Departmen of Epidemiology, University of California Los Angeles, Los Angeles, CA, USA.
Neuroepidemiology. 2010;35(3):191-5. doi: 10.1159/000315157. Epub 2010 Jul 24.
Although of great interest and suggested in prior reports, possible α-synuclein (SNCA) gene-environment interactions have not been well investigated in humans.
We used a population-based approach to examine whether the risk of Parkinson's disease (PD) depended on the combined presence of SNCA variations and two important environmental factors, pesticide exposures and smoking.
RESULTS/CONCLUSIONS: Similar to recent meta- and pooled analyses, our data suggest a lower PD risk in subjects who were either homozygous or heterozygous for the SNCA REP1 259 genotype, and a higher risk in subjects who were either homozygous or heterozygous for the REP1 263 genotype, especially among subjects with an age of onset ≤68 years. More importantly, while analyses of interactions were limited by small cell sizes, risk due to SNCA variations seemed to vary with pesticide exposure and smoking, especially in younger onset cases, suggesting an age-of-onset effect.
尽管先前的报告表明存在α-突触核蛋白(SNCA)基因-环境相互作用的可能性,但在人类中尚未对此进行充分研究。
我们采用基于人群的方法,研究 SNCA 变异与两种重要环境因素(农药暴露和吸烟)的共同存在是否会影响帕金森病(PD)的发病风险。
结果/结论:与最近的荟萃分析和汇总分析相似,我们的数据表明,在 SNCA REP1 259 基因型纯合或杂合的个体中,PD 风险较低,而在 REP1 263 基因型纯合或杂合的个体中,PD 风险较高,尤其是在发病年龄≤68 岁的个体中。更重要的是,尽管交互作用的分析受到细胞数量小的限制,但由于 SNCA 变异引起的风险似乎与农药暴露和吸烟有关,尤其是在发病年龄较轻的病例中,提示存在发病年龄效应。