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Cited by 281Parkinson's Disease Mechanisms and TreatmentsNuclear Receptors and SignalingNeuroinflammation and Neurodegeneration Mechanisms

The DOI matches its Crossref record; 18 of the 19 references it cites were found in a registry or an index.

Lack of Nigral Pathology in Transgenic Mice Expressing Human α-Synuclein Driven by the Tyrosine Hydroxylase Promoter

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Matsuoka, Yasuji, Vila, Miquel, Lincoln, Sarah, McCormack, Alison, Picciano, Melanie, LaFrancois, John, Yu, Xin, Dickson, Dennis, Langston, William J., McGowan, Eileen, Farrer, Matt, Hardy, John, Duff, Karen, Przedborski, Serge, Di Monte, Donato A.·2001·Neurobiology of Disease
DOI 10.1006/nbdi.2001.0392
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Abstract

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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  1. Goldberg, 2000, Studies of human α-synuclein in transgenic mice, Abstr. Soc. Neurosci.

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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)
ORCID
Venue
Neurobiology of Disease
Publisher
Elsevier BV
Published
2001-06
Volume
8
Issue
3
Pages
535-539
ISSN
0969-9961 (ISSN-L)
DOI
10.1006/nbdi.2001.0392
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
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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