ArticleBrain : a journal of neurology2024
Distinct ultrastructural phenotypes of glial and neuronal alpha-synuclein inclusions in multiple system atrophy.
Article in Brain : a journal of neurology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Exploring the therapeutic potential of Astragalin in Parkinson's disease: a network pharmacology approach.Annals of medicine and surgery (2012) · 2026Article
- A Structure-Activity Relationship Study of Alpha Synuclein PET Radiotracer M503-1619.Molecules (Basel, Switzerland) · 2026Article
- Modeling Parkinson's pathology in human iPSC dopaminergic neurons uncovers key mechanisms of Lewy body formation and heterogeneity.Science advances · 2026Article
- Myelin damage in donor skin differentiates between synucleinopathies.NPJ Parkinson's disease · 2026Article
- α-Synuclein in Lewy Body Diseases: Progress, Remaining Challenges and Future Perspectives.Expert reviews in molecular medicine · 2026Review
- Multiple system atrophy: integrating clinical phenotypes and multimodal biomarkers for early diagnosis.Frontiers in aging neuroscience · 2026Review
- Article
- Autophagy-Lysosome Pathway in Multiple System Atrophy Pathogenesis: The Best Is Yet to Come.International journal of molecular sciences · 2025Review
- Correlative light and electron microscopy for human brain and other biological models.Nature protocols · 2025Review
- Limbic Alzheimer's co-pathology in multiple system atrophy is associated with cognitive impairment and diagnostic inaccuracy.Acta neuropathologica · 2025Article
- Biological definitions of synucleinopathies should be anchored in clinical trajectories and encompass the complex biology of the disease.Journal of Parkinson's disease · 2025Review
- Neuronal α-synuclein toxicity is the key driver of neurodegeneration in multiple system atrophy.Brain : a journal of neurology · 2025Article
- Multiple sclerosis: what have we learned and can we still learn from electron microscopy.Cellular and molecular life sciences : CMLS · 2025Review
- Pathomechanisms of neuropsychiatric disturbances in atypical parkinsonian disorders: a current view.Journal of neural transmission (Vienna, Austria : 1996) · 2025Review
- Correlative light and electron microscopy imaging of proteinaceous deposits in cell cultures and brain tissues.Acta neuropathologica communications · 2025Article
- The Spectrum of Cognitive Impairment in Atypical Parkinsonism Syndromes: A Comprehensive Review of Current Understanding and Research.Diseases (Basel, Switzerland) · 2025Review
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9 authors.
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Abstract
Multiple system atrophy is characterized pathologically by the accumulation of alpha-synuclein (aSyn) into glial cytoplasmic inclusions (GCIs). The mechanism underlying the formation of GCIs is not well understood. In this study, correlative light and electron microscopy was employed to investigate aSyn pathology in the substantia nigra and putamen of post-mortem multiple system atrophy brain donors. Three distinct types of aSyn immuno-positive inclusions were identified in oligodendrocytes, neurons and dark cells presumed to be dark microglia. Oligodendrocytes contained fibrillar GCIs that were consistently enriched with lysosomes and peroxisomes, supporting the involvement of the autophagy pathway in aSyn aggregation in multiple system atrophy. Neuronal cytoplasmic inclusions exhibited ultrastructural heterogeneity resembling both fibrillar and membranous inclusions, linking multiple systems atrophy and Parkinson's disease. The novel aSyn pathology identified in the dark cells, displayed GCI-like fibrils or non-GCI-like ultrastructures suggesting various stages of aSyn accumulation in these cells. The observation of GCI-like fibrils within dark cells suggests these cells may be an important contributor to the origin or spread of pathological aSyn in multiple system atrophy. Our results suggest a complex interplay between multiple cell types that may underlie the formation of aSyn pathology in multiple system atrophy brain and highlight the need for further investigation into cell-specific disease pathologies in multiple system atrophy.
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