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@ARTICLE{Zhang:263624,
      author       = {Zhang, Shuyu and Dauer, Karina and Strohäker, Timo and
                      Tatenhorst, Lars and Caldi Gomes, Lucas and Mayer, Simon and
                      Jung, Byung Chul and Kim, Woojin S and Lee, Seung-Jae and
                      Becker, Stefan and Liesche-Starnecker, Friederike and
                      Zweckstetter, Markus and Lingor, Paul},
      title        = {{A}lpha-synuclein fibrils amplified from multiple system
                      atrophy and {P}arkinson's disease patient brain spread after
                      intracerebral injection into mouse brain.},
      journal      = {Brain pathology},
      volume       = {33},
      number       = {5},
      issn         = {1015-6305},
      address      = {Oxford},
      publisher    = {Wiley-Blackwell},
      reportid     = {DZNE-2023-00843},
      pages        = {e13196},
      year         = {2023},
      abstract     = {Parkinson's disease (PD), multiple system atrophy (MSA),
                      and dementia with Lewy bodies (DLB) are neurodegenerative
                      disorders with alpha-synuclein (α-syn) aggregation
                      pathology. Different strains of α-syn with unique
                      properties are suggested to cause distinct clinical and
                      pathological manifestations resulting in PD, MSA, or DLB. To
                      study individual α-syn spreading patterns, we injected
                      α-syn fibrils amplified from brain homogenates of two MSA
                      patients and two PD patients into the brains of C57BI6/J
                      mice. Antibody staining against pS129-α-syn showed that
                      α-syn fibrils amplified from the brain homogenates of the
                      four different patients caused different levels of α-syn
                      spreading. The strongest α-syn pathology was triggered by
                      α-syn fibrils of one of the two MSA patients, followed by
                      comparable pS129-α-syn induction by the second MSA and one
                      PD patient material. Histological analysis using an antibody
                      against Iba1 further showed that the formation of
                      pS129-α-syn is associated with increased microglia
                      activation. In contrast, no differences in dopaminergic
                      neuron numbers or co-localization of α-syn in
                      oligodendrocytes were observed between the different groups.
                      Our data support the spreading of α-syn pathology in MSA,
                      while at the same time pointing to spreading heterogeneity
                      between different patients potentially driven by individual
                      patient immanent factors.},
      keywords     = {Animals / Mice / alpha-Synuclein: metabolism / Parkinson
                      Disease: pathology / Multiple System Atrophy: pathology /
                      Brain: pathology / Synucleinopathies: pathology / Antibodies
                      / Snca protein, mouse (NLM Chemicals) / Parkinson's disease
                      (Other) / alpha-synuclein (Other) / microglia (Other) /
                      multiple system atrophy (Other) / patient-derived fibrils
                      (Other) / alpha-Synuclein (NLM Chemicals) / Antibodies (NLM
                      Chemicals)},
      cin          = {AG Zweckstetter},
      ddc          = {610},
      cid          = {I:(DE-2719)1410001},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC10467043},
      pubmed       = {pmid:37485772},
      doi          = {10.1111/bpa.13196},
      url          = {https://pub.dzne.de/record/263624},
}