Environment Gene Interaction in Parkinson's disease (EGI-PD) Mohamed M. Salama1, Thomas W. Rösler2, Ali Shalash3, Abdelhaleem Tantawy4, , Günter U. Höglinger2,5 1Toxicology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt 2Department for Translational Neurodegeneration, German Center for Neurodegenerative Diseases (DZNE), Munich, Germany 3. Department of Neurology, Faculty of Medicine, Ain Shams University, Cairo, Egypt 4. Department of Neurology, Faculty of Medicine, Mansoura University, Mansoura, Egypt 3 Department of Neurology, Technical University, Munich, Germany Introduction: The prevalence of PD is increased in Egypt compared to reports in other countries. Both genetic and environmental causes might be responsible. E.g. a high rate of LRRK2 mutations has been reported in other North African countries, but has not been systematically studied in Egypt. Also, several epidemiologic studies have supported the hypothesis that broadly defined pesticide exposure may increase the risk of PD. A high degree of pesticide use occurs in Egypt due to the limited availability of agricultural areas in the country. Moreover, lack of precautionary measures on applying pesticides leads to increased pesticide exposures. We aimed to study the link between genes encoding detoxifying enzymes and PD-risk genes on one hand and exposure to pesticides on the other hand in the etiology of PD in Egypt. Methods: This work is undertaken in collaboration between the Technische Universtität München, Germany and a network of 16 Egyptian Universities leaded by Mansoura University (Egyptian Network of Neurodegenerative Diseases [ENND]). PD cases from all over Egypt are recruited. Half of the cases were chosen in areas of low pesticide exposure, the other half with high pesticides exposure (farmers 50 years of age or older). Similar numbers of non-PD controls are chosen from two sources; first, patients arriving to outpatient clinic who are not suffering from any other neurodegenerative disorder; secondly, persons accompanying participating PD patients. Controls are further stratified into low pesticides and high pesticides controls, as described for the PD cases. Patients are assessed with a standardized questionnaire to evaluate past exposure to pesticides or other Parkinson-related environmental factors, a standardized clinical neurological examination to verify presence of PD (UK brain bank criteria) and to quantify disease severity (Hoehn & Yahr stage, UPDRS motor part) and genotyping for presence or absence of risk-carrying alleles in detoxification and Parkinson's associated genes. Results: We were able to establish ENND which is the first collaborative network of this type in Egypt. Moreover, we established a functional Standard Operation Procedure to collect and ship clinical data and blood for analysis to the German cooperation partner at TUM. So far, we collected blood and epidemiological data from 70 cases and 80 controls. Preliminary data on the analysis of gene-environment interaction analysis will be presented. Conclusion: This work will provide further insights into the mechanisms of gene environment interplay in the etiology of PD and hopefully insights which allow the establishment of primary preventive measures. Funding: DAAD-funded Al-Tawasul project EGI-PD


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