% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Decker:138082,
      author       = {Decker, Jochen Martin and Krüger, Lars and Sydow, Astrid
                      and Zhao, Shanting and Frotscher, Michael and Mandelkow,
                      Eckhard and Mandelkow, Eva-Maria},
      title        = {{P}ro-aggregant {T}au impairs mossy fiber plasticity due to
                      structural changes and {C}a(++) dysregulation.},
      journal      = {Acta Neuropathologica Communications},
      volume       = {3},
      number       = {1},
      issn         = {2051-5960},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {DZNE-2020-04404},
      pages        = {23},
      year         = {2015},
      abstract     = {We used an inducible mouse model expressing the Tau repeat
                      domain with the pro-aggregant mutation ΔK280 to analyze
                      presynaptic Tau pathology in the hippocampus.Expression of
                      pro-aggregant Tau(RDΔ) leads to phosphorylation,
                      aggregation and missorting of Tau in area CA3. To test
                      presynaptic pathophysiology we used electrophysiology in the
                      mossy fiber tract. Synaptic transmission was severely
                      disturbed in pro-aggregant Tau(RDΔ) and Tau-knockout mice.
                      Long-term depression of the mossy fiber tract failed in
                      pro-aggregant Tau(RDΔ) mice. We observed an increase in
                      bouton size, but a decline in numbers and presynaptic
                      markers. Both pre-and postsynaptic structural deficits are
                      preventable by inhibition of Tau(RDΔ) aggregation. Calcium
                      imaging revealed progressive calcium dysregulation in
                      boutons of pro-aggregant Tau(RDΔ) mice. In N2a cells we
                      observed this even in cells without tangle load, whilst in
                      primary hippocampal neurons transient Tau(RDΔ) expression
                      alone caused similar Ca(++) dysregulation. Ultrastructural
                      analysis revealed a severe depletion of synaptic vesicles
                      pool in accordance with synaptic transmission impairments.We
                      conclude that oligomer formation by Tau(RDΔ) causes pre-
                      and postsynaptic structural deterioration and Ca(++)
                      dysregulation which leads to synaptic plasticity deficits.},
      keywords     = {Animals / Calcium: physiology / Calcium Signaling:
                      physiology / Cell Culture Techniques / Disease Models,
                      Animal / Electrophysiology / Hippocampus: physiology /
                      Long-Term Potentiation: physiology / Mice / Mice, Knockout /
                      Mossy Fibers, Hippocampal: physiology / Neuronal Plasticity:
                      physiology / Synaptic Transmission: physiology / tau
                      Proteins: deficiency / tau Proteins: genetics / tau
                      Proteins: metabolism / tau Proteins (NLM Chemicals) /
                      Calcium (NLM Chemicals)},
      cin          = {AG Mandelkow 2 / Tech Transfer / AG Mandelkow 1},
      ddc          = {610},
      cid          = {I:(DE-2719)1013015 / I:(DE-2719)1030028 /
                      I:(DE-2719)1013014},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25853683},
      pmc          = {pmc:PMC4384391},
      doi          = {10.1186/s40478-015-0193-3},
      url          = {https://pub.dzne.de/record/138082},
}