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Researchers announced that may have found the ideal tool for testing new disease therapies.
For the past ten years, Parkinson's disease researchers have relied on a very heavy handed approach to test new therapies for the disease, which may be a reason that the clinical trials of promising neuroprotective drugs have failed.
"We believe we've found an approach that is most relevant to humans, in that our models of gene dysfunction mimic the etiology of Parkinson's disease rather than its pathology -- meaning its beginning rather than its end," says Matthew Farrer, who is the study's lead investigator and one of the researchers at the Djavad Mowafaghian Centre for Brain Health at UBC. "This means we're looking at the disease before it becomes symptomatic, before it begins affecting an individual's motor skills or cognition."
The new model, developed by Farrer and his team could provide the precise tool that researchers have long wished would deliver the impact of LRRK2 inhibitors and other disease-modifying medications.