Kleinknecht, Alexander

[["dc.bibliographiccitation.firstpage","300"],["dc.bibliographiccitation.journal","Journal of the neurological sciences"],["dc.bibliographiccitation.lastpage","304"],["dc.bibliographiccitation.volume","372"],["dc.contributor.author","Maier, Ilko L."],["dc.contributor.author","Behme, Daniel"],["dc.contributor.author","Schnieder, Marlena"],["dc.contributor.author","Tsogkas, Ioannis"],["dc.contributor.author","Schregel, Katharina"],["dc.contributor.author","Kleinknecht, Alexander"],["dc.contributor.author","Wasser, Katrin"],["dc.contributor.author","Bähr, Mathias"],["dc.contributor.author","Knauth, Michael"],["dc.contributor.author","Psychogios, Marios"],["dc.contributor.author","Liman, Jan"],["dc.date.accessioned","2018-01-09T10:18:58Z"],["dc.date.available","2018-01-09T10:18:58Z"],["dc.date.issued","2017"],["dc.description.abstract","Although endovascular treatment for proximal cerebral vessel occlusion is very effective, it remains controversial if intravenous thrombolysis (IVT) prior to endovascular treatment is superior compared to endovascular treatment alone. In this study we compared functional outcomes and recanalization rates of endovascularly treated stroke patients with and without bridging IVT."],["dc.identifier.doi","10.1016/j.jns.2016.12.001"],["dc.identifier.pmid","28017233"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11576"],["dc.language.iso","en"],["dc.notes.status","final"],["dc.relation.eissn","1878-5883"],["dc.title","Bridging-therapy with intravenous recombinant tissue plasminogen activator improves functional outcome in patients with endovascular treatment in acute stroke"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","619"],["dc.bibliographiccitation.issue","5"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","631"],["dc.bibliographiccitation.volume","130"],["dc.contributor.author","Wagner, J."],["dc.contributor.author","Krauss, S."],["dc.contributor.author","Shi, S."],["dc.contributor.author","Ryazanov, S."],["dc.contributor.author","Steffen, J."],["dc.contributor.author","Miklitz, C."],["dc.contributor.author","Leonov, A."],["dc.contributor.author","Kleinknecht, A."],["dc.contributor.author","Goericke, Bettina"],["dc.contributor.author","Weishaupt, J. H."],["dc.contributor.author","Weckbecker, D."],["dc.contributor.author","Reiner, A. M."],["dc.contributor.author","Zinth, W."],["dc.contributor.author","Levin, J."],["dc.contributor.author","Ehninger, D."],["dc.contributor.author","Remy, S."],["dc.contributor.author","Kretzschmar, Hans A."],["dc.contributor.author","Griesinger, C."],["dc.contributor.author","Giese, A."],["dc.contributor.author","Fuhrmann, M."],["dc.date.accessioned","2017-09-07T11:43:27Z"],["dc.date.available","2017-09-07T11:43:27Z"],["dc.date.issued","2015"],["dc.description.abstract","Pathological tau aggregation leads to filamentous tau inclusions and characterizes neurodegenerative tauopathies such as Alzheimer's disease and frontotemporal dementia and parkinsonism linked to chromosome 17. Tau aggregation coincides with clinical symptoms and is thought to mediate neurodegeneration. Transgenic mice overexpressing mutant human P301S tau exhibit many neuropathological features of human tauopathies including behavioral deficits and increased mortality. Here, we show that the di-phenyl-pyrazole anle138b binds to aggregated tau and inhibits tau aggregation in vitro and in vivo. Furthermore, anle138b treatment effectively ameliorates disease symptoms, increases survival time and improves cognition of tau transgenic PS19 mice. In addition, we found decreased synapse and neuron loss accompanied by a decreased gliosis in the hippocampus. Our results suggest that reducing tau aggregates with anle138b may represent an effective and promising approach for the treatment of human tauopathies."],["dc.identifier.doi","10.1007/s00401-015-1483-3"],["dc.identifier.gro","3141799"],["dc.identifier.isi","000363270100002"],["dc.identifier.pmid","26439832"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1201"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.eissn","1432-0533"],["dc.relation.issn","0001-6322"],["dc.title","Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dspace.entity.type","Publication"]]