α-Synuclein and the Pathogenesis of Parkinson's Disease

Francis L. Martin; Sally J.M. Williamson; Katerina E. Paleologou; David Allsop; Omar M.A. El-Agnaf

doi:10.2174/0929866043407138

ISSN: 0929-8665
E-ISSN: 1875-5305

α-Synuclein and the Pathogenesis of Parkinson's Disease
Authors: Francis L. Martin¹, Sally J.M. Williamson², Katerina E. Paleologou³, David Allsop⁴ and Omar M.A. El-Agnaf⁵
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¹ Department of Biological Sciences, I.E.N.S., Lancaster University, Lancaster LA1 4YQ, UK ² Department of Biological Sciences, I.E.N.S., Lancaster University, Lancaster LA1 4YQ, UK ³ Department of Biological Sciences, I.E.N.S., Lancaster University, Lancaster LA1 4YQ, UK ⁴ Department of Biological Sciences, I.E.N.S., Lancaster University, Lancaster LA1 4YQ, UK ⁵ Department of Biological Sciences, I.E.N.S., Lancaster University, Lancaster LA1 4YQ, UK
Source: Protein and Peptide Letters, Volume 11, Issue 3, Jun 2004, p. 229 - 237
DOI: https://doi.org/10.2174/0929866043407138
- Available online: 01 Jun 2004

Abstract

Lesions known as Lewy bodies (LBs) and Lewy neurites (LNs) characterise brains of Parkinson's disease (PD) patients. Intracellular aggregation of α-synuclein (α-syn) appears to play a key role in the generation of LBs and LNs. Such aggregation in the presence of redox metals may initiate Fenton reaction-mediated generation of reactive oxygen species (ROS). ROS thus generated may result in cytotoxic mechanisms such as the induction of DNA single-strand breaks.

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2004-06-01

2025-12-15

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Article Type: Review Article

Keyword(s): comet assay; dna single-strand breaks; environmental causation; reactive oxygen species

α-Synuclein and the Pathogenesis of Parkinson's Disease

Abstract

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