experimental model of autoimmune optic neuritis in rodents. Moreover, in comparing RNFL thickness decline with histopathological analyses of the optic nerve, these results suggest an early, and in part, inflammation-independent process of RNFL degeneration in autoimmune optic neuritis."],["dc.identifier.doi","10.1167/iovs.11-8092"],["dc.identifier.gro","3142601"],["dc.identifier.isi","000302694500026"],["dc.identifier.pmid","22131393"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/23"],["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","0146-0404"],["dc.title","An Optical Coherence Tomography Study on Degeneration of Retinal Nerve Fiber Layer in Rats with 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.journal","MULTIPLE SCLEROSIS"],["dc.bibliographiccitation.volume","12"],["dc.contributor.author","Saettler, M. B."],["dc.contributor.author","Merkler, Doron"],["dc.contributor.author","Togni, M."],["dc.contributor.author","Gadjanski, I."],["dc.contributor.author","Stadelmann, Christine"],["dc.contributor.author","Baehr, M."],["dc.contributor.author","Diem, Ricarda"],["dc.date.accessioned","2018-11-07T09:22:56Z"],["dc.date.available","2018-11-07T09:22:56Z"],["dc.date.issued","2006"],["dc.format.extent","S56"],["dc.identifier.isi","000241921400183"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/29457"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Sage Publications Ltd"],["dc.publisher.place","London"],["dc.relation.eventlocation","Madrid, SPAIN"],["dc.relation.issn","1352-4585"],["dc.title","Neuronal damage in MOG-induced optic neuritis correlates well with T-cell infiltration"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["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"]]