The DOI matches its Crossref record; 9 of the 9 references it cites were found in a registry or an index.
Mechanisms of Suppression of α-Synuclein Neurotoxicity by Geldanamycin in Drosophila
Open accessAbstract
Parkinson's disease is a common neurodegenerative disease characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta and the accumulation of the protein alpha-synuclein into aggregates called Lewy bodies and Lewy neurites. Parkinson's disease can be modeled in Drosophila where directed expression of alpha-synuclein induces compromise of dopaminergic neurons and the formation of Lewy body-like aggregates. The molecular chaperone Hsp70 protects cells from the deleterious effects of alpha-synuclein, indicating a potential therapeutic approach to enhance neuron survival in Parkinson's disease. We have now investigated the molecular mechanisms by which the drug geldanamycin protects neurons against alpha-synuclein toxicity. Our studies show that geldanamycin sensitizes the stress response within normal physiological parameters to enhance chaperone activation, offering protection against alpha-synuclein neurotoxicity. Further, geldanamycin uncouples neuronal toxicity from Lewy body and Lewy neurite formation such that dopaminergic neurons are protected from the effects of alpha-synuclein expression despite the continued presence of (and even increase in) inclusion pathology. These studies indicate that compounds that modulate the stress response are a promising approach to treat Parkinson's disease.
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Mutation in the α-Synuclein Gene Identified in Families with Parkinson's Disease
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Chaperone Suppression of α-Synuclein Toxicity in a Drosophila Model for Parkinson's Disease
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Whitesell, L., & Lindquist, S. L. (2005) · Nature Reviews Cancer · doi:10.1038/nrc1716 · Cited by 2,502
Genetics of Parkinson disease: paradigm shifts and future prospects
Farrer, M. J. (2006) · Nature Reviews Genetics · doi:10.1038/nrg1831 · Cited by 707
α-synuclein acts in the nucleus to inhibit histone acetylation and promote neurotoxicity
Kontopoulos, E., Parvin, J. D., & Feany, M. B. (2006) · Human Molecular Genetics · doi:10.1093/hmg/ddl243 · Cited by 537
NEURODEGENERATIVE DISEASES: New Concepts of Pathogenesis and Their Therapeutic Implications
Skovronsky, D. M., Lee, V. M.-Y., & Trojanowski, J. Q. (2006) · Annual Review of Pathology: Mechanisms of Disease · doi:10.1146/annurev.pathol.1.110304.100113 · Cited by 425
Zhou, W., & Freed, C. R. (2005) · Journal of Biological Chemistry · doi:10.1074/jbc.m507124200 · Cited by 346
Metadata
- Authors
- Auluck, P. K., Meulener, M. C., & Bonini, N. M.
- Venue
- Journal of Biological Chemistry
- Publisher
- Elsevier BV
- Published
- 2005-01
- Volume
- 280
- Issue
- 4
- Pages
- 2873-2878
- ISSN
- 0021-9258 (ISSN-L)
- OpenAlex
- W2039425688
- Cited by
- 203
- References
- 9
- FWCI
- 11.81
- Type
- journal article
- Language
- en
- Open access
- hybrid
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- Auluck, P. K., Meulener, M. C., & Bonini, N. M. (2005). Mechanisms of Suppression of α-Synuclein Neurotoxicity by Geldanamycin in Drosophila. Journal of Biological Chemistry. https://doi.org/10.1074/jbc.m412106200
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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.
Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).
Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.
