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@ARTICLE{Wagner:138181,
      author       = {Wagner, Jens and Krauß, Sybille and Shi, Song and
                      Ryazanov, Sergey and Steffen, Julia and Miklitz, Carolin and
                      Leonov, Andrei and Kleinknecht, Alexander and Göricke,
                      Bettina and Weishaupt, Jochen H and Weckbecker, Daniel and
                      Reiner, Anne M and Zinth, Wolfgang and Levin, Johannes and
                      Ehninger, Dan and Remy, Stefan and Kretzschmar, Hans A and
                      Griesinger, Christian and Giese, Armin and Fuhrmann, Martin},
      title        = {{R}educing tau aggregates with anle138b delays disease
                      progression in a mouse model of tauopathies.},
      journal      = {Acta neuropathologica},
      volume       = {130},
      number       = {5},
      issn         = {0001-6322},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2020-04503},
      pages        = {619-631},
      year         = {2015},
      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.},
      keywords     = {Animals / Benzodioxoles: pharmacology / Cell Death: drug
                      effects / Cell Death: physiology / Disease Models, Animal /
                      Disease Progression / Female / Gliosis: drug therapy /
                      Gliosis: pathology / Gliosis: physiopathology / Hippocampus:
                      drug effects / Hippocampus: pathology / Hippocampus:
                      physiopathology / Male / Mice, Transgenic / Motor Activity:
                      drug effects / Motor Activity: physiology / Neurons: drug
                      effects / Neurons: pathology / Neurons: physiology /
                      Neuroprotective Agents: pharmacology / Protein Aggregates:
                      drug effects / Pyrazoles: pharmacology / Random Allocation /
                      Recognition, Psychology: drug effects / Recognition,
                      Psychology: physiology / Tauopathies: drug therapy /
                      Tauopathies: pathology / tau Proteins: genetics / tau
                      Proteins: metabolism /
                      3-(1,3-benzodioxol-5-yl)-5-(3-bromophenyl)-1H-pyrazole (NLM
                      Chemicals) / Benzodioxoles (NLM Chemicals) / MAPT protein,
                      human (NLM Chemicals) / Mapt protein, mouse (NLM Chemicals)
                      / Neuroprotective Agents (NLM Chemicals) / Protein
                      Aggregates (NLM Chemicals) / Pyrazoles (NLM Chemicals) / tau
                      Proteins (NLM Chemicals)},
      cin          = {AG Fuhrmann / AG Krauß / AG Remy / AG Ehninger},
      ddc          = {610},
      cid          = {I:(DE-2719)1011004 / I:(DE-2719)1011006 /
                      I:(DE-2719)1013006 / I:(DE-2719)1013005},
      pnm          = {341 - Molecular Signaling (POF3-341) / 342 - Disease
                      Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-341 / G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26439832},
      pmc          = {pmc:PMC4612332},
      doi          = {10.1007/s00401-015-1483-3},
      url          = {https://pub.dzne.de/record/138181},
}