From the Faculty of Medicine:
Under the collaborative umbrella of the uOttawa Brain and Mind Research Institute (uOBMRI), past papers from Dr. Park and fellow researchers have shown PINK1 to be associated with Parkinson’s. However, this week’s paper marks a deeper understanding of the molecular mechanisms behind it.
Mitochondria are the organelles that process nutrients within a cell, including calcium. Dr. Park’s team found that a protein in the PINK1 gene modifies mitochondrial protein LETM1, a process that plays a critical role in calcium transport in mitochondria. Deactivation of the PINK1 gene—knocking the gene out of mouse models mimics a natural mutation in humans—causes dysfunction of LETM1. This interrupts mitochondria’s normal processing of calcium and leads to brain cell death.
By identifying the specific mechanism causing a cell to mishandle calcium, new targets for drugs have been revealed, opening doors for potential new treatments for Parkinson’s. Five years of research have culminated in these results which En Huang, research associate in the Faculty’s Department of Cellular and Molecular Medicine and co-author of the paper, confirms can proceed to new avenues of drug testing.
“We’ve uncovered a novel molecular pathway in the pathogenesis of Parkinson’s,” Huang says. “Essentially, this means we’ve identified potential targets for new drugs.”