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Glial cytoplasmic inclusions in white matter oligodendrocytes of multiple system atrophy brains contain insoluble α‐synuclein
Abstract
Recently, α‐synuclein was shown to be a structural component of the filaments in Lewy bodies (LBs) of Parkinson's disease (PD), dementia with LBs (DLB) as well as the LB variant of Alzheimer's disease, and this suggests that α‐synuclein could play a mechanistic role in the pathogenesis of these disorders. To determine whether α‐synuclein is a building block of inclusions in other neurodegenerative movement disorders, we examined brains from patients with multiple system atrophy (MSA) and detected α‐synuclein, but not β‐ or γ‐synuclein, in glial cytoplasmic inclusions (GCIs) throughout the MSA brain. In MSA white matter, α‐synuclein–positive GCIs were restricted to oligodendrocytes, and α‐synuclein accumulated selectively in MSA white matter with α‐synuclein–positive GCIs. Taken together with evidence that LBs contain insoluble α‐synuclein, our data suggest that a reduction in the solubility of α‐synuclein may induce this protein to form filaments that aggregate into cytoplasmic inclusions, which contribute to the dysfunction or death of glial cells as well as neurons in neurodegenerative disorders with different phenotypes.
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“MSA is a synucleinopathy, however, unlike PD and dementia with Lewy bodies, in which α-syn accumulates and aggregates in neurons, MSA is characterized neuropathologically by α-syn-positive glial cytoplasmic inclusions (GCIs) in oligodendroglia [1, 42, 54, 58, 59].”
From Novel oligodendroglial alpha synuclein viral vector models of multiple system atrophy: studies in rodents and nonhuman primates (2017) · cites this paper as [54]
In the citing paper
“The pathological hallmark of MSA is the abnormal accumulation of α-syn in the cytoplasm of oligodendrocytes, named glial cytoplasmic inclusions (GCIs).271–275”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [272]
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“MSA is a synucleinopathy, however, unlike PD and dementia with Lewy bodies, in which α-syn accumulates and aggregates in neurons, MSA is characterized neuropathologically by α-syn-positive glial cytoplasmic inclusions (GCIs) in oligodendroglia [1, 42, 54, 58, 59].”
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“-Synuclein is the precursor protein of the non-A component of Alzheimer’s disease amyloid.9 Missense mutations in the -synuclein gene are linked to some cases of autosomal dominant familial PD.10,11 Furthermore, Lewy bodies, which are neuronal inclusions characteristic of PD,12 contain -synuclein.13,14 Recently, not o…”
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Detecting Alpha Synuclein Seeding Activity in Formaldehyde-Fixed MSA Patient Tissue by PMCA
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“The neuropathologic hallmark of MSA is the formation of argyrophilic glial cytoplasmic inclusions (GCIs) in oligodendroglia [13,14], consisting of α-synuclein (α-syn) [15-19].”
BackgroundDecreased α-synuclein expression in the aging mouse substantia nigra
Mak, S. K., McCormack, A. L., Langston, J. W., Kordower, J. H., & Monte, D. A. D. (2009) · Experimental Neurology · doi:10.1016/j.expneurol.2009.09.021 · Cited by 44
“…diseases. α-Synuclein is a major component of the intraneuronal inclusions, called Lewy bodies and Lewy neurites, which characterize the brain of patients affected by Parkinson's disease (PD), dementia with Lewy bodies, and multiple system atrophy (Spillantini et al., 1998; Tu et al., 1998).”
α-Synuclein binding to rab3a in multiple system atrophy
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NACP/α-synuclein immunoreactivity in diffuse neurofibrillary tangles with calcification (DNTC)
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“…and Lewy neurites in the brains of patients with PD and dementia with Lewy bodies (DLB), and in glial cytoplasmic inclusions in oligodendrocytes and in neuronal inclusions in patients with multiple system atrophy (MSA) (Spillantini et al. 1997, 1998a, b; Tu et al. 1998; Wakabayashi et al. 1998).”
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α-Synuclein Inclusions in Alzheimer and Lewy Body Diseases
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“Synucleinopathies, including Parkinson’s disease without (PD) and with dementia (PDD), dementia with Lewy bodies (DLBs), and multiple system atrophy (MSA) are a group of neurodegenerative diseases characterized by the abnormal accumulations of -synuclein (Spillantini et al., 1997, 1998a, b; Goedert and Spillantini, 19…”
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Metadata
- Authors
- Tu, P., Galvin, J. E., Baba, M., Giasson, B., Tomita, T., Leight, S., Nakajo, S., Iwatsubo, T., Trojanowski, J. Q., & Lee, V. M. ‐.
- Affiliations
- University of Pennsylvania (US)
- The University of Tokyo (JP)
- SHOWA Medical University (JP)
- Corresponding author
- Lee, Virginia M.‐Y.
- ORCID
- Venue
- Annals of Neurology
- Publisher
- Wiley
- Published
- 1998-09
- Volume
- 44
- Issue
- 3
- Pages
- 415-422
- ISSN
- 0364-5134 (ISSN-L)
- 1531-8249
- OpenAlex
- W2133068803
- Cited by
- 686
- References
- 43
- Citations by year
- 2026: 14 · 2025: 21 · 2024: 33 · 2023: 23 · 2022: 25 · 2021: 28 · 2020: 21 · 2019: 24 · 2018: 21 · 2017: 23 · 2016: 12 · 2015: 20 · 2014: 24 · 2013: 18 · 2012: 17
- FWCI
- 30.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Annals of Neurology (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Mental Health (MH.NS 31862)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- alpha-synuclein, glial cytoplasmic inclusions, multiple system atrophy, oligodendrocytes, white matter, Lewy bodies, protein aggregation, neurodegenerative movement disorders, immunoelectron microscopy, synuclein
- MeSH terms
- Adult, Aged, Aged, 80 and over, Antibodies, Inclusion Bodies, Female, Humans, Male, Actin Cytoskeleton, Middle Aged, Myelin Sheath, Nerve Tissue Proteins, Neuroglia, Oligodendroglia, Solubility, Multiple System Atrophy, Synucleins, alpha-Synuclein, gamma-Synuclein
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