Parkinson’s Disease (PD) is a neurodegenerative disease caused by the death of dopaminergic neurons in the substantia nigra region of the brain. PD is characterized by the presence of dysfunctional mitochondria and increased levels of oxidative stress. Though a handful of genes, such as parkin and PINK1, have been identified in familial forms of PD, most cases are sporadic. Therefore, it is thought that environmental factors may act on genetic risk factors to promote disease onset. Therefore, we are exploring the relationship between copper toxicity, which has been linked to other neurological disorders, and parkin and PINK1. We are testing the effect of environmental exposure to copper as well as altering copper levels genetically by manipulating the copper transporter ATP7, which is mutated in the neurodegenerative disorder, Menkes disease. Preliminary findings have shown that increased extracellular copper, from over-expression of ATP7, in conjunction with knockdown of parkin and PINK1 exasperate Parkinson’s symptoms.