The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.
Sensitivity to MPTP is not increased in Parkinson's disease‐associated mutant α‐synuclein transgenic mice: RAPID COMMUNICATION
Abstract
Environmental and genetic factors that contribute to the pathogenesis of Parkinson's disease are discussed. Mutations in the α‐synuclein (α SYN ) gene are associated with rare cases of autosomal‐dominant Parkinson's disease. We have analysed the dopaminergic system in transgenic mouse lines that expressed mutant [A30P]αSYN under the control of a neurone‐specific Thy‐1 or a tyrosine hydroxylase (TH) promoter. The latter mice showed somal and neuritic accumulation of transgenic [A30P]αSYN in TH‐positive neurones in the substantia nigra. However, there was no difference in the number of TH‐positive neurones in the substantia nigra and the concentrations of catecholamines in the striatum between these transgenic mice and non‐transgenic littermates. To investigate whether forced expression of [A30P]αSYN increased the sensitivity to putative environmental factors we subjected transgenic mice to a chronic 1‐methyl‐4‐phenyl‐1,2,3,6‐tetrahydropyridine (MPTP) regimen. The MPTP‐induced decrease in the number of TH‐positive neurones in the substantia nigra and the concentrations of catecholamines in the striatum did not differ in any of the [A30P]α SYN transgenic mouse lines compared with wild‐type controls. These results suggest that mutations and forced expression of αSYN are not likely to increase the susceptibility to environmental toxins in vivo.
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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 [118]
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Metadata
- Authors
- Rathke‐Hartlieb, S., Kahle, P. J., Neumann, M., Ozmen, L., Haid, S., Okochi, M., Haass, C., & Schulz, J. B.
- Affiliations
- University of Tübingen (DE)
- Ludwig-Maximilians-Universität München (DE)
- F. Hoffmann-La Roche AG (CH)
- Corresponding author
- Schulz, Jörg B.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2001-05-15
- Volume
- 77
- Issue
- 4
- Pages
- 1181-1184
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W1516811504
- Cited by
- 128
- References
- 21
- Citations by year
- 2026: 1 · 2025: 1 · 2024: 1 · 2022: 1 · 2021: 5 · 2020: 2 · 2019: 2 · 2018: 1 · 2017: 4 · 2015: 2 · 2014: 6 · 2013: 3 · 2012: 4
- FWCI
- 12.32
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neurochemistry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Deutsche Forschungsgemeinschaft
- International Society for Neurochemistry
- 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
- Parkinson's disease, alpha-synuclein, A30P mutation, MPTP, dopaminergic neurons, substantia nigra, tyrosine hydroxylase promoter, catecholamines, striatum, transgenic mice, autosomal dominant Parkinson's disease
- MeSH terms
- Animals, Corpus Striatum, Dopamine, Homovanillic Acid, Humans, Mice, Transgenic, Nerve Tissue Proteins, Neurons, Parkinson Disease, Promoter Regions, Genetic, Substantia Nigra, Tyrosine 3-Monooxygenase, 3,4-Dihydroxyphenylacetic Acid, 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine, Neurites, Thy-1 Antigens, Amino Acid Substitution, Parkinsonian Disorders, Mice, Synucleins, alpha-Synuclein
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