Meuer, Katrin

[["dc.bibliographiccitation.firstpage","651"],["dc.bibliographiccitation.issue","4"],["dc.bibliographiccitation.journal","Cell Death and Differentiation"],["dc.bibliographiccitation.lastpage","661"],["dc.bibliographiccitation.volume","14"],["dc.contributor.author","Meuer, K."],["dc.contributor.author","Suppanz, I. E."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Planchamp, V."],["dc.contributor.author","Göricke, B."],["dc.contributor.author","Fichtner, L."],["dc.contributor.author","Braus, G. H."],["dc.contributor.author","Dietz, G. P. H."],["dc.contributor.author","Jakobs, S."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Weishaupt, J. H."],["dc.date.accessioned","2017-09-07T11:49:50Z"],["dc.date.available","2017-09-07T11:49:50Z"],["dc.date.issued","2007"],["dc.description.abstract","Under physiological conditions, mitochondrial morphology dynamically shifts between a punctuate appearance and tubular networks. However, little is known about upstream signal transduction pathways that regulate mitochondrial morphology. We show that mitochondrial fission is a very early and kinetically invariant event during neuronal cell death, which causally contributes to cytochrome c release and neuronal apoptosis. Using a small molecule CDK5 inhibitor, as well as a dominant-negative CDK5 mutant and RNAi knockdown experiments, we identified CDK5 as an upstream signalling kinase that regulates mitochondrial fission during apoptosis of neurons. Vice versa, our study shows that mitochondrial fission is a modulator contributing to CDK5-mediated neurotoxicity. Thereby, we provide a link that allows integration of CDK5 into established neuronal apoptosis pathways."],["dc.identifier.doi","10.1038/sj.cdd.4402087"],["dc.identifier.gro","3143515"],["dc.identifier.isi","000245102900002"],["dc.identifier.pmid","17218957"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1038"],["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","1350-9047"],["dc.title","Cyclin-dependent kinase 5 is an upstream regulator of mitochondrial fission during neuronal apoptosis"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","61"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Brain Research"],["dc.bibliographiccitation.lastpage","66"],["dc.bibliographiccitation.volume","1082"],["dc.contributor.author","Dietz, Gunnar P. H."],["dc.contributor.author","Valbuena, Paola C."],["dc.contributor.author","Dietz, Birgit"],["dc.contributor.author","Meuer, Katrin"],["dc.contributor.author","Müller, Patrick"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.contributor.author","Bähr, Mathias"],["dc.date.accessioned","2017-09-07T11:53:10Z"],["dc.date.available","2017-09-07T11:53:10Z"],["dc.date.issued","2006"],["dc.description.abstract","Glial-cell-line-derived neurotrophic factor (GDNF) promotes mesencephalic dopaminergic neuronal survival in several in vitro and in vivo models. As the demise of dopaminergic neurons is the cause for Parkinson's disease (PD) symptoms, GDNF is a promising agent for its treatment However, this neurotrophin is unable to cross the blood-brain barrier, which has complicated its clinical use. Therefore, ways to deliver GDNF into the central nervous system in an effective manner are needed. The HIV-1-Tat-derived cell-penetrating peptide (CPP) provides a means to deliver fusion proteins into the brain. We generated a fusion protein between the 11 amino acid CPP of Tat and the rat GDNF mature protein to deliver GDNF across the blood-brain barrier. We showed previously that Tat-GDNF enhances the neuroprotective effect of GDNF in in vivo models for nerve trauma and ischemia. Here, we tested its effect in a subchronic scheme of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) application into the mouse as a model for PD to evaluate the effect of Tat-GDNF fusion protein in dopaminergic neuron survival. We showed that the fusion protein did indeed reach the dopaminergic neurons. However, the in vivo application of Tat-GDNF did not provide neuroprotection of dopaminergic neurons, as revealed by immunohistochemistry and counting of the number of tyrosine-hydroxylase-immunoreactive neurons in the substantia nigra pars compacta. Possibly, GDNF does protect nigro-striatal projections of those neurons that survive MPTP treatment but does not increase the number of surviving dopaminergic neurons. A concomitant treatment of Tat-GDNF with an anti-apoptotic Tat-fusion protein might be beneficial. (c) 2006 Elsevier B.V. All rights reserved."],["dc.identifier.doi","10.1016/j.brainres.2006.01.083"],["dc.identifier.gro","3143709"],["dc.identifier.isi","000236931400007"],["dc.identifier.pmid","16703672"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1253"],["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","0006-8993"],["dc.subject","Cell-penetrating peptide (CPP); Protein transduction domain (PTD); Blood–brain barrier; Neuroprotection; MPTP mouse model"],["dc.title","Application of a blood-brain-barrier-penetrating form of GDNF in a mouse model for Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","249"],["dc.bibliographiccitation.issue","2"],["dc.bibliographiccitation.journal","Journal of Neural Transmission"],["dc.bibliographiccitation.lastpage","250"],["dc.bibliographiccitation.volume","116"],["dc.contributor.author","Frank, T."],["dc.contributor.author","Meuer, K."],["dc.contributor.author","Klinker, Florian"],["dc.contributor.author","Liebetanz, David"],["dc.contributor.author","Schulz, Joerg B."],["dc.contributor.author","Baehr, M."],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.date.accessioned","2018-11-07T08:33:12Z"],["dc.date.available","2018-11-07T08:33:12Z"],["dc.date.issued","2009"],["dc.identifier.isi","000269823900093"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/17516"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","Najko"],["dc.publisher","Springer"],["dc.publisher.place","Wien"],["dc.relation.eventlocation","Marburg, GERMANY"],["dc.relation.issn","0300-9564"],["dc.title","Granulocyte-colony stimulating factor for the treatment of Parkinson's disease"],["dc.type","conference_abstract"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.status","published"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","757"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","765"],["dc.bibliographiccitation.volume","104"],["dc.contributor.author","Dietz, G. P. H."],["dc.contributor.author","Stockhausen (née Peters), K. V."],["dc.contributor.author","Dietz, B."],["dc.contributor.author","Falkenburger, B. H."],["dc.contributor.author","Valbuena, P."],["dc.contributor.author","Opazo, F."],["dc.contributor.author","Lingor, P."],["dc.contributor.author","Meuer, K."],["dc.contributor.author","Weishaupt, J. H."],["dc.contributor.author","Schulz, J. B."],["dc.contributor.author","Bähr, M."],["dc.date.accessioned","2017-09-07T11:48:48Z"],["dc.date.available","2017-09-07T11:48:48Z"],["dc.date.issued","2008"],["dc.description.abstract","The anti-apoptotic Bcl-x(L) is a promising agent to prevent neurodegeneration in Parkinson's disease, which is characterized by a demise of dopaminergic neurons. We linked Bcl-x(L) to a peptide that allows its delivery across biological membranes and the blood-brain barrier. We tested the fusion protein in two models of Parkinson's Disease. Cell-permeable Bcl-x(L) protected neuroblastoma cells from the selective neurotoxin 1-methyl-4-phenylpyridinium. Furthermore, its systemic application in aged mice protected dopaminergic neurons following administration of MPTP as revealed by counting of tyrosine hydroxylase-immunoreactive neurons in the substantia nigra pars compacta. Hence, we present that a cell-permeable form of an anti-apoptotic protein can be delivered to CNS neurons through its systemic application, and we provide the proof that the delivery of this protein to the CNS neurons effectively prevents neuronal cell death in models of chronic neurodegenerative diseases."],["dc.identifier.doi","10.1111/j.1471-4159.2007.05028.x"],["dc.identifier.gro","3143353"],["dc.identifier.isi","000252322600015"],["dc.identifier.pmid","17995935"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/858"],["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","0022-3042"],["dc.title","Membrane-permeable Bcl-x(L) prevents MPTP-induced dopaminergic neuronal loss in the substantia nigra"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","207"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Experimental Neurology"],["dc.bibliographiccitation.lastpage","213"],["dc.bibliographiccitation.volume","205"],["dc.contributor.author","Liebetanz, D."],["dc.contributor.author","Baier, P. C."],["dc.contributor.author","Paulus, W."],["dc.contributor.author","Meuer, K."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Weishaupt, J. H."],["dc.date.accessioned","2017-09-07T11:49:48Z"],["dc.date.available","2017-09-07T11:49:48Z"],["dc.date.issued","2007"],["dc.description.abstract","The subchronic 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridin (MPTP) paradigm is one of the most widely used in vivo models of Parkinson's disease (PD). However, particularly in the mouse model it has remained difficult to reliably detect behavioural correlates for PD. In the present study we apply a novel murine motor test, the motor skill sequence (MOSS) based on computerized recording of voluntary running wheel activity, and found latent motor skill deficits in the subchronic MPTP mouse model. Mice are first subjected to a 2-week training phase. The animals then receive either MPTP injections according to the standard subchronic MPTP paradigm (30 mg/kg) or vehicle injections for 5 consecutive days. Running performance transiently fell during the injection phase but returned to baseline within few days. The animals were then exposed to complex wheels with irregularly spaced crossbars demanding high central motor coordination abilities. Though both groups showed clear improvement of running performance in the learning phase oil the complex wheel, MPTP animals displayed clear central motor deficits oil the complex wheels, as indicated by a reduced maximum speed and running distance, despite unchanged running motivation. Our results demonstrate latent motor deficits in MPTP-treated mice, which can be unmasked by MOSS. MOSS is thus capable of detecting and quantifying central motor deficits in this widely used model of PD with high sensitivity. The automated full time data collection of several different running parameters makes it also a suitable test for efficient in vivo screening of potential therapeutic compound ill this model for PD. (C) 2007 Elsevier Inc. All rights reserved."],["dc.identifier.doi","10.1016/j.expneurol.2007.01.030"],["dc.identifier.gro","3143506"],["dc.identifier.isi","000246403400023"],["dc.identifier.pmid","17341420"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1028"],["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.title","A highly sensitive automated complex running wheel test to detect latent motor deficits in the mouse MPTP model of Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","675"],["dc.bibliographiccitation.issue","3"],["dc.bibliographiccitation.journal","Journal of Neurochemistry"],["dc.bibliographiccitation.lastpage","686"],["dc.bibliographiccitation.volume","97"],["dc.contributor.author","Meuer, Katrin"],["dc.contributor.author","Pitzer, Claudia"],["dc.contributor.author","Teismann, Peter"],["dc.contributor.author","Krüger, Carola"],["dc.contributor.author","Göricke, Bettina"],["dc.contributor.author","Laage, Rico"],["dc.contributor.author","Lingor, Paul"],["dc.contributor.author","Peters, Kerstin"],["dc.contributor.author","Schlachetzki, Johannes C. M."],["dc.contributor.author","Kobayashi, Kazuto"],["dc.contributor.author","Dietz, Gunnar P. H."],["dc.contributor.author","Weber, Daniela"],["dc.contributor.author","Ferger, Boris"],["dc.contributor.author","Schäbitz, Wolf-Rüdiger"],["dc.contributor.author","Bach, Alfred"],["dc.contributor.author","Schulz, Jörg B."],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Schneider, Armin"],["dc.contributor.author","Weishaupt, Jochen H."],["dc.date.accessioned","2017-09-07T11:53:06Z"],["dc.date.available","2017-09-07T11:53:06Z"],["dc.date.issued","2006"],["dc.description.abstract","We have recently shown that the hematopoietic Granulocyte-Colony Stimulating Factor (G-CSF) is neuroprotective in rodent stroke models, and that this action appears to be mediated via a neuronal G-CSF receptor. Here, we report that the G-CSF receptor is expressed in rodent dopaminergic substantia nigra neurons, suggesting that G-CSF might be neuroprotective for dopaminergic neurons and a candidate molecule for the treatment of Parkinson's disease. Thus, we investigated protective effects of G-CSF in 1-methyl-4-phenylpyridinium (MPP+)-challenged PC12 cells and primary neuronal midbrain cultures, as well as in the mouse 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) model of Parkinson's disease. Substantial protection was found against MPP+-induced dopaminergic cell death in vitro. Moreover, subcutaneous application of G-CSF at a dose of 40 mu g/Kg body weight daily over 13 days rescued dopaminergic substantia nigra neurons from MPTP-induced death in aged mice, as shown by quantification of tyrosine hydroxylase-positive substantia nigra cells. Using HPLC, a corresponding reduction in striatal dopamine depletion after MPTP application was observed in G-CSF-treated mice. Thus our data suggest that G-CSF is a novel therapeutic opportunity for the treatment of Parkinson's disease, because it is well-tolerated and already approved for the treatment of neutropenic conditions in humans."],["dc.identifier.doi","10.1111/j.1471-4159.2006.03727.x"],["dc.identifier.gro","3143697"],["dc.identifier.isi","000236798600007"],["dc.identifier.pmid","16573658"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1240"],["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","0022-3042"],["dc.title","Granulocyte-colony stimulating factor is neuroprotective in a model of Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","10"],["dc.bibliographiccitation.journal","BMC Neuroscience"],["dc.contributor.author","Weishaupt, Jochen Hans"],["dc.contributor.author","Dietz, Gunnar"],["dc.contributor.author","Göricke, Bettina"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Frank, Tobias"],["dc.contributor.author","Schlachetzki, Johannes C. M."],["dc.contributor.author","Meuer, Katrin"],["dc.contributor.author","Rohde, Gundula"],["dc.contributor.author","Schneider, Armin"],["dc.date.accessioned","2019-07-10T08:13:27Z"],["dc.date.available","2019-07-10T08:13:27Z"],["dc.date.issued","2009"],["dc.description.abstract","Background: The hematopoietic Granulocyte-Colony Stimulating Factor (G-CSF) plays a crucial role in controlling the number of neutrophil progenitor cells. Its function is mediated via the G-CSF receptor, which was recently found to be expressed also in the central nervous system. In addition, G-CSF provided neuroprotection in models of neuronal cell death. Here we used the retinal ganglion cell (RGC) axotomy model to compare effects of local and systemic application of neuroprotective molecules. Results: We found that the G-CSF receptor is robustly expressed by RGCs in vivo and in vitro. We thus evaluated G-CSF as a neuroprotectant for RGCs and found a dose-dependent neuroprotective effect of G-CSF on axotomized RGCs when given subcutaneously. As stem stell mobilization had previously been discussed as a possible contributor to the neuroprotective effects of G-CSF, we compared the local treatment of RGCs by injection of G-CSF into the vitreous body with systemic delivery by subcutaneous application. Both routes of application reduced retinal ganglion cell death to a comparable extent. Moreover, G-CSF enhanced the survival of immunopurified RGCs in vitro. Conclusion: We thus show that G-CSF neuroprotection is at least partially independent of potential systemic effects and provide further evidence that the clinically applicable G-CSF could become a treatment option for both neurodegenerative diseases and glaucoma"],["dc.identifier.fs","568091"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/5954"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/61250"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.relation.issn","1471-2202"],["dc.relation.orgunit","Universitätsmedizin Göttingen"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.subject.ddc","610"],["dc.title","Both systemic and local application of granulocyte-colony stimulating factor (G-CSF) is neuroprotective after retinal ganglion cell axotomy."],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]