Study of genetic and environmental exposures on neuroendocrine and immune disorders
Our study aims to 1) quantify and understand the role of genetic variants, environment, and their interaction on outcomes related to neuroendocrine and immune disorders, which may provide accurate targets for further mechanistic studies. 2) examine crosstalk between neuroendocrine and immune systems by an interdisciplinary approach. 3) Ultimately, provide a reliable approach for the precise prediction and treatment of neuroendocrine-immune disorders based on genetic and environmental factors.
The interactions of the neuroendocrine system with the immune system and its importance in mediating diseases are receiving increasing attention from the scientific community. Numerous studies showed that changes in the neuroendocrine system profoundly modify the activities and functions of the immune system. Similarly, functional alterations in the activity of the immune system can cause alteration in both the nervous and endocrine systems. Previous studies have identified a range of risk SNP associated with those disorders but still lack fine mapping of causal variants. In addition, population stratification and disease prediction based on genetic and environmental factors lack reliable evidence support from long-term large sample cohorts.
Therefore, we propose to harness the power of large-scale genomic analysis to understand the interactions between human genetic variants, environmental exposures, complex neuroendocrine and immune disorders of major public health importance. Due to the interdisciplinary complexity, our study is expected to be finished in 3 years. We aim to provide high-quality prospective population-based evidence for the prevention and intervention of neuroendocrine and immune diseases. By combining the advantage of the animal model, we will verify the function of candidate targets during the pathophysiological process and further develop a large-scale drug screen. Hence, our studies may ease the burden of disease worldwide.