ReviewMolecular neurodegeneration2022
Multiple system atrophy: α-Synuclein strains at the neuron-oligodendrocyte crossroad.
Review in Molecular neurodegeneration, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed.
- Beyond the Wiring: White Matter as a Dynamic Regulator of Brain Function and Disease.Neuroscience bulletin · 2026Review
- Setting shapes the strain: Untangling alpha-synuclein heterogeneity.Neural regeneration research · 2026Article
- Lipidomic perspectives on the role of lactosylceramides in inflammation and disease: A narrative review.Expert reviews in molecular medicine · 2026Review
- Single-nucleus brain transcriptomics reveals microglia dysfunction in multiple system atrophy.Nature communications · 2026Article
- Alpha-Synuclein in Neurodegeneration: From Shared Biology to Disease-Specific Phenotypes.Cells · 2026Review
- Multiple system atrophy: integrating clinical phenotypes and multimodal biomarkers for early diagnosis.Frontiers in aging neuroscience · 2026Review
- Systemic delivery of anti-sense oligonucleotide targeting α-synuclein for treatment in a mouse model of multiple system atrophy.Frontiers in aging neuroscience · 2026Article
- Internalized SNCA/α-synuclein fibrils become truncated and resist degradation in neurons while glial cells rapidly degrade SNCA fibrils.Autophagy · 2026Article
- Generation and characterization of human induced pluripotent stem cells from neuropathologically confirmed multiple system atrophy patient-derived fibroblasts.Frontiers in immunology · 2026Article
- Serum Neurofilament light chain predicts autonomic symptoms in early Parkinson's disease.Neurodegenerative disease management · 2025Article
- Distinct AQP4 Alterations in Movement Disorders with Primary Synucleinopathy.Movement disorders : official journal of the Movement Disorder Society · 2025Article
- Exploring the skin as an open window onto neurodegenerative diseases.Translational neurodegeneration · 2025Review
- Systemic delivery of anti-sense oligonucleotide targeting a-synuclein for the treatment of multiple system atrophy.Research square · 2025Article
- Neuronal α-synuclein toxicity is the key driver of neurodegeneration in multiple system atrophy.Brain : a journal of neurology · 2025Article
- GATA Transcription Factors: A Cross-Road for Erythropoiesis, Neurodevelopment, and Synucleinopathies.Developmental neurobiology · 2025Review
- Role of the Intestinal Microbiota in the Molecular Pathogenesis of Atypical Parkinsonian Syndromes.International journal of molecular sciences · 2025Review
- Parkinson's Spectrum Mechanisms in Pregnancy: Exploring Hypothetical Scenarios for MSA in the Era of ART.International journal of molecular sciences · 2025Review
- Fibrinogen degradation products exacerbate alpha-synuclein aggregation by inhibiting autophagy via downregulation of Beclin1 in multiple system atrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- Emerging targets of α-synuclein spreading in α-synucleinopathies: a review of mechanistic pathways and interventions.Molecular neurodegeneration · 2025Review
- Subtle concentration changes in zinc hold the key to fibrillation of α-synuclein: an updated insight on the micronutrient's role in prevention of neurodegenerative disorders.Frontiers in molecular biosciences · 2025Review
Corrections and comments
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Authors and funding
2 authors.
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Abstract
The aberrant accumulation of α-Synuclein within oligodendrocytes is an enigmatic, pathological feature specific to Multiple system atrophy (MSA). Since the characterization of the disease in 1969, decades of research have focused on unravelling the pathogenic processes that lead to the formation of oligodendroglial cytoplasmic inclusions. The discovery of aggregated α-Synuclein (α-Syn) being the primary constituent of glial cytoplasmic inclusions has spurred several lines of research investigating the relationship between the pathogenic accumulation of the protein and oligodendrocytes. Recent developments have identified the ability of α-Syn to form conformationally distinct "strains" with varying behavioral characteristics and toxicities. Such "strains" are potentially disease-specific, providing insight into the enigmatic nature of MSA. This review discusses the evidence for MSA-specific α-Syn strains, highlighting the current methods for detecting and characterizing MSA patient-derived α-Syn. Given the differing behaviors of α-Syn strains, we explore the seeding and spreading capabilities of MSA-specific strains, postulating their influence on the aggressive nature of the disease. These ideas culminate into one key question: What causes MSA-specific strain formation? To answer this, we discuss the interplay between oligodendrocytes, neurons and α-Syn, exploring the ability of each cell type to contribute to the aggregate formation while postulating the effect of additional variables such as protein interactions, host characteristics and environmental factors. Thus, we propose the idea that MSA strain formation results from the intricate interrelation between neurons and oligodendrocytes, with deficits in each cell type required to initiate α-Syn aggregation and MSA pathogenesis.
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