Inside cells, organelles called mitochondria carry out a medley of vital tasks. These structures generate energy and help to keep the cells’ interior environment in a state of healthy equilibrium, among other functions. Now, scientists show in detail how alpha-synuclein, a protein associated with Parkinson’s disease, can damage these cellular powerhouses.

Now, scientists show how a protein associated with Parkinson’s disease can damage these cellular powerhouses.

The findings come from experiments in which fruit fly larvae were genetically engineered to produce unusually high amounts of the protein, called alpha-synuclein.

«When fruit fly larvae expressed alpha-synuclein at elevated levels similar to what is seen in Parkinson’s disease, many of the mitochondria we observed became unhealthy, and many became fragmented. Through detailed experiments, we also showed that different parts of the alpha-synuclein protein seem to be responsible for these two problems, and that fragmented mitochondria can actually be healthy. This is a key finding, because before, people thought fragmented mitochondria were unhealthy mitochondria,» says Shermali Gunawardena, PhD, associate professor of biological sciences in the University at Buffalo College of Arts and Sciences.

The results could be of interest in the context of drug development, as abnormal aggregates of alpha-synuclein in brain cells are a hallmark of Parkinson’s disease, and mitochondrial damage has also been observed in patients.

«This research showcases the advantage of using fruit fly larvae as a model organism to study how neurons become damaged during devastating diseases such as Parkinson’s disease,» says TJ Krzystek, UB PhD candidate in biological sciences. «Through this approach, we pieced together a new understanding for how the Parkinson’s disease-related protein alpha-synuclein disrupts the health and movement of mitochondria — the epicenter for energy production in cells. We believe this work emphasizes a promising path that can be explored for potential therapeutics aimed at improving mitochondrial health in Parkinson’s disease patients.»

The study was published on Aug. 17 in the journal Cell Death and Disease.

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Materials provided by University at Buffalo. Original written by Charlotte Hsu. Note: Content may be edited for style and length.