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  Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies.

Wagner, J., Krauss, S., Shi, S., Ryazanov, S., Steffen, J., Miklitz, C., et al. (2015). Reducing tau aggregates with anle138b delays disease progression in a mouse model of tauopathies. Acta Neuropathologica, 130(5), 619-631. doi:10.1007/s00401-015-1483-3.

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Item Permalink: http://hdl.handle.net/11858/00-001M-0000-0029-06FA-0 Version Permalink: http://hdl.handle.net/11858/00-001M-0000-0029-1E2F-4
Genre: Journal Article

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 Creators:
Wagner, J., Author
Krauss, S., Author
Shi, S., Author
Ryazanov, S.1, Author              
Steffen, J., Author
Miklitz, C., Author
Leonov, A.2, Author              
Kleinknecht, A., Author
Göricke, B., Author
Weishaupt, J. H., Author
Weckbecker, D., Author
Reiner, A. M., Author
Zinth, W., Author
Levin, J., Author
Ehninger, D., Author
Remy, S., Author
Kretzschmar, H. A., Author
Griesinger, C.2, Author              
Giese, A., Author
Fuhrmann, M., Author
Affiliations:
1Department of NMR-based Structural Biology, MPI for biophysical chemistry, Max Planck Society, escidoc:578567              
2Department of NMR Based Structural Biology, MPI for biophysical chemistry, Max Planck Society, escidoc:578567              

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Free keywords: Alzheimer's disease; Tauopathy; Tau; Protein aggregation; Anle138b; Tau aggregation inhibitor
 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.

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Language(s): eng - English
 Dates: 2015-11
 Publication Status: Published in print
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 Rev. Method: Peer
 Identifiers: DOI: 10.1007/s00401-015-1483-3
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Title: Acta Neuropathologica
Source Genre: Journal
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Pages: - Volume / Issue: 130 (5) Sequence Number: - Start / End Page: 619 - 631 Identifier: -