ArticleStem cell reports2018
Pathological Endogenous α-Synuclein Accumulation in Oligodendrocyte Precursor Cells Potentially Induces Inclusions in Multiple System Atrophy.
Article in Stem cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.
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Who cites it
53 citing papers in PubMed, 97 citations in OpenAlex.
- α-Synuclein overexpression increases the tropism of pre-formed fibrils and MSA-patient derived seeds towards oligodendroglia.Acta neuropathologica communications · 2026Article
- Alpha-Synuclein in Neurodegeneration: From Shared Biology to Disease-Specific Phenotypes.Cells · 2026Review
- Anti-TLR2 immunotherapy modulates neuron-to-oligodendrocyte propagation of α-synuclein in mouse and human models.Nature communications · 2026Article
- Multiple system atrophy: advances in pathogenesis and emerging therapeutic strategies.Journal of neurology · 2025Review
- Autophagy-Lysosome Pathway in Multiple System Atrophy Pathogenesis: The Best Is Yet to Come.International journal of molecular sciences · 2025Review
- Dysregulation of Monounsaturated Fatty Acids is Related to α-Synuclein in Multiple System Atrophy.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Neuronal α-synuclein toxicity is the key driver of neurodegeneration in multiple system atrophy.Brain : a journal of neurology · 2025Article
- Protein Pathologies in Oligodendroglia in Neurodegenerative Diseases.Advances in neurobiology · 2025Review
- A lipid nanoparticle-based oligodendrocyte-specific mRNA therapy.Molecular therapy. Nucleic acids · 2024Article
- A novel mouse model for investigating α-synuclein aggregates in oligodendrocytes: implications for the glial cytoplasmic inclusions in multiple system atrophy.Molecular brain · 2024Article
- A topographical atlas of α-synuclein dosage and cell type-specific expression in adult mouse brain and peripheral organs.NPJ Parkinson's disease · 2024Article
- GBA1 inactivation in oligodendrocytes affects myelination and induces neurodegenerative hallmarks and lipid dyshomeostasis in mice.Molecular neurodegeneration · 2024Article
- Perspective Strategies for Interventions in Parkinsonism: Remedying the Neglected Role of TPPP.Cells · 2024Article
- Relationship among α‑synuclein, aging and inflammation in Parkinson's disease (Review).Experimental and therapeutic medicine · 2024Review
- What Are the Roles of Oligodendrocyte Precursor Cells in Normal and Pathologic Conditions?Neurology · 2023Article
- A functional role for alpha-synuclein in neuroimmune responses.Journal of neuroimmunology · 2023Review
- Review
- Understanding the Role of CDH4 in Multiple System Atrophy Brain.Journal of Parkinson's disease · 2023Article
- Multiple system atrophy: α-Synuclein strains at the neuron-oligodendrocyte crossroad.Molecular neurodegeneration · 2022Review
- Autophagy mediates the clearance of oligodendroglial SNCA/alpha-synuclein and TPPP/p25A in multiple system atrophy models.Autophagy · 2022Article
Corrections and comments
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Authors and funding
17 authors at 7 institutions in 2 countries.
Funding
Abstract
Glial cytoplasmic inclusions (GCIs), commonly observed as α-synuclein (α-syn)-positive aggregates within oligodendrocytes, are the pathological hallmark of multiple system atrophy. The origin of α-syn in GCIs is uncertain; there is little evidence of endogenous α-syn expression in oligodendrocyte lineage cells, oligodendrocyte precursor cells (OPCs), and mature oligodendrocytes (OLGs). Here, based on in vitro analysis using primary rat cell cultures, we elucidated that preformed fibrils (PFFs) generated from recombinant human α-syn trigger multimerization and an upsurge of endogenous α-syn in OPCs, which is attributable to insufficient autophagic proteolysis. RNA-seq analysis of OPCs revealed that α-syn PFFs interfered with the expression of proteins associated with neuromodulation and myelination. Furthermore, we detected cytoplasmic α-syn inclusions in OLGs through differentiation of OPCs pre-incubated with PFFs. Overall, our findings suggest the possibility of endogenous α-syn accumulation in OPCs that contributes to GCI formation and perturbation of neuronal/glial support in multiple system atrophy brains.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.