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@ARTICLE{Hllerhage:137713,
      author       = {Höllerhage, Matthias and Deck, Roman and De Andrade,
                      Anderson and Respondek, Gesine and Xu, Hong and Rösler,
                      Thomas W and Salama, Mohamed and Carlsson, Thomas and
                      Yamada, Elizabeth S and Gad El Hak, Seham A and Goedert,
                      Michel and Oertel, Wolfgang H and Höglinger, Günter U},
      title        = {{P}iericidin {A} aggravates {T}au pathology in {P}301{S}
                      transgenic mice.},
      journal      = {PLOS ONE},
      volume       = {9},
      number       = {12},
      issn         = {1932-6203},
      address      = {San Francisco, California, US},
      publisher    = {PLOS},
      reportid     = {DZNE-2020-04035},
      pages        = {e113557},
      year         = {2014},
      abstract     = {The P301S mutation in exon 10 of the tau gene causes a
                      hereditary tauopathy. While mitochondrial complex I
                      inhibition has been linked to sporadic tauopathies.
                      Piericidin A is a prototypical member of the group of the
                      piericidins, a class of biologically active natural complex
                      I inhibitors, isolated from streptomyces spp. with global
                      distribution in marine and agricultural habitats. The aim of
                      this study was to determine whether there is a pathogenic
                      interaction of the environmental toxin piericidin A and the
                      P301S mutation.Transgenic mice expressing human tau with the
                      P301S-mutation (P301S+/+) and wild-type mice at 12 weeks of
                      age were treated subcutaneously with vehicle (N = 10
                      P301S+/+, N = 7 wild-type) or piericidin A (N = 9
                      P301S+/+, N = 9 wild-type mice) at a dose of 0.5 mg/kg/d
                      for a period of 28 days via osmotic minipumps. Tau pathology
                      was measured by stereological counts of cells immunoreative
                      with antibodies against phosphorylated tau (AD2, AT8, AT180,
                      and AT100) and corresponding Western blot
                      analysis.Piericidin A significantly increased the number of
                      phospho-tau immunoreactive cells in the cerebral cortex in
                      P301S+/+ mice, but only to a variable and mild extent in
                      wild-type mice. Furthermore, piericidin A led to increased
                      levels of pathologically phosphorylated tau only in P301S+/+
                      mice. While we observed no apparent cell loss in the frontal
                      cortex, the synaptic density was reduced by piericidin A
                      treatment in P301S+/+ mice.This study shows that exposure to
                      piericidin A aggravates the course of genetically determined
                      tau pathology, providing experimental support for the
                      concept of gene-environment interaction in the etiology of
                      tauopathies.},
      keywords     = {Animals / Cerebral Cortex: drug effects / Cerebral Cortex:
                      pathology / Exons: genetics / Gene-Environment Interaction /
                      Humans / Mice / Mice, Transgenic / Mutation /
                      Phosphorylation: drug effects / Pyridines: toxicity /
                      Synapses: drug effects / Synapses: pathology / Tauopathies:
                      genetics / Tauopathies: metabolism / Tauopathies: pathology
                      / tau Proteins: genetics / tau Proteins: metabolism /
                      Pyridines (NLM Chemicals) / tau Proteins (NLM Chemicals) /
                      piericidin A (NLM Chemicals)},
      cin          = {AG Höglinger 1},
      ddc          = {610},
      cid          = {I:(DE-2719)1110002},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25437199},
      pmc          = {pmc:PMC4249965},
      doi          = {10.1371/journal.pone.0113557},
      url          = {https://pub.dzne.de/record/137713},
}