Physiological and Pathological Role of Alpha-Synuclein in Parkinson’s Disease through Iron Mediated Oxidative Stress; The Role of a Putative Iron-Responsive Element

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Physiological and Pathological Role of Alpha-Synuclein in Parkinson’s Disease through Iron Mediated Oxidative Stress; The Role of a Putative Iron-Responsive Element

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Title: Physiological and Pathological Role of Alpha-Synuclein in Parkinson’s Disease through Iron Mediated Oxidative Stress; The Role of a Putative Iron-Responsive Element
Author: Olivares, David; Branden, Lars; Greig, Nigel H.; Huang, Xudong; Rogers, Jack Timothy

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Citation: Olivares, David, Xudong Huang, Lars Branden, Nigel H. Greig, and Jack T. Rogers. 2009. Physiological and pathological role of alpha-synuclein in Parkinson’s disease through iron mediated oxidative stress; The role of a putative iron-responsive element. International Journal of Molecular Sciences 10(3): 1226-1260.
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Abstract: Parkinson’s disease (PD) is the second most common progressive neurodegenerative disorder after Alzheimer’s disease (AD) and represents a large health burden to society. Genetic and oxidative risk factors have been proposed as possible causes, but their relative contribution remains unclear. Dysfunction of alpha-synuclein (\(\alpha\)-syn) has been associated with PD due to its increased presence, together with iron, in Lewy bodies. Brain oxidative damage caused by iron may be partly mediated by \(\alpha\)-syn oligomerization during PD pathology. Also, \(\alpha\)-syn gene dosage can cause familial PD and inhibition of its gene expression by blocking translation via a newly identified Iron Responsive Element-like RNA sequence in its 5’-untranslated region may provide a new PD drug target.
Published Version: doi://10.3390/ijms10031226
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2672027/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:10246870
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