Analyzing the Link between PINK1 and Neurodegenerative Disease Using C. elegans

Mitochondria are organelles in the cell that are responsible for producing energy in the form of ATP through the electron transport chain in the mitochondrial membrane. Mitophagy is the programmed destruction of damaged mitochondria, and PINK1 is a protein kinase that flags these unhealthy mitochondria for mitophagy. Existing evidence shows a link between mutations in pink1 and familial Parkinson’s disease and other neurodegenerative diseases. The mechanism as to how PINK1 loss of function can cause Parkinson’s disease is unknown, but it has been suggested that the disruption of the mitophagy pathway plays a key role. To assess mitochondrial health and energy production, this study tracks the overall fitness of different strains of C. elegans with pink1 mutations by recording their lifespans and brood sizes. C. elegans are an ideal model organism for this study due to their homology to human pink1, their short lifespans, and their fast regeneration. Each strain has a different type of deletion in the PINK1 coding gene that causes its loss of function. This study reports a significant difference between the effects of each deletion on different aspects of the worms’ health. The data supports the theory that different domains of PINK1 are responsible for different functions, and further research into these domains can help elucidate the mechanism by which pink1 mutations attribute to the disease state.