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Collaborative Success Stories: Turning the ‘Tide


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University of Missouri researchers say a peptide in brain cells could be the key to treatment for early onset Parkinson’s disease.

Cells are powered by tiny structures called mitochondria. Eventually they wear out, and special proteins move them to the cell’s lysosome, a “recycling center” that restores them to function. However, in early onset Parkinson’s disease, these proteins mutate and stop transporting mitochondria—causing a buildup that kills brain cells, with debilitating results.

MU Bond Life Science Center (LSC) researchers have identified a molecule that could circumvent the problem. The team, led by biochemist Mark Hannink, located an alternative pathway which bypasses the mutated proteins, using a different protein called PGAM5 to recycle the mitochondria. PGAM5 can be triggered to create the pathway by a peptide that acts as an “on/off switch.” Switching it on could restore mitochondrial recycling, lessening the disease’s severity.

Hannink says the next step is to search for a drug molecule that can control PGAM5 just as the peptide did. If further studies are successful, researchers may be on the road to developing new treatments for early onset Parkinson’s disease.

Dr. Mark Hannink is a researcher at Bond LSC and a professor in the division of Biochemistry, an interdisciplinary unit of the School of Medicine and the College of Agriculture, Food and Natural Resources.

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Related Initiative(s):
One Health/One Medicine