ArticleCerebellum (London, England)2024
Neuropathology of Multiple System Atrophy, a Glioneuronal Degenerative Disease.
Article in Cerebellum (London, England), 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 14 citations in OpenAlex.
- Review
- Autonomic dysfunction in multiple system atrophy: from pathophysiology to clinical manifestations.Annals of medicine · 2025Review
- Limbic Alzheimer's co-pathology in multiple system atrophy is associated with cognitive impairment and diagnostic inaccuracy.Acta neuropathologica · 2025Article
- Neuronal α-synuclein toxicity is the key driver of neurodegeneration in multiple system atrophy.Brain : a journal of neurology · 2025Article
- Tubulin Polymerization Promoting Proteins: Functional Diversity With Implications in Neurological Disorders.Journal of neuroscience research · 2025Review
- Protein Pathologies in Oligodendroglia in Neurodegenerative Diseases.Advances in neurobiology · 2025Review
- N-terminus α-synuclein detection reveals new and more diverse aggregate morphologies in multiple system atrophy and Parkinson's disease.Translational neurodegeneration · 2024Article
- Multiple system atrophy: at the crossroads of cellular, molecular and genetic mechanisms.Nature reviews. Neuroscience · 2023Review
- Alpha synuclein post translational modifications: potential targets for Parkinson's disease therapy?Frontiers in molecular neuroscience · 2023Review
- Multiple system atrophy: α-Synuclein strains at the neuron-oligodendrocyte crossroad.Molecular neurodegeneration · 2022Review
- Multiple system atrophy prions transmit neurological disease to mice expressing wild-type human α-synuclein.Acta neuropathologica · 2022Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Multiple system atrophy (MSA) is a fatal disease characterized pathologically by the widespread occurrence of aggregated α-synuclein in the oligodendrocytes referred to as glial cytoplasmic inclusions (GCIs). α-Synuclein aggregates are also found in the oligodendroglial nuclei and neuronal cytoplasm and nuclei. It is uncertain whether the primary source of α-synuclein in GCIs is originated from neurons or oligodendrocytes. Accumulating evidence suggests that there are two degenerative processes in this disease. One possibility is that numerous GCIs are associated with the impairment of oligo-myelin-axon-neuron complex, and the other is that neuronal inclusion pathology is also a primary event from the early stage. Both oligodendrocytes and neurons may be primarily affected in MSA, and the damage of one cell type contributes to the degeneration of the other. Vesicle-mediated transport plays a key role in the nuclear translocation of α-synuclein as well as in the formation of glial and neuronal α-synuclein inclusions. Recent studies have shown that impairment of autophagy can occur along with or as a result of α-synuclein accumulation in the brain of MSA and Lewy body disease. Activated autophagy may be implicated in the therapeutic approach for α-synucleinopathies.
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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.