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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 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]
Experimental — accuracy not yet measuredIn the citing paper
“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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Metadata
- 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 › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Health Sciences › Medicine › Clinical Neurology › Deep Brain Stimulation and Movement Disorders
- 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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