ArticleMolecular and cellular neurosciences2014
Intracellular alpha-synuclein affects early maturation of primary oligodendrocyte progenitor cells.
Article in Molecular and cellular neurosciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 55 citations in OpenAlex.
- Sex-Dependent Effects of CSF1R-Mediated Myeloid Cell Depletion in a Mouse Model of Multiple System Atrophy.The European journal of neuroscience · 2026Article
- Alpha synuclein-mediated cytoskeletal dysfunction impairs myelination in human oligodendrocytes.Acta neuropathologica · 2025Article
- GBA1 inactivation in oligodendrocytes affects myelination and induces neurodegenerative hallmarks and lipid dyshomeostasis in mice.Molecular neurodegeneration · 2024Article
- Review
- Transcriptional and bioinformatic analysis of GABAFrontiers in molecular neuroscience · 2023Article
- Cellular Models of Alpha-Synuclein Aggregation: What Have We Learned and Implications for Future Study.Biomedicines · 2022Review
- Parkinson's disease and multiple system atrophy patient iPSC-derived oligodendrocytes exhibit alpha-synuclein-induced changes in maturation and immune reactive properties.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Review
- A historical review of multiple system atrophy with a critical appraisal of cellular and animal models.Journal of neural transmission (Vienna, Austria : 1996) · 2021Review
- Neurons and Glia Interplay in α-Synucleinopathies.International journal of molecular sciences · 2021Review
- Human alpha-synuclein overexpressing MBP29 mice mimic functional and structural hallmarks of the cerebellar subtype of multiple system atrophy.Acta neuropathologica communications · 2021Article
- BCAS1-positive immature oligodendrocytes are affected by the α-synuclein-induced pathology of multiple system atrophy.Acta neuropathologica communications · 2020Article
- alpha-Synuclein: a Modulator During Inflammatory CNS Demyelination.Journal of molecular neuroscience : MN · 2020Article
- T cell infiltration in both human multiple system atrophy and a novel mouse model of the disease.Acta neuropathologica · 2020Article
- In Search of Effective Treatments Targeting α-Synuclein Toxicity in Synucleinopathies: Pros and Cons.Frontiers in cell and developmental biology · 2020Review
- From Synaptic Protein to Prion: The Long and Controversial Journey of α-Synuclein.Frontiers in synaptic neuroscience · 2020Review
- Endogenous oligodendroglial alpha-synuclein and TPPP/p25α orchestrate alpha-synuclein pathology in experimental multiple system atrophy models.Acta neuropathologica · 2019Article
- Understanding the pathogenesis of multiple system atrophy: state of the art and future perspectives.Acta neuropathologica communications · 2019Review
- In vitro models of multiple system atrophy from primary cells to induced pluripotent stem cells.Journal of cellular and molecular medicine · 2018Review
- An Inducible Alpha-Synuclein Expressing Neuronal Cell Line Model for Parkinson's Disease1.Journal of Alzheimer's disease : JAD · 2018Article
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
Abstract
Myelin loss is a widespread neuropathological hallmark of the atypical parkinsonian disorder multiple system atrophy (MSA). On a cellular level, MSA is characterized by alpha-synuclein (aSyn)-positive glial cytoplasmic inclusions (GCIs) within mature oligodendrocytes leading to demyelination as well as axonal and neuronal loss. Oligodendrocyte progenitor cells (OPCs) represent a proliferative cell population distributed throughout the adult mammalian central nervous system. During remyelination, OPCs are recruited to sites of demyelination, differentiate, and finally replace dysfunctional mature oligodendrocytes. However, comprehensive studies investigating OPCs and remyelination processes in MSA are lacking. In the present study, we therefore investigate the effect of human aSyn (h-aSyn) on early primary rat OPC maturation. Upon lentiviral transduction, h-aSyn expressing OPCs exhibit fewer and shorter primary processes at the initiation of differentiation. Until day 4 of a 6day differentiation paradigm, h-aSyn expressing OPCs further show a severely delayed maturation evidenced by reduced myelin gene expression and increased levels of the progenitor marker platelet derived growth factor receptor-alpha (PDGFRα). Matching these results, OPCs that take up extracellular recombinant h-aSyn exhibit a similar delayed differentiation. In both experimental setups however, myelin gene expression is restored at day 6 of differentiation paralleled by decreased intracellular h-aSyn levels indicating a reverse correlation of h-aSyn and the differentiation potential of OPCs. Taken together, these findings suggest a tight link between the intracellular level of h-aSyn and maturation capacity of primary OPCs.
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