Animal modeling an oligodendrogliopathy – multiple system atrophy
Open accessAbstract
Multiple system atrophy (MSA) is a rare, yet rapidly-progressive neurodegenerative disease that presents clinically with autonomic failure in combination with parkinsonism or cerebellar ataxia. The definitive neuropathology differentiating MSA from Lewy body diseases is the presence of α-synuclein aggregates in oligodendrocytes (called glial cytoplasmic inclusion or GCI) rather than the fibrillar aggregates in neurons (called Lewy bodies). This makes the pathological pathway(s) in MSA unique in that oligodendrocytes are involved rather than predominantly neurons, as is most other neurodegenerative disorders. MSA is therefore regarded as an oligodendrogliopathy. The etiology of MSA is unknown. No definitive risk factors have been identified, although α-synuclein and other genes have been variably linked to MSA risk. Utilization of postmortem brain tissues has greatly advanced our understanding of GCI pathology and the subsequent neurodegeneration. However, extrapolating the early pathogenesis of MSA from such resource has been difficult and limiting. In recent years, cell and animal models developed for MSA have been instrumental in delineating unique MSA pathological pathways, as well as aiding in clinical phenotyping. The purpose of this review is to bring together and discuss various animal models that have been developed for MSA and how they have advanced our understanding of MSA pathogenesis, particularly the dynamics of α-synuclein aggregation. This review will also discuss how animal models have been used to explore potential therapeutic avenues for MSA, and future directions of MSA modeling.
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To date, none of the available transgenic mouse lines have been able to recapitulate the specific striatonigral degeneration or olivopontocerebellar atrophy seen in human MSA.
“To date, none of the available tg mouse lines have been able to recapitulate the specific striatonigral degeneration or olivopontocerebellar atrophy as seen in the human disorder [3].”
From Novel oligodendroglial alpha synuclein viral vector models of multiple system atrophy: studies in rodents and nonhuman primates (2017) · cites this paper as [3]
Variability of pathology is seen across the 3 mouse lines, with none of the models being able to model the distinct SND or OPCA observed in MSA patients.
“Variability of pathology is seen across the 3 mouse lines, with none of the models being able to model the distinct SND or OPCA observed in MSA patients [3].”
From Novel oligodendroglial alpha synuclein viral vector models of multiple system atrophy: studies in rodents and nonhuman primates (2017) · cites this paper as [3]
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“A more recent study [54] reported widespread α-synuclein pathology with distribution analysis revealing the highest burden in the globus pallidus.”
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Multiple System Atrophy: An Oligodendroglioneural Synucleinopathy
Jellinger, K. A. (2017) · Journal of Alzheimer s Disease · doi:10.3233/jad-170397 · Cited by 209 · see citing works
Multiple system atrophy: pathogenic mechanisms and biomarkers
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Multiple system atrophy - a clinicopathological update
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“Multiple system atrophy: experimental models and reality”.
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Potential clinical utility of multiple system atrophy biomarkers
Jellinger, K. A. (2017) · Expert Review of Neurotherapeutics · doi:10.1080/14737175.2017.1392239 · Cited by 18 · see citing works
Nuccio, F. D., Kashyrina, M., Serinelli, F. C., Laferrière, F., Lofrumento, D. D., Giorgi, F. D., & Ichas, F. (2023) · Biomolecules · doi:10.3390/biom13020269 · Cited by 17 · see citing works
TNFα inhibitors as targets for protective therapies in MSA: a viewpoint
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Oligodendrocytes, the Forgotten Target of Gene Therapy
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Recent advances in multiple system atrophy
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Chang, C. C., Liu, J., Chen, B. C., Jiang, Z. S., Tu, C. T., Su, C. H., Yang, H. H., Liu, Z. Q., Deng, Y. C., Chen, C. Y., et al. (2020) · Cell Transplantation · doi:10.1177/0963689720960185 · Cited by 1 · see citing works
- Authors
- Bleasel, J. M., Halliday, G. M., & Kim, W. S.
- Affiliations
- UNSW Sydney (AU)
- Corresponding author
- Kim, Woojin Scott
- Venue
- Acta Neuropathologica Communications
- Published
- 2016-02-09
- Volume
- 4
- Issue
- 1
- Pages
- 12-12
- ISSN
- 2051-5960 (ISSN-L)
- PMC
- PMC4748629
- OpenAlex
- W2255583736
- Cited by
- 19
- References
- 146
- Citations by year
- 2024: 1 · 2023: 1 · 2020: 4 · 2019: 5 · 2018: 1 · 2017: 5 · 2016: 2
- FWCI
- 0.60
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- cc-by
- Locations
- Acta Neuropathologica Communications (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- Medical Research Council
- National Health and Medical Research Council
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Keywords
- multiple system atrophy, animal models, alpha-synuclein aggregation, glial cytoplasmic inclusions, oligodendrocytes, neurodegeneration, therapeutic target, Lewy bodies, autonomic failure, parkinsonism, cerebellar ataxia
- MeSH terms
- Animals, Disease Models, Animal, Humans, Oligodendroglia, Multiple System Atrophy, alpha-Synuclein
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
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