Interactions between PARK7, PINK1, and Parkin, and their function in the pathophysiology of Parkinson’s disease

Abstract

Parkinson’s disease is a slow onset, neurodegenerative disease that affects some 500,000 people in the United States alone. Mitochondrial dysfunctions, caused by mutations within dopamine generating cells, lead to the slow loss of functioning neurons. Three important genes have been identified in the causation and prevention of Parkinson’s disease. PARK7, PINK1, and Parkin work as cofactors within the mitochondria. PARK7 plays an important role in reducing free radicals (reactive oxygen species, ROS) in mitochondria. Likewise, PINK1 and Parkin are involved in mitochondrial morphology and function. Recent studies have indicated that PINK1 and Parkin work in series, which is parallel to the function of PARK7. These studies have brought insight into the interactions between the three complimentary genes, as little was known regarding their interaction previously. Additionally, studies of PARK7 have indicated two variants of the gene, which may determine the pathology of the disease. Wild type PARK7 encodes elongated mitochondria, which promotes normal function. In contrast, mutated PARK7 causes increased fragmentation of the mitochondria, thereby leading to a decrease in function. While a great deal of knowledge has been acquired about the pathophysiology of Parkinson’s disease, more research is needed to determine exact mechanisms and potential treatments.