A Progressive Mouse Model of Parkinson’s Disease: The Thy1-aSyn (“Line 61”) Mice
Open accessAbstract
Identification of mutations that cause rare familial forms of Parkinson's disease (PD) and subsequent studies of genetic risk factors for sporadic PD have led to an improved understanding of the pathological mechanisms that may cause nonfamilial PD. In particular, genetic and pathological studies strongly suggest that alpha-synuclein, albeit very rarely mutated in PD patients, plays a critical role in the vast majority of individuals with the sporadic form of the disease. We have extensively characterized a mouse model over-expressing full-length, human, wild-type alpha-synuclein under the Thy-1 promoter. We have also shown that this model reproduces many features of sporadic PD, including progressive changes in dopamine release and striatal content, alpha-synuclein pathology, deficits in motor and nonmotor functions that are affected in pre-manifest and manifest phases of PD, inflammation, and biochemical and molecular changes similar to those observed in PD. Preclinical studies have already demonstrated improvement with promising new drugs in this model, which provides an opportunity to test novel neuroprotective strategies during different phases of the disorder using endpoint measures with high power to detect drug effects.
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The α-syn transgenic mouse model overexpressing human wild-type α-synuclein under the murine Thy1 promoter reproduces most features of synucleinopathies, including neuropathology and deficits in motor and non-motor function.
“The mouse model utilized in current study is known to reproduce most features of synucleinopathies, including neuropathology and deficits in motor and non-motor function (46).”
From LRRK2 mediates microglial neurotoxicity via NFATc2 in rodent models of synucleinopathies (2020) · cites this paper as [46]
The General Description identifies the model as mice overexpressing human wild-type α-synuclein under the murine Thy-1 promoter. The conclusion reports motor and nonmotor deficits and pathological changes resembling Parkinson’s disease, but describes these as key features of PD, not most features of synucleinopathies broadly; it also notes that the mice do not develop measurable loss of dopaminergic cell bodies. (LLM, conf=0.86)
Experimental — accuracy not yet measuredThe ASO mouse model of PD develops progressive deficits in motor function as well as in gut motility.
“Importantly, ASO (overexpressing a-synuclein under Thy1 promoter) mouse model of PD develops progressive deficits in motor function as well as in gut motility (182, 183).”
From The gut-brain axis: how microbiota and host inflammasome influence brain physiology and pathology (2020) · cites this paper as [182]
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Systems biology of neurodegenerative diseases
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Neuronal Oxidative Stress Promotes α-Synuclein Aggregation In Vivo
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Microglial dynamics and neuroinflammation in prodromal and early Parkinson’s disease
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- Authors
- Chesselet, M.-F., Richter, F., Zhu, C., Magen, I., Watson, M. B., & Subramaniam, S. R.
- Affiliations
- University of California, Los Angeles (US)
- Venue
- Neurotherapeutics
- Publisher
- Elsevier BV
- Published
- 2012-04
- Volume
- 9
- Issue
- 2
- Pages
- 297-314
- ISSN
- 1878-7479 (ISSN-L)
- PMC
- PMC3337020
- OpenAlex
- W2169324918
- Cited by
- 346
- References
- 88
- Citations by year
- 2026: 18 · 2025: 38 · 2024: 38 · 2023: 30 · 2022: 33 · 2021: 40 · 2020: 23 · 2019: 20 · 2018: 26 · 2017: 26 · 2016: 12 · 2015: 13 · 2014: 21 · 2013: 5 · 2012: 3
- FWCI
- 1.88
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Neurotherapeutics (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (P50-NS 38367, P50NS038367)
- Topics
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
- Health Sciences › Medicine › Neurology › Neurological disorders and treatments
- Keywords
- Parkinson's disease, alpha-synuclein, mouse model, sporadic Parkinson's disease, dopamine release, striatum, motor impairment, neuroinflammation, neuroprotection, preclinical drug testing, alpha-synuclein pathology
- MeSH terms
- Animals, Disease Models, Animal, Humans, Mice, Neurologic Mutants, Parkinson Disease, Promoter Regions, Genetic, Disease Progression, Mice, alpha-Synuclein
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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.
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