Previous research has demonstrated that alpha-synuclein can damage mitochondria, the organelle responsible for cellular energy production, contributing to the progression of Parkinson’s disease. New research from the State University of New York at Buffalo sheds light on the previously undiscovered ways that alpha-synuclein affects mitochondria.
In a paper published in August in Cell Death and Disease, fruit fly larvae were genetically altered to overexpress alpha-synuclein, which caused their mitochondria to fragment, become damaged, and get marked for destruction. Researchers discovered that one end of alpha-synuclein interacts with the PINK1 and Parkin proteins to influence the health of mitochondria while the other end interacts with DRP1 to fragment the mitochondria. They also discovered that fragmented mitochondria are not necessarily unhealthy, as previously believed.
The discovery that different parts of the alpha-synuclein protein are responsible for affecting mitochondria in different ways offers potential pathways for the exploration of future therapies for Parkinson’s disease.