Absence of α-synuclein mRNA expression in normal and multiple system atrophy oligodendroglia
Abstract
alpha-Synuclein is a major constituent of glial cytoplasmic inclusions (GCIs), which are pathognomic for multiple system atrophy (MSA). We have previously demonstrated that in normal human brain, alpha-synuclein mRNA has a restricted pattern of neuronal expression and no apparent glial expression. The current study used double-label in situ hybridization to determine if alpha-synuclein mRNA is expressed by oligodendroglia of MSA cases. Analysis of MSA brain tissue revealed depletion of regional signal for this transcript in many brain areas due to extensive neurodegeneration. Cellular analysis of oligodendroglia in crus cerebri, a GCI-rich region ventral to substantia nigra, revealed an absence of alpha-synuclein mRNA signal in control and MSA cases. However, an abundance of this transcript was detected in melanin-containing neurons of substantia nigra. Therefore, oligodendroglia do not express alpha-synuclein mRNA in control and MSA cases suggesting that involvement of alpha-synuclein in GCI pathology of MSA is due to its ectopic presence in oligodendroglia.
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α-syn is transiently expressed in oligodendroglia precursor cells during development, but reduced in mature oligodendrocytes.
“It has been shown that α-syn is transiently expressed in oligodendroglia precursor cells during development, but reduced in mature oligodendrocytes [30, 37, 48].”
From Novel oligodendroglial alpha synuclein viral vector models of multiple system atrophy: studies in rodents and nonhuman primates (2017) · cites this paper as [37]
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References 34 · Cited by 198
- Authors
- Miller, D. W., Johnson, J. M., Solano, S. M., Hollingsworth, Z. R., Standaert, D. G., & Young, A. B.
- Affiliations
- National Institutes of Health (US)
- Massachusetts General Hospital (US)
- Venue
- Journal of Neural Transmission
- Published
- 2005-12
- Volume
- 112
- Issue
- 12
- Pages
- 1613-1624
- ISSN
- 0300-9564 (ISSN-L)
- 1435-1463
- OpenAlex
- W1999883522
- Cited by
- 198
- References
- 34
- Citations by year
- 2026: 3 · 2025: 8 · 2024: 15 · 2023: 7 · 2022: 15 · 2021: 13 · 2020: 9 · 2019: 15 · 2018: 12 · 2017: 14 · 2016: 5 · 2015: 15 · 2014: 18 · 2013: 11 · 2012: 7
- FWCI
- 2.81
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Journal of Neural Transmission (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5p50ns038372-10)
- National Institute of Mental Health (R24MH068855, MH 068855)
- National Institute of Neurological Disorders and Stroke (NS 038372)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Keywords
- alpha-synuclein, multiple system atrophy, oligodendroglia, glial cytoplasmic inclusions, mRNA expression, substantia nigra, neurodegeneration, ectopic protein expression
- MeSH terms
- Aged, Aged, 80 and over, Brain, Gene Expression Regulation, Humans, Middle Aged, Oligodendroglia, RNA, Messenger, Multiple System Atrophy, alpha-Synuclein
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