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@ARTICLE{Ulusoy:138081,
      author       = {Ulusoy, Ayse and Musgrove, Ruth E and Rusconi, Raffaella
                      and Klinkenberg, Michael and Helwig, Michael and Schneider,
                      Anja and Di Monte, Donato A},
      title        = {{N}euron-to-neuron α-synuclein propagation in vivo is
                      independent of neuronal injury.},
      journal      = {Acta Neuropathologica Communications},
      volume       = {3},
      number       = {1},
      issn         = {2051-5960},
      address      = {London},
      publisher    = {Biomed Central},
      reportid     = {DZNE-2020-04403},
      pages        = {13},
      year         = {2015},
      abstract     = {Interneuronal propagation of α-synuclein has been
                      demonstrated in a variety of experimental models and may be
                      involved in disease progression during the course of human
                      synucleinopathies. The aim of this study was to assess the
                      role that neuronal injury or, vice versa, cell integrity
                      could have in facilitating interneuronal α-synuclein
                      transfer and consequent protein spreading in an in vivo
                      animal model.Viral vectors carrying the DNA for human
                      α-synuclein were injected into the rat vagus nerve to
                      trigger protein overexpression in the medulla oblongata and
                      consequent spreading of human α-synuclein toward pons,
                      midbrain and forebrain. Two vector preparations sharing the
                      same viral construct were manufactured using identical
                      procedures with the exception of methods for their
                      purification. They were also injected at concentrations that
                      induced comparable levels of α-synuclein
                      transduction/overexpression in the medulla oblongata.
                      α-Synuclein load was associated with damage (at 6 weeks
                      post injection) and death (at 12 weeks) of medullary neurons
                      after treatment with only one of the two vector
                      preparations. Of note, neuronal injury and degeneration was
                      accompanied by a substantial reduction of caudo-rostral
                      propagation of human α-synuclein.Interneuronal α-synuclein
                      transfer, which underlies protein spreading from the medulla
                      oblongata to more rostral brain regions in this rat model,
                      is not a mere consequence of passive release from damaged or
                      dead neurons. Neuronal injury and degeneration did not
                      exacerbate α-synuclein propagation. In fact, data suggest
                      that cell-to-cell passage of α-synuclein may be
                      particularly efficient between intact, relatively healthy
                      neurons.},
      keywords     = {Animals / Brain: metabolism / Disease Models, Animal /
                      Female / Gene Transfer Techniques / Humans / Medulla
                      Oblongata: metabolism / Nerve Degeneration: metabolism /
                      Nerve Degeneration: pathology / Neural Pathways: metabolism
                      / Neural Pathways: pathology / Neurons: metabolism /
                      Neurons: pathology / Parkinson Disease: metabolism / Rats /
                      Rats, Sprague-Dawley / alpha-Synuclein: metabolism / SNCA
                      protein, human (NLM Chemicals) / alpha-Synuclein (NLM
                      Chemicals)},
      cin          = {AG Di Monte / AG Schneider Göttingen},
      ddc          = {610},
      cid          = {I:(DE-2719)1013008 / I:(DE-2719)1440011},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 344
                      - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25853980},
      pmc          = {pmc:PMC4369863},
      doi          = {10.1186/s40478-015-0198-y},
      url          = {https://pub.dzne.de/record/138081},
}