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@ARTICLE{SalazarCampos:275862,
      author       = {Salazar Campos, José María and Burbulla, Lena F and
                      Jäkel, Sarah},
      title        = {{A}re oligodendrocytes bystanders or drivers of
                      {P}arkinson's disease pathology?},
      journal      = {PLoS biology},
      volume       = {23},
      number       = {1},
      issn         = {1544-9173},
      address      = {Lawrence, KS},
      publisher    = {PLoS},
      reportid     = {DZNE-2025-00097},
      pages        = {e3002977},
      year         = {2025},
      abstract     = {The major pathological feature of Parkinson 's disease
                      (PD), the second most common neurodegenerative disease and
                      most common movement disorder, is the predominant
                      degeneration of dopaminergic neurons in the substantia
                      nigra, a part of the midbrain. Despite decades of research,
                      the molecular mechanisms of the origin of the disease remain
                      unknown. While the disease was initially viewed as a purely
                      neuronal disorder, results from single-cell transcriptomics
                      have suggested that oligodendrocytes may play an important
                      role in the early stages of Parkinson's. Although these
                      findings are of high relevance, particularly to the search
                      for effective disease-modifying therapies, the actual
                      functional role of oligodendrocytes in Parkinson's disease
                      remains highly speculative and requires a concerted
                      scientific effort to be better understood. This Unsolved
                      Mystery discusses the limited understanding of
                      oligodendrocytes in PD, highlighting unresolved questions
                      regarding functional changes in oligodendroglia, the role of
                      myelin in nigral dopaminergic neurons, the impact of the
                      toxic environment, and the aggregation of alpha-synuclein
                      within oligodendrocytes.},
      keywords     = {Oligodendroglia: metabolism / Oligodendroglia: pathology /
                      Parkinson Disease: pathology / Parkinson Disease: metabolism
                      / Parkinson Disease: genetics / Humans / alpha-Synuclein:
                      metabolism / Dopaminergic Neurons: metabolism / Dopaminergic
                      Neurons: pathology / Substantia Nigra: metabolism /
                      Substantia Nigra: pathology / Animals / Myelin Sheath:
                      metabolism / Myelin Sheath: pathology / alpha-Synuclein (NLM
                      Chemicals)},
      cin          = {AG Burbulla},
      ddc          = {610},
      cid          = {I:(DE-2719)5000074},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:39777410},
      pmc          = {pmc:PMC11709285},
      doi          = {10.1371/journal.pbio.3002977},
      url          = {https://pub.dzne.de/record/275862},
}