Wagner, Jens

[["dc.bibliographiccitation.firstpage","924"],["dc.bibliographiccitation.issue","9"],["dc.bibliographiccitation.journal","Journal of Neuropathology and Experimental Neurology"],["dc.bibliographiccitation.lastpage","933"],["dc.bibliographiccitation.volume","74"],["dc.contributor.author","Shi, Song"],["dc.contributor.author","Wagner, Jens"],["dc.contributor.author","Mitteregger-Kretzschmar, Gerda"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Giese, Armin"],["dc.date.accessioned","2017-09-07T11:43:35Z"],["dc.date.available","2017-09-07T11:43:35Z"],["dc.date.issued","2015"],["dc.description.abstract","Prion diseases are fatal neurodegenerative diseases characterized by accumulation of the pathogenic prion protein PrPSc in the brain. We established quantitative real-time quaking-induced conversion for the measurement of minute amounts of PrPSc in body fluids such as urine. Using this approach, we monitored the efficacy of antiprion therapy by quantifying the seeding activity of PrPSc from the brain and urine of mice after prion infection. We found that the aggregation inhibitor anle138b decreased the levels of PrPSc in the brain and urine. Importantly, variations of PrPSc levels in the urine closely corresponded to those in the brain. Our findings indicate that quantification of urinary PrPSc enables measurement of prion disease progression in body fluids and can substitute for immunodetection in brain tissue. We expect PrPSc quantification biologic fluids (such as urine and cerebrospinal fluid) with quantitative real-time quaking-induced conversion to emerge as a valuable noninvasive diagnostic tool for monitoring disease progression and the efficacy of therapeutic approaches in animal studies and human clinical trials of prion diseases. Moreover, highly sensitive methods for quantifying pathologic aggregate seeds might provide novel molecular biomarkers for other neurodegenerative diseases that may involve prion-like mechanisms (protein aggregation and spreading), such as Alzheimer disease and Parkinson disease."],["dc.identifier.doi","10.1097/NEN.0000000000000233"],["dc.identifier.gro","3141840"],["dc.identifier.isi","000360142900007"],["dc.identifier.pmid","26247395"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/1656"],["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","0022-3069"],["dc.title","Quantitative Real-Time Quaking-Induced Conversion Allows Monitoring of Disease-Modifying Therapy in the Urine of Prion-Infected Mice"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","32"],["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","EMBO molecular medicine"],["dc.bibliographiccitation.lastpage","47"],["dc.bibliographiccitation.volume","10"],["dc.contributor.author","Martinez-Hernandez, Ana"],["dc.contributor.author","Urbanke, Hendrik"],["dc.contributor.author","Gillman, Alan L."],["dc.contributor.author","Lee, Joon"],["dc.contributor.author","Ryazanov, Sergey"],["dc.contributor.author","Agbemenyah, Hope Y."],["dc.contributor.author","Benito, Eva"],["dc.contributor.author","Jain, Gaurav"],["dc.contributor.author","Kaurani, Lalit"],["dc.contributor.author","Grigorian, Gayane"],["dc.contributor.author","Leonov, Andrei"],["dc.contributor.author","Rezaei-Ghaleh, Nasrollah"],["dc.contributor.author","Wilken, Petra"],["dc.contributor.author","Teran Arce, Fernando"],["dc.contributor.author","Wagner, Jens"],["dc.contributor.author","Fuhrman, Martin"],["dc.contributor.author","Caruana, Mario"],["dc.contributor.author","Camilleri, Angelique"],["dc.contributor.author","Vassallo, Neville"],["dc.contributor.author","Zweckstetter, Markus"],["dc.contributor.author","Benz, Roland"],["dc.contributor.author","Giese, Armin"],["dc.contributor.author","Schneider, Anja"],["dc.contributor.author","Korte, Martin"],["dc.contributor.author","Lal, Ratnesh"],["dc.contributor.author","Griesinger, Christian"],["dc.contributor.author","Eichele, Gregor"],["dc.contributor.author","Fischer, Andre"],["dc.date.accessioned","2018-01-09T14:58:18Z"],["dc.date.available","2018-01-09T14:58:18Z"],["dc.date.issued","2017-12-05"],["dc.description.abstract","Alzheimer's disease is a devastating neurodegenerative disease eventually leading to dementia. An effective treatment does not yet exist. Here we show that oral application of the compound anle138b restores hippocampal synaptic and transcriptional plasticity as well as spatial memory in a mouse model for Alzheimer's disease, when given orally before or after the onset of pathology. At the mechanistic level, we provide evidence that anle138b blocks the activity of conducting Aβ pores without changing the membrane embedded Aβ-oligomer structure. In conclusion, our data suggest that anle138b is a novel and promising compound to treat AD-related pathology that should be investigated further."],["dc.identifier.doi","10.15252/emmm.201707825"],["dc.identifier.pmid","29208638"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/15064"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/11613"],["dc.language.iso","en"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","final"],["dc.relation.eissn","1757-4684"],["dc.rights","CC BY 4.0"],["dc.rights.uri","https://creativecommons.org/licenses/by/4.0"],["dc.title","The diphenylpyrazole compound anle138b blocks Aβ channels and rescues disease phenotypes in a mouse model for amyloid pathology"],["dc.type","journal_article"],["dc.type.internalPublication","unknown"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.firstpage","795"],["dc.bibliographiccitation.issue","6"],["dc.bibliographiccitation.journal","Acta Neuropathologica"],["dc.bibliographiccitation.lastpage","813"],["dc.bibliographiccitation.volume","125"],["dc.contributor.author","Wagner, J."],["dc.contributor.author","Ryazanov, S."],["dc.contributor.author","Leonov, A."],["dc.contributor.author","Levin, J."],["dc.contributor.author","Shi, S."],["dc.contributor.author","Schmidt, F."],["dc.contributor.author","Prix, C."],["dc.contributor.author","Pan-Montojo, F."],["dc.contributor.author","Bertsch, U."],["dc.contributor.author","Mitteregger-Kretzschmar, G."],["dc.contributor.author","Geissen, M."],["dc.contributor.author","Eiden, M."],["dc.contributor.author","Leidel, F."],["dc.contributor.author","Hirschberger, T."],["dc.contributor.author","Deeg, A. A."],["dc.contributor.author","Krauth, J. J."],["dc.contributor.author","Zinth, W."],["dc.contributor.author","Tavan, P."],["dc.contributor.author","Pilger, J."],["dc.contributor.author","Zweckstetter, M."],["dc.contributor.author","Frank, T."],["dc.contributor.author","Bähr, M."],["dc.contributor.author","Weishaupt, J. H."],["dc.contributor.author","Uhr, M."],["dc.contributor.author","Urlaub, H."],["dc.contributor.author","Teichmann, U."],["dc.contributor.author","Samwer, M."],["dc.contributor.author","Bötzel, K."],["dc.contributor.author","Groschup, M."],["dc.contributor.author","Kretzschmar, Hans"],["dc.contributor.author","Griesinger, C."],["dc.contributor.author","Giese, A."],["dc.date.accessioned","2017-09-07T11:47:41Z"],["dc.date.available","2017-09-07T11:47:41Z"],["dc.date.issued","2013"],["dc.description.abstract","In neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD) and prion diseases, deposits of aggregated disease-specific proteins are found. Oligomeric aggregates are presumed to be the key neurotoxic agent. Here we describe the novel oligomer modulator anle138b [3-(1,3-benzodioxol-5-yl)-5-(3-bromophenyl)-1H-pyrazole], an aggregation inhibitor we developed based on a systematic high-throughput screening campaign combined with medicinal chemistry optimization. In vitro, anle138b blocked the formation of pathological aggregates of prion protein (PrPSc) and of alpha-synuclein (alpha-syn), which is deposited in PD and other synucleinopathies such as dementia with Lewy bodies (DLB) and multiple system atrophy (MSA). Notably, anle138b strongly inhibited all prion strains tested including BSE-derived and human prions. Anle138b showed structure-dependent binding to pathological aggregates and strongly inhibited formation of pathological oligomers in vitro and in vivo both for prion protein and alpha-synuclein. Both in mouse models of prion disease and in three different PD mouse models, anle138b strongly inhibited oligomer accumulation, neuronal degeneration, and disease progression in vivo. Anle138b had no detectable toxicity at therapeutic doses and an excellent oral bioavailability and blood-brain-barrier penetration. Our findings indicate that oligomer modulators provide a new approach for disease-modifying therapy in these diseases, for which only symptomatic treatment is available so far. Moreover, our findings suggest that pathological oligomers in neurodegenerative diseases share structural features, although the main protein component is disease-specific, indicating that compounds such as anle138b that modulate oligomer formation by targeting structure-dependent epitopes can have a broad spectrum of activity in the treatment of different protein aggregation diseases."],["dc.identifier.doi","10.1007/s00401-013-1114-9"],["dc.identifier.gro","3142347"],["dc.identifier.isi","000319357900002"],["dc.identifier.pmid","23604588"],["dc.identifier.purl","https://resolver.sub.uni-goettingen.de/purl?gs-1/10301"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/7275"],["dc.language.iso","en"],["dc.notes.intern","WoS Import 2017-03-10"],["dc.notes.intern","Merged from goescholar"],["dc.notes.status","zu prüfen"],["dc.notes.submitter","PUB_WoS_Import"],["dc.relation.issn","0001-6322"],["dc.rights","Goescholar"],["dc.rights.uri","https://goescholar.uni-goettingen.de/licenses"],["dc.title","Anle138b: a novel oligomer modulator for disease-modifying therapy of neurodegenerative diseases such as prion and Parkinson's disease"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.peerReviewed","yes"],["dc.type.subtype","original"],["dc.type.version","published_version"],["dspace.entity.type","Publication"]]

[["dc.bibliographiccitation.issue","1"],["dc.bibliographiccitation.journal","Journal of Physics. Conference Series"],["dc.bibliographiccitation.volume","2374"],["dc.contributor.affiliation","Bäni, L;"],["dc.contributor.affiliation","Artuso, M;"],["dc.contributor.affiliation","Bachmair, F;"],["dc.contributor.affiliation","Bartosik, M;"],["dc.contributor.affiliation","Beck, H;"],["dc.contributor.affiliation","Bellini, V;"],["dc.contributor.affiliation","Belyaev, V;"],["dc.contributor.affiliation","Bentele, B;"],["dc.contributor.affiliation","Bergonzo, P;"],["dc.contributor.affiliation","Bes, A;"],["dc.contributor.affiliation","Brom, J-M;"],["dc.contributor.affiliation","Chiodini, G;"],["dc.contributor.affiliation","Chren, D;"],["dc.contributor.affiliation","Cindro, V;"],["dc.contributor.affiliation","Claus, G;"],["dc.contributor.affiliation","Collot, J;"],["dc.contributor.affiliation","Cumalat, J;"],["dc.contributor.affiliation","Curtoni, S;"],["dc.contributor.affiliation","Dabrowski, A;"],["dc.contributor.affiliation","D’Alessandro, R;"],["dc.contributor.affiliation","Dauvergne, D;"],["dc.contributor.affiliation","de Boer, W;"],["dc.contributor.affiliation","Dorfer, C;"],["dc.contributor.affiliation","Dünser, M;"],["dc.contributor.affiliation","Eigen, G;"],["dc.contributor.affiliation","Eremin, V;"],["dc.contributor.affiliation","Forneris, J;"],["dc.contributor.affiliation","Gallin-Martel, L;"],["dc.contributor.affiliation","Gallin-Martel, M-L;"],["dc.contributor.affiliation","Gan, K K;"],["dc.contributor.affiliation","Gastal, M;"],["dc.contributor.affiliation","Ghimouz, A;"],["dc.contributor.affiliation","Goffe, M;"],["dc.contributor.affiliation","Goldstein, J;"],["dc.contributor.affiliation","Golubev, A;"],["dc.contributor.affiliation","Gorišek, A;"],["dc.contributor.affiliation","Grigoriev, E;"],["dc.contributor.affiliation","Grosse-Knetter, J;"],["dc.contributor.affiliation","Grummer, A;"],["dc.contributor.affiliation","Hiti, B;"],["dc.contributor.affiliation","Hits, D;"],["dc.contributor.affiliation","Hoeferkamp, M;"],["dc.contributor.affiliation","Hofmann, T;"],["dc.contributor.affiliation","Hosselet, J;"],["dc.contributor.affiliation","Hügging, F;"],["dc.contributor.affiliation","Hutson, C;"],["dc.contributor.affiliation","Jackman, R;"],["dc.contributor.affiliation","Janssen, J;"],["dc.contributor.affiliation","Jennings-Moors, R;"],["dc.contributor.affiliation","Kagan, H;"],["dc.contributor.affiliation","Kanxheri, K;"],["dc.contributor.affiliation","Kis, M;"],["dc.contributor.affiliation","Kramberger, G;"],["dc.contributor.affiliation","Kuleshov, S;"],["dc.contributor.affiliation","Lacoste, A;"],["dc.contributor.affiliation","Lagomarsino, S;"],["dc.contributor.affiliation","Giudice, A Lo;"],["dc.contributor.affiliation","Paz, I López;"],["dc.contributor.affiliation","Lukosi, E;"],["dc.contributor.affiliation","Maazouzi, C;"],["dc.contributor.affiliation","Mandić, I;"],["dc.contributor.affiliation","Marcatili, S;"],["dc.contributor.affiliation","Marino, A;"],["dc.contributor.affiliation","Mathieu, C;"],["dc.contributor.affiliation","Menichelli, M;"],["dc.contributor.affiliation","Mikuž, M;"],["dc.contributor.affiliation","Morozzi, A;"],["dc.contributor.affiliation","Moscatelli, F;"],["dc.contributor.affiliation","Moss, J;"],["dc.contributor.affiliation","Mountain, R;"],["dc.contributor.affiliation","Oh, A;"],["dc.contributor.affiliation","Olivero, P;"],["dc.contributor.affiliation","Pakpour-Tabrizi, A;"],["dc.contributor.affiliation","Passeri, D;"],["dc.contributor.affiliation","Pernegger, H;"],["dc.contributor.affiliation","Perrino, R;"],["dc.contributor.affiliation","Picollo, F;"],["dc.contributor.affiliation","Pomorski, M;"],["dc.contributor.affiliation","Porter, A;"],["dc.contributor.affiliation","Potenza, R;"],["dc.contributor.affiliation","Quadt, A;"],["dc.contributor.affiliation","Rarbi, F;"],["dc.contributor.affiliation","Re, A;"],["dc.contributor.affiliation","Reichmann, M;"],["dc.contributor.affiliation","Roe, S;"],["dc.contributor.affiliation","Rossetto, O;"],["dc.contributor.affiliation","Becerra, D A Sanz;"],["dc.contributor.affiliation","Schmidt, C;"],["dc.contributor.affiliation","Schnetzer, S;"],["dc.contributor.affiliation","Sciortino, S;"],["dc.contributor.affiliation","Scorzoni, A;"],["dc.contributor.affiliation","Seidel, S;"],["dc.contributor.affiliation","Servoli, L;"],["dc.contributor.affiliation","Smith, D S;"],["dc.contributor.affiliation","Sopko, B;"],["dc.contributor.affiliation","Sopko, V;"],["dc.contributor.affiliation","Spagnolo, S;"],["dc.contributor.affiliation","Spanier, S;"],["dc.contributor.affiliation","Stenson, K;"],["dc.contributor.affiliation","Stone, R;"],["dc.contributor.affiliation","Stugu, B;"],["dc.contributor.affiliation","Sutera, C;"],["dc.contributor.affiliation","Traeger, M;"],["dc.contributor.affiliation","Trischuk, W;"],["dc.contributor.affiliation","Truccato, M;"],["dc.contributor.affiliation","Tuvê, C;"],["dc.contributor.affiliation","Velthuis, J;"],["dc.contributor.affiliation","Wagner, S;"],["dc.contributor.affiliation","Wallny, R;"],["dc.contributor.affiliation","Wang, J C;"],["dc.contributor.affiliation","Welch, J;"],["dc.contributor.affiliation","Wermes, N;"],["dc.contributor.affiliation","Wickramasinghe, J;"],["dc.contributor.affiliation","Yamouni, M;"],["dc.contributor.affiliation","Zalieckas, J;"],["dc.contributor.affiliation","Zavrtanik, M;"],["dc.contributor.author","Bäni, L."],["dc.contributor.author","Artuso, M."],["dc.contributor.author","Bachmair, F."],["dc.contributor.author","Bartosik, M."],["dc.contributor.author","Beck, H."],["dc.contributor.author","Bellini, V."],["dc.contributor.author","Belyaev, V."],["dc.contributor.author","Bentele, B."],["dc.contributor.author","Bergonzo, P."],["dc.contributor.author","Bes, A."],["dc.contributor.author","Brom, J.-M."],["dc.contributor.author","Chiodini, G."],["dc.contributor.author","Chren, D."],["dc.contributor.author","Cindro, V."],["dc.contributor.author","Claus, G."],["dc.contributor.author","Collot, J."],["dc.contributor.author","Cumalat, J."],["dc.contributor.author","Curtoni, S."],["dc.contributor.author","Dabrowski, A."],["dc.contributor.author","D’Alessandro, R."],["dc.contributor.author","Dauvergne, D."],["dc.contributor.author","de Boer, W."],["dc.contributor.author","Dorfer, C."],["dc.contributor.author","Dünser, M."],["dc.contributor.author","Eigen, G."],["dc.contributor.author","Eremin, V."],["dc.contributor.author","Forneris, J."],["dc.contributor.author","Gallin-Martel, L."],["dc.contributor.author","Gallin-Martel, M.-L."],["dc.contributor.author","Gan, K. K."],["dc.contributor.author","Gastal, M."],["dc.contributor.author","Ghimouz, A."],["dc.contributor.author","Goffe, M."],["dc.contributor.author","Goldstein, J."],["dc.contributor.author","Golubev, A."],["dc.contributor.author","Gorišek, A."],["dc.contributor.author","Grigoriev, E."],["dc.contributor.author","Grosse-Knetter, J."],["dc.contributor.author","Grummer, A."],["dc.contributor.author","Hiti, B."],["dc.contributor.author","Hits, D."],["dc.contributor.author","Hoeferkamp, M."],["dc.contributor.author","Hofmann, T."],["dc.contributor.author","Hosselet, J."],["dc.contributor.author","Hügging, F."],["dc.contributor.author","Hutson, C."],["dc.contributor.author","Jackman, R."],["dc.contributor.author","Janssen, J."],["dc.contributor.author","Jennings-Moors, R."],["dc.contributor.author","Kagan, H."],["dc.contributor.author","Kanxheri, K."],["dc.contributor.author","Kis, M."],["dc.contributor.author","Kramberger, G."],["dc.contributor.author","Kuleshov, S."],["dc.contributor.author","Lacoste, A."],["dc.contributor.author","Lagomarsino, S."],["dc.contributor.author","Giudice, A. Lo"],["dc.contributor.author","Paz, I. López"],["dc.contributor.author","Lukosi, E."],["dc.contributor.author","Maazouzi, C."],["dc.contributor.author","Mandić, I."],["dc.contributor.author","Marcatili, S."],["dc.contributor.author","Marino, A."],["dc.contributor.author","Mathieu, C."],["dc.contributor.author","Menichelli, M."],["dc.contributor.author","Mikuž, M."],["dc.contributor.author","Morozzi, A."],["dc.contributor.author","Moscatelli, F."],["dc.contributor.author","Moss, J."],["dc.contributor.author","Mountain, R."],["dc.contributor.author","Oh, A."],["dc.contributor.author","Olivero, P."],["dc.contributor.author","Pakpour-Tabrizi, A."],["dc.contributor.author","Passeri, D."],["dc.contributor.author","Pernegger, H."],["dc.contributor.author","Perrino, R."],["dc.contributor.author","Picollo, F."],["dc.contributor.author","Pomorski, M."],["dc.contributor.author","Porter, A."],["dc.contributor.author","Potenza, R."],["dc.contributor.author","Quadt, A."],["dc.contributor.author","Rarbi, F."],["dc.contributor.author","Re, A."],["dc.contributor.author","Reichmann, M."],["dc.contributor.author","Roe, S."],["dc.contributor.author","Rossetto, O."],["dc.contributor.author","Becerra, D. A. Sanz"],["dc.contributor.author","Schmidt, C."],["dc.contributor.author","Schnetzer, S."],["dc.contributor.author","Sciortino, S."],["dc.contributor.author","Scorzoni, A."],["dc.contributor.author","Seidel, S."],["dc.contributor.author","Servoli, L."],["dc.contributor.author","Smith, D. S."],["dc.contributor.author","Sopko, B."],["dc.contributor.author","Sopko, V."],["dc.contributor.author","Spagnolo, S."],["dc.contributor.author","Spanier, S."],["dc.contributor.author","Stenson, K."],["dc.contributor.author","Stone, R."],["dc.contributor.author","Stugu, B."],["dc.contributor.author","Sutera, C."],["dc.contributor.author","Traeger, M."],["dc.contributor.author","Trischuk, W."],["dc.contributor.author","Truccato, M."],["dc.contributor.author","Tuvê, C."],["dc.contributor.author","Velthuis, J."],["dc.contributor.author","Wagner, S."],["dc.contributor.author","Wallny, R."],["dc.contributor.author","Wang, J. C."],["dc.contributor.author","Welch, J."],["dc.contributor.author","Wermes, N."],["dc.contributor.author","Wickramasinghe, J."],["dc.contributor.author","Yamouni, M."],["dc.contributor.author","Zalieckas, J."],["dc.contributor.author","Zavrtanik, M."],["dc.date.accessioned","2022-12-09T09:09:57Z"],["dc.date.available","2022-12-09T09:09:57Z"],["dc.date.issued","2022"],["dc.date.updated","2022-12-09T04:21:29Z"],["dc.description.abstract","Diamond is used as detector material in high energy physics experiments due to its inherent radiation tolerance. The RD42 collaboration has measured the radiation tolerance of chemical vapour deposition (CVD) diamond against proton, pion, and neutron irradiation. Results of this study are summarized in this article. The radiation tolerance of diamond detectors can be further enhanced by using a 3D electrode geometry. We present preliminary results of a poly-crystalline CVD (pCVD) diamond detector with a 3D electrode geometry after irradiation and compare to planar devices of roughly the same thickness."],["dc.identifier.doi","10.1088/1742-6596/2374/1/012172"],["dc.identifier.uri","https://resolver.sub.uni-goettingen.de/purl?gro-2/118491"],["dc.language.iso","en"],["dc.relation.eissn","1742-6596"],["dc.relation.issn","1742-6588"],["dc.rights.uri","http://creativecommons.org/licenses/by/3.0/"],["dc.title","Radiation tolerance of diamond detectors"],["dc.type","journal_article"],["dc.type.internalPublication","yes"],["dc.type.version","published_version"],["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"]]