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Cited by 128Parkinson's Disease Mechanisms and TreatmentsNuclear Receptors and SignalingNeuroinflammation and Neurodegeneration Mechanisms

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

Rathke‐Hartlieb, Silvia, Kahle, Philipp J., Neumann, Manuela, Ozmen, Laurence, Haid, Sibylle, Okochi, Masayasu, Haass, Christian, Schulz, Jörg B.·2001·Journal of Neurochemistry
DOI 10.1046/j.1471-4159.2001.00366.x
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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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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.
ORCID
Venue
Journal of Neurochemistry
Publisher
Wiley
Published
2001-05-15
Volume
77
Issue
4
Pages
1181-1184
ISSN
  • 0022-3042 (ISSN-L)
  • 1471-4159
DOI
10.1046/j.1471-4159.2001.00366.x
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
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 219 d)
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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