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@ARTICLE{Stuendl:138377,
      author       = {Stuendl, Anne and Kunadt, Marcel and Kruse, Niels and
                      Bartels, Claudia and Moebius, Wiebke and Danzer, Karin M and
                      Mollenhauer, Brit and Schneider, Anja},
      title        = {{I}nduction of α-synuclein aggregate formation by {CSF}
                      exosomes from patients with {P}arkinson's disease and
                      dementia with {L}ewy bodies.},
      journal      = {Brain},
      volume       = {139},
      number       = {2},
      issn         = {0006-8950},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {DZNE-2020-04699},
      pages        = {481-494},
      year         = {2016},
      abstract     = {Extracellular α-synuclein has been proposed as a crucial
                      mechanism for induction of pathological aggregate formation
                      in previously healthy cells. In vitro, extracellular
                      α-synuclein is partially associated with exosomal vesicles.
                      Recently, we have provided evidence that exosomal
                      α-synuclein is present in the central nervous system in
                      vivo. We hypothesized that exosomal α-synuclein species
                      from patients with α-synuclein related neurodegeneration
                      serve as carriers for interneuronal disease transmission. We
                      isolated exosomes from cerebrospinal fluid from patients
                      with Parkinson's disease, dementia with Lewy bodies,
                      progressive supranuclear palsy as a non-α-synuclein related
                      disorder that clinically overlaps with Parkinson's disease,
                      and neurological controls. Cerebrospinal fluid exosome
                      numbers, α-synuclein protein content of cerebrospinal fluid
                      exosomes and their potential to induce oligomerization of
                      α-synuclein were analysed. The quantification of
                      cerebrospinal fluid exosomal α-synuclein showed distinct
                      differences between patients with Parkinson's disease and
                      dementia with Lewy bodies. In addition, exosomal
                      α-synuclein levels correlated with the severity of
                      cognitive impairment in cross-sectional samples from
                      patients with dementia with Lewy bodies. Importantly,
                      cerebrospinal fluid exosomes derived from Parkinson's
                      disease and dementia with Lewy bodies induce oligomerization
                      of α-synuclein in a reporter cell line in a dose-dependent
                      manner. Our data suggest that cerebrospinal fluid exosomes
                      from patients with Parkinson's disease and dementia with
                      Lewy bodies contain a pathogenic species of α-synuclein,
                      which could initiate oligomerization of soluble α-synuclein
                      in target cells and confer disease pathology.},
      keywords     = {Cerebrospinal Fluid: metabolism / Cohort Studies /
                      Cross-Sectional Studies / Exosomes: metabolism / Female /
                      Follow-Up Studies / Humans / Lewy Body Disease:
                      cerebrospinal fluid / Lewy Body Disease: metabolism /
                      Longitudinal Studies / Male / Parkinson Disease:
                      cerebrospinal fluid / Parkinson Disease: metabolism /
                      Protein Aggregates: physiology / alpha-Synuclein:
                      biosynthesis / alpha-Synuclein: cerebrospinal fluid /
                      Protein Aggregates (NLM Chemicals) / alpha-Synuclein (NLM
                      Chemicals)},
      cin          = {AG Schneider Göttingen},
      ddc          = {610},
      cid          = {I:(DE-2719)1440011},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26647156},
      pmc          = {pmc:PMC4805087},
      doi          = {10.1093/brain/awv346},
      url          = {https://pub.dzne.de/record/138377},
}