The DOI matches its Crossref record; 19 of the 19 references it cites were found in a registry or an index.
The A53T α-Synuclein Mutation Increases Iron-Dependent Aggregation and Toxicity
Open accessAbstract
Parkinson9s disease (PD) is the most common motor disorder affecting the elderly. PD is characterized by the formation of Lewy bodies and death of dopaminergic neurons. The mechanisms underlying PD are unknown, but the discoveries that mutations in α-synuclein can cause familial PD and that α-synuclein accumulates in Lewy bodies suggest that α-synuclein participates in the pathophysiology of PD. Using human BE-M17 neuroblastoma cells overexpressing wild-type, A53T, or A30P α-synuclein, we now show that iron and free radical generators, such as dopamine or hydrogen peroxide, stimulate the production of intracellular aggregates that contain α-synuclein and ubiquitin. The aggregates can be identified by immunocytochemistry, electron microscopy, or the histochemical stain thioflavine S. The amount of aggregation occurring in the cells is dependent on the amount of α-synuclein expressed and the type of α-synuclein expressed, with the amount of α-synuclein aggregation following a rank order of A53T > A30P > wild-type > untransfected. In addition to stimulating aggregate formation, α-synuclein also appears to induce toxicity. BE-M17 neuroblastoma cells overexpressing α-synuclein show up to a fourfold increase in vulnerability to toxicity induced by iron. The vulnerability follows the same rank order as for aggregation. These data raise the possibility that α-synuclein acts in concert with iron and dopamine to induce formation of Lewy body pathology in PD and cell death in PD.
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Cites
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The relevance of the Lewy body to the pathogenesis of idiopathic Parkinson's disease.
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A Drosophila model of Parkinson's disease
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Hydrogen peroxide mediates amyloid β protein toxicity
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The ubiquitin pathway in Parkinson's disease
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Polymeropoulos, M. H., Higgins, J. J., Golbe, L. I., Johnson, W. G., Ide, S. E., Di Iorio, G., Sanges, G., Stenroos, E. S., Pho, L. T., Schaffer, A. A., et al. (1996) · Science · doi:10.1126/science.274.5290.1197 · Cited by 788 · cited 2×
“The only defined causes of the disease are A53T and A30P mutations in the a-synuclein gene (Polymeropoulos et al., 1997; Goedert et al., 1999; Papadimitriou et al., 1999), but there has been much circumstantial evidence implicating oxidative stress in the etiology of the disease (Jenner and Olanow,…”
BackgroundUnderstanding cell death in parkinson's disease
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α-Synuclein Shares Physical and Functional Homology with 14-3-3 Proteins
Ostrerova, N., Petrucelli, L., Farrer, M., Mehta, N., Choi, P., Hardy, J., & Wolozin, B. (1999) · The Journal of Neuroscience · doi:10.1523/jneurosci.19-14-05782.1999 · Cited by 564
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Cited by
Oxidative stress in neurodegeneration: Cause or consequence?
Andersen, J. K. (2004) · Nature Medicine · doi:10.1038/nrn1434 · Cited by 1,869
The Role of Oxidative Stress in Parkinson's Disease
Dias, V., Junn, E., & Mouradian, M. M. (2013) · Journal of Parkinson’s Disease · doi:10.3233/jpd-130230 · Cited by 1,845
Iron, brain ageing and neurodegenerative disorders
Zecca, L., Youdim, M. B. H., Riederer, P., Connor, J. R., & Crichton, R. R. (2004) · Nature Reviews Neuroscience · doi:10.1038/nrn1537 · Cited by 1,801
Halliwell, B. (2001) · Drugs & Aging · doi:10.2165/00002512-200118090-00004 · Cited by 1,502
-Synuclein in Parkinson's Disease
Stefanis, L. (2012) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a009399 · Cited by 1,446
Metadata
- Authors
- Ostrerova-Golts, N., Petrucelli, L., Hardy, J., Lee, J. M., Farer, M., & Wolozin, B.
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2000-08-15
- Volume
- 20
- Issue
- 16
- Pages
- 6048-6054
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- OpenAlex
- W4295689620
- Cited by
- 466
- References
- 19
- FWCI
- 15.37
- Type
- journal article
- Language
- en
- Open access
- bronze
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