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Sci Rep. 2018 Nov 8;8(1):16525. doi: 10.1038/s41598-018-35003-4.

K-variant BCHE and pesticide exposure: Gene-environment interactions in a case-control study of Parkinson's disease in Egypt.

Author information

German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Department of Neurology, Technical University of Munich, Munich, Germany.
Medical Experimental Research Center (MERC), Mansoura University, Mansoura, Egypt.
Toxicology Department, Mansoura University, Mansoura, Egypt.
Department of Neurology, Ain Shams University, Cairo, Egypt.
Department of Neurology, Assiut University, Assiut, Egypt.
Department of Neurology, Mansoura University, Mansoura, Egypt.
Department of Neurology, Sohag University, Sohag, Egypt.
Department of Neurology, Zagazig University, Zagazig, Egypt.
Department of Neurology, Tanta University, Tanta, Egypt.
Institute for Human Genetics, Justus Liebig University Giessen, Giessen, Germany.
Institute of Medical Informatics and Statistics, Kiel University, Kiel, Germany.
Department of Neurology, Kiel University, Kiel, Germany.
German Center for Neurodegenerative Diseases (DZNE), Munich, Germany.
Department of Neurology, Technical University of Munich, Munich, Germany.
Munich Cluster for Systems Neurology (SyNergy), Ludwig-Maximilians-University, Munich, Germany.


Pesticide exposure is associated with increased risk of Parkinson's disease (PD). We investigated in Egypt whether common variants in genes involved in pesticide detoxification or transport might modify the risk of PD evoked by pesticide exposure. We recruited 416 PD patients and 445 controls. Information on environmental factors was collected by questionnaire-based structured interviews. Candidate single-nucleotide polymorphisms (SNPs) in 15 pesticide-related genes were genotyped. We analyzed the influence of environmental factors and SNPs as well as the interaction of pesticide exposure and SNPs on the risk of PD. The risk of PD was reduced by coffee consumption [OR = 0.63, 95% CI: 0.43-0.90, P = 0.013] and increased by pesticide exposure [OR = 7.09, 95% CI: 1.12-44.01, P = 0.036]. The SNP rs1126680 in the butyrylcholinesterase gene BCHE reduced the risk of PD irrespective of pesticide exposure [OR = 0.38, 95% CI: 0.20-0.70, P = 0.002]. The SNP rs1803274, defining K-variant BCHE, interacted significantly with pesticide exposure (P = 0.007) and increased the risk of PD only in pesticide-exposed individuals [OR = 2.49, 95% CI: 1.50-4.19, P = 0.0005]. The K-variant BCHE reduces serum activity of butyrylcholinesterase, a known bioscavenger for pesticides. Individuals with K-variant BCHE appear to have an increased risk for PD when exposed to pesticides.

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