Although the exact cause of Parkinson’s disease (PD) is unknown, scientific research suggests that mutations in genes such as Parkin and PINK1 have a significant role in the progression of PD. These genes are involved in helping to maintain the health of cells, in part through their actions on mitochondria, the part of the cell whose function is to produce energy and to regulate metabolism.

Some of the world’s most important research into the mechanism of Parkinson’s disease is being conducted at McGill University in a collaboration among researchers of the Neurodegenerative Diseases Group of the Montreal Neurological Institute and Hospital (The Neuro), the Department of Pharmacology and Therapeutics, and the Groupe de Recherche Axé sur la Structure des Protéines.

In a paper published in the journal Nature Communications, researchers Matthew Y. Tang, Marta Vranas, Andrea I. Krahn, Shayal Pundlik, Jean–François Trempe and Edward A. Fon uncover more about the function of Parkin, a protein that, when dysfunctional, contributes to the development of PD.

The researchers showed that introducing activating mutations that relax Parkin into an “open” conformation can enhance its function – activated Parkin can remove damaged mitochondria faster. So the idea is if you get this inhibited pathway to be fully functional it may have benefits for patients with PD. The goal is to find a drug that can activate the pathway better and thus give the cell a greater chance to survive. The mechanism by which Parkin is activated is crucial to finding such a drug that would open up Parkin and activate it.