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Lack of Nigral Pathology in Transgenic Mice Expressing Human α-Synuclein Driven by the Tyrosine Hydroxylase Promoter
Open accessAbstract
alpha-Synuclein has been identified as a major component of Lewy body inclusions, which are one of the pathologic hallmarks of idiopathic Parkinson's disease. Mutations in alpha-synuclein have been found to be responsible for rare familial cases of Parkinsonism. To test whether overexpression of human alpha-synuclein leads to inclusion formation and neuronal loss of dopaminergic cells in the substantia nigra, we made transgenic mice in which the expression of wild-type or mutant (A30P and A53T) human alpha-synuclein protein was driven by the promoter from the tyrosine hydroxylase gene. Even though high levels of human alpha-synuclein accumulated in dopaminergic cell bodies, Lewy-type-positive inclusions did not develop in the nigrostriatal system. In addition, the number of nigral neurons and the levels of striatal dopamine were unchanged relative to non-transgenic littermates, in mice up to one year of age. These findings suggest that overexpression of alpha-synuclein within nigrostriatal dopaminergic neurons is not in itself sufficient to cause aggregation into Lewy body-like inclusions, nor does it trigger overt neurodegenerative changes.
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“Because the overexpression of wild-type or mutant human α-synuclein caused by the TH promoter did not result in the formation of pathological inclusions nor alter the behavior and sensitivity to 1-methyl-4-phenyl-1,2,3,6- tetrahydropyridine (MPTP) in C57BL/6 mice [117,118,119]”
From Degradation of Tyrosine Hydroxylase by the Ubiquitin-Proteasome System in the Pathogenesis of Parkinson’s Disease and Dopa-Responsive Dystonia (2020) · cites this paper as [117]
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Metadata
- Authors
- Matsuoka, Y., Vila, M., Lincoln, S., McCormack, A., Picciano, M., LaFrancois, J., Yu, X., Dickson, D., Langston, W. J., McGowan, E., Farrer, M., Hardy, J., Duff, K., Przedborski, S., & Di Monte, D. A.
- Affiliations
- New York University (US)
- Columbia University (US)
- Mayo Clinic (US)
- Parkinson's Institute and Clinical Center (US)
- Venue
- Neurobiology of Disease
- Publisher
- Elsevier BV
- Published
- 2001-06
- Volume
- 8
- Issue
- 3
- Pages
- 535-539
- ISSN
- 0969-9961 (ISSN-L)
- OpenAlex
- W1976148085
- Cited by
- 281
- References
- 19
- Citations by year
- 2026: 2 · 2025: 3 · 2024: 9 · 2023: 5 · 2022: 9 · 2021: 8 · 2020: 5 · 2019: 4 · 2018: 6 · 2017: 14 · 2016: 2 · 2015: 3 · 2014: 8 · 2013: 11 · 2012: 11
- FWCI
- 17.21
- Type
- journal article
- Language
- en
- Open access
- green
- doaj.org
- Licence
- Locations
- Neurobiology of Disease (publishedVersion)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
- UCL Discovery (University College London) (submittedVersion)
- Funders
- National Institute of Environmental Health Sciences (R01ES010442, ES10442)
- 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
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- alpha-synuclein, Lewy bodies, Parkinson's disease, substantia nigra, dopaminergic neurons, tyrosine hydroxylase promoter, transgenic mice, protein aggregation, nigrostriatal pathway, striatal dopamine, neurodegeneration
- MeSH terms
- Animals, Disease Models, Animal, Humans, Mice, Inbred C57BL, Mice, Inbred DBA, Nerve Tissue Proteins, Phenotype, Promoter Regions, Genetic, Substantia Nigra, Tyrosine 3-Monooxygenase, Lewy Bodies, Parkinsonian Disorders, Mice, Synucleins, alpha-Synuclein
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