Reshaping Mitochondrial Efficiency and Integrity to Treat Parkinson’s Disease
- Ruth Slack, University of Ottawa
- David Park, University of Ottawa
- Louis-Eric Trudeau, Université de Montréal
- Laura Trinkle-Mulcahy, University of Ottawa
- Krembil Foundation
Parkinson’s Disease (PD) is a debilitating neurodegenerative disease for which there is no cure. This movement disorder is thought to be due to the loss of a specific population of nerve cells, the dopamine (DA)-containing neurons located in the substantia nigra pars compacta (SNc). The question as to why this small population of cells die and cause PD has been an enigma for decades and understanding the unique vulnerability of these neurons would provide important clues to the successful treatment of PD. Dr. Slack and her team have recently discovered that, in these neurons, the mitochondria (the cell’s energy provider) are producing energy at ‘burn-out’ levels, unlike other cells in the brain. When mitochondria work at such excessively high levels, they leak a damaging byproduct called reactive oxygen species (ROS), which can cause massive damage leading to cell death. For this project, the team is studying mitochondrial function and understanding how they adapt to environmental changes and respond to stress. They are using number of different approaches to identify new molecules to trigger mitochondrial reconfiguration to increase their efficiency and resistance to stress. Their study is designed to identify new molecular targets that can be triggered by pharmacological approaches to enhance mitochondrial energetic efficiency and protect this vulnerable neuronal population in PD. They predict that activating mitochondrial reconfiguration will provide a novel approach to treat PD.