Parkinson’s disease (PD), the most common neurodegenerative movement disorder, is characterized by degeneration of the nigrostriatal dopaminergic pathway and other monoaminergic regions and the formation of cytoplasmic inclusions. The majority of cases of PD are sporadic (i.e. not caused by an inherited monogenic mutation). The etiology of these sporadic cases is thought to involve an interaction between genetic and environmental factors. Epidemiological studies suggest that exposure to environmental toxicants increases the risk of PD; many of these compounds have also been associated
with PD by post-mortem analysis of brain tissue. Many labs have shown that a variety of these compounds cause oxidative stress and disrupt expression and function of dopaminergic-related and PD-related proteins, resulting in increased susceptibility of dopaminergic neurons to toxicants that target the dopaminergic system in adult and developmental models. It has been proposed that epigenetic modulations serve as an intermediate process that imprints dynamic environmental experiences on the “fixed” genome, resulting in stable alterations in phenotype and changes in neuronal vulnerability. Our work focuses on understanding the epigenetic changes that occur in PD and in response to toxicant exposures and how these epigenetic changes affect neuronal vulnerability and disease risk.