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@ARTICLE{Emmenegger:162869,
      author       = {Emmenegger, Marc and De Cecco, Elena and Hruska-Plochan,
                      Marian and Eninger, Timo and Schneider, Matthias M and
                      Barth, Melanie and Tantardini, Elena and de Rossi, Pierre
                      and Bacioglu, Mehtap and Langston, Rebekah G and Kaganovich,
                      Alice and Bengoa-Vergniory, Nora and Gonzalez-Guerra,
                      Andrès and Avar, Merve and Heinzer, Daniel and Reimann,
                      Regina and Häsler, Lisa M and Herling, Therese W and
                      Matharu, Naunehal S and Landeck, Natalie and Luk, Kelvin and
                      Melki, Ronald and Kahle, Philipp J and Hornemann, Simone and
                      Knowles, Tuomas P J and Cookson, Mark R and Polymenidou,
                      Magdalini and Jucker, Mathias and Aguzzi, Adriano},
      title        = {{LAG}3 is not expressed in human and murine neurons and
                      does not modulate α-synucleinopathies.},
      journal      = {EMBO molecular medicine},
      volume       = {13},
      number       = {9},
      issn         = {1757-4684},
      address      = {Heidelberg},
      publisher    = {EMBO Press},
      reportid     = {DZNE-2021-01524},
      pages        = {e14745},
      year         = {2021},
      note         = {(CC BY)},
      abstract     = {While the initial pathology of Parkinson's disease and
                      other α-synucleinopathies is often confined to
                      circumscribed brain regions, it can spread and progressively
                      affect adjacent and distant brain locales. This process may
                      be controlled by cellular receptors of α-synuclein fibrils,
                      one of which was proposed to be the LAG3 immune checkpoint
                      molecule. Here, we analysed the expression pattern of LAG3
                      in human and mouse brains. Using a variety of methods and
                      model systems, we found no evidence for LAG3 expression by
                      neurons. While we confirmed that LAG3 interacts with
                      α-synuclein fibrils, the specificity of this interaction
                      appears limited. Moreover, overexpression of LAG3 in
                      cultured human neural cells did not cause any worsening of
                      α-synuclein pathology ex vivo. The overall survival of
                      A53T α-synuclein transgenic mice was unaffected by LAG3
                      depletion, and the seeded induction of α-synuclein lesions
                      in hippocampal slice cultures was unaffected by LAG3
                      knockout. These data suggest that the proposed role of LAG3
                      in the spreading of α-synucleinopathies is not universally
                      valid.},
      keywords     = {Animals / Humans / Mice / Mice, Transgenic / Neurons /
                      Parkinson Disease / Synucleinopathies / alpha-Synuclein:
                      genetics / LAG3 (Other) / neurodegeneration (Other) /
                      prionoids (Other) / α-synuclein (Other) / alpha-Synuclein
                      (NLM Chemicals)},
      cin          = {AG Jucker / AG Kahle 2},
      ddc          = {610},
      cid          = {I:(DE-2719)1210001 / I:(DE-2719)1210000-4},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34309222},
      pmc          = {pmc:PMC8422075},
      doi          = {10.15252/emmm.202114745},
      url          = {https://pub.dzne.de/record/162869},
}