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@ARTICLE{Kim:169133,
      author       = {Kim, Tae-Kyung and Bae, Eun-Jin and Jung, Byung Chul and
                      Choi, Minsun and Shin, Soo Jean and Park, Sung Jun and Kim,
                      Jeong Tae and Jung, Min Kyo and Ulusoy, Ayse and Song,
                      Mi-Young and Lee, Jun Sung and Lee, He-Jin and Di Monte,
                      Donato A and Lee, Seung-Jae},
      title        = {{I}nflammation promotes synucleinopathy propagation.},
      journal      = {Experimental $\&$ molecular medicine},
      volume       = {54},
      number       = {12},
      issn         = {2092-6413},
      address      = {Seoul},
      publisher    = {Soc.},
      reportid     = {DZNE-2023-00012},
      pages        = {2148-2161},
      year         = {2022},
      note         = {ISSN 2092-6413 not unique: **2 hits**.},
      abstract     = {The clinical progression of neurodegenerative diseases
                      correlates with the spread of proteinopathy in the brain.
                      The current understanding of the mechanism of proteinopathy
                      spread is far from complete. Here, we propose that
                      inflammation is fundamental to proteinopathy spread. A
                      sequence variant of α-synuclein (V40G) was much less
                      capable of fibril formation than wild-type α-synuclein
                      (WT-syn) and, when mixed with WT-syn, interfered with its
                      fibrillation. However, when V40G was injected
                      intracerebrally into mice, it induced aggregate spreading
                      even more effectively than WT-syn. Aggregate spreading was
                      preceded by sustained microgliosis and inflammatory
                      responses, which were more robust with V40G than with
                      WT-syn. Oral administration of an anti-inflammatory agent
                      suppressed aggregate spreading, inflammation, and behavioral
                      deficits in mice. Furthermore, exposure of cells to
                      inflammatory cytokines increased the cell-to-cell
                      propagation of α-synuclein. These results suggest that the
                      inflammatory microenvironment is the major driver of the
                      spread of synucleinopathy in the brain.},
      keywords     = {Mice / Animals / alpha-Synuclein: genetics /
                      alpha-Synuclein: metabolism / Synucleinopathies / Brain:
                      metabolism / Neurodegenerative Diseases / Inflammation /
                      Disease Models, Animal / alpha-Synuclein (NLM Chemicals)},
      cin          = {AG Di Monte},
      ddc          = {540},
      cid          = {I:(DE-2719)1013008},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC9794777},
      pubmed       = {pmid:36473937},
      doi          = {10.1038/s12276-022-00895-w},
      url          = {https://pub.dzne.de/record/169133},
}