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.

Background: The brain is a productive source of a variety of enzymes and any brain injury like a stroke to brain tissue could similarly result in an increase in these enzymes in cerebrospinal fluid and serum. Evaluation of these enzymes represents a simple method for the ischemic stroke subtype diagnosis and prognosis. Objective: This study aimed to determine the role of brain natriuretic peptide (BNP), D-dimer, creatine-kinase-MB (CK-MB), C-reactive protein (CRP) serum levels, and globulin/albumin ratio in the diagnosis of CES stroke and its ability to predict short-term outcome. Methods: This study was conducted on 96 patients with acute ischemic stroke, subdivided into two groups: group Ι was 48 patients with cardio-embolic stroke and group ΙΙ was 48 patients with non-cardio-embolic. All patients were subjected to the assessment of serum BNP, D-dimer and CK-MB, and CRP and globulin/albumin ratio within the first 24 h of stroke. In the third week, they were assessed by mRS. Results: The mean levels of BNP, D-dimer level, and CK-MB were significantly higher in patients with cardio-embolic stroke than in patients with non-cardio-embolic stroke (P < 0.001) and also were associated with poor short-term outcome. Conclusion: Elevated plasma levels of BNP, D-dimer levels, and CK-MB can be used as surrogate biomarkers for the diagnosis of cardio-embolic stroke and prediction of poor short-term outcomes.

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