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Updated: Jan 6, 2026

Gene-environment Interaction Models to Unmask Susceptibility Mechanisms in Parkinson's Disease
Published on: January 7, 2014
Superoxide dismutase coding of gene polymorphisms associated with susceptibility to Parkinson's disease
Chunlei Liu1, Jinju Fang2, Wenke Liu1
1Department of Neurosurgery, West China Hospital of Sichuan University, Chengdu, Sichuan Province 610041, P. R. China.
Abstract:
Oxidative stress linked to the etiology of Parkinson's disease, which is characterized by chronic and progressive neurodegeneration of dopamine neurons. Superoxide dismutase enzymes (SODs) regarded as the first line of defense against oxidative damage. This study assessed the potential associations of gene polymorphisms in SOD1 (encoding Cu/Zn-SOD), SOD2 (encoding Mn-SOD) and SOD3 (encoding extracellular-SOD) with susceptibility to Parkinson's disease. A case-control study, including Parkinson's disease cases (n = 356) and controls (n = 370). Single nucleotide polymorphisms of SOD1 (rs2070424 A/G), SOD2 (rs4880 T/C) and SOD3 (rs1799895, C/G) were genotyped. Results indicated that AG or GG genotype carriers in SOD1 had a much greater risk of Parkinson's disease compared to corresponding AA genotypes, and allele G carriers had increased risk versus allele A carriers in the single nucleotide polymorphism (rs2070424 A/G) in SOD1. Further, TC or CC genotype carriers in SOD2 had a much higher risk of Parkinson's disease compared with corresponding TT genotypes, and the C carriers had an increased risk over allele T carriers in the single nucleotide polymorphism (rs4880 T/C) in SOD2. Together, carrying allele G in the single nucleotide polymorphism (rs2070424 A/G) in SOD1, or allele C in the single nucleotide polymorphism (rs4880 T/C) in SOD2, enhances genetic susceptibility to Parkinson's disease.
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