Dr. Mattia Volta, University of British Columbia
$100,000 over 2 years during the 2014 – 2016 research funding cycle
Project description:
“We hope to develop a therapeutic strategy, a treatment avenue that can be tested in other models and ultimately in humans, but that will take time.”
Although researchers haven’t pinpointed what triggers most forms of Parkinson’s disease, the interaction or collaboration among multiple genes and proteins is almost certainly critical to the spread of the illness from one damaged brain cell to another.
At the University of British Columbia, neuroscientist Mattia Volta concentrates on the relationship between the proteins alpha-synuclein and LRRK2 – and what happens if you can take one of those proteins out of the equation. Volta, who began studying Parkinson’s disease in his native Italy, works with animal models missing the LRRK2 protein. He documents what happens when mice without LRRK2 are treated with a substance to replicate the alpha-synuclein protein.
Clumps of alpha-synuclein are present in the brain cells of people with Parkinson’s disease, and mutated forms of both proteins cause familial forms of Parkinson’s. Volta has collected preliminary data indicating mice without LRRK2 are free from the cognitive impairment or memory loss that occurs in mice that have both LRRK2 and alpha-synuclein present in their brains.
“Removing LRRK2 appears to be protective when it’s early in the disease’s progression,” Volta says. Now he’s investigating whether the absence of LRRK2 in mice also protects them against the motor problems and progression of the disease that follow cognitive changes and memory loss in Parkinson’s disease. Eventually, Volta will knock out LRRK2 to see if removing the first protein can reverse or stop the brain cell death that clumps of alpha-synuclein cause.