ПЕРСПЕКТИВЫ ПЕРВИЧНОЙ ПРОФИЛАКТИКИ БОЛЕЗНИ ПАРКИНСОНА

Abstract

The incidence of Parkinson's disease currently outpaces the rate of aging and is growing disproportionately in newly industrialized areas of the globe. Scientific evidence suggests that exposure to environmental toxicants during neurodevelopment, whether in utero, perinatal or childhood, may have a significant impact on the risk of developing Parkinson's disease in the future. More often we have a combination of factors/triggers that last for decades, such as pesticides, organic solvents, metals and air pollution. The relationship between exposure and disease is variable, meaning that gene-environment and environment-environment interactions and other exposure dynamics contribute to the disease phenotype. Since all disease phenotypes are the result of our genes (intrinsic factors) and environment (extrinsic factors), there is no doubt that gene-environment interactions account for most cases of idiopathic Parkinson's disease. Unraveling key aspects of our understanding of the environmental risk associated with Parkinson's disease in the human population requires experimental work. Collaboration between interdisciplinary teams and new technologies combined with basic toxicological principles is required. With both laboratory and analytical support, incorporating biomarkers, transcriptomics or metabolomics, and gene-environment interactions into research projects would be an ideal mechanism for PD research, both in the preclinical and clinical areas. Understanding the contribution of the environment to PD is critical as it could potentially help prevent the development and/or progression of this as yet incurable disease in some percentage of cases.