Aug. 21 (UPI) -- Researchers have developed a new tool that can evaluate new therapies for Parkinson's disease, which they say could lead to quicker development of drugs to treat the neurological condition.
In a test of mice, the new model induces the biology of a disease-causing gene rather than the symptoms. Researchers at the University of British Columbia's Djavad Mowafaghian Center for Brain Health published their findings Tuesday in the journal Nature Parkinson's Disease.
Parkinson's disease is a chronic, degenerative neurological disorder that affects the body's motor system, causing people to shake and have difficulty with movements. In the United States, about 10 million people have the illness, according to the Parkinson's Disease Foundation.
Many patients have mutations in a gene called LRRK2, which researchers in British Columbia discovered in 2004.
"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," lead investigator Dr. Matthew Farrer, a researcher at the center, said in a press release. "This means we're looking at the disease before it becomes symptomatic, before it begins affecting an individual's motor skills or cognition."
An available experimental model involved flooding the brain with alpha-synuclein, which is a protein that, when it accumulates abnormally into clumps, is linked to Parkinson's. Another method is using neurotoxins to destroy dopamine-producing cells. But with these methods, inducing the disease means the cells die before any of the subtle changes can be measured.
No LRRK2-specific drugs have been developed to treat Parkinson's.
The new method, which is known as a VPS35 D620N knock-in, or VKI, induces the biology of a disease-causing gene rather dealing with the symptoms.
The VKI model shows an important relationship to dopamine neurotransmission, which plays roles in the brain.
The British Columbia researchers first suspected a relationship between LRRK2 and VPS35 in 2012, but it was the first time they observe activity-dependent changes in dopamine release and reuptake from a single mutation.
"What's really exciting for us is that everything we're seeing is pointing to an early change in synaptic activity," Igor Tatarnikov, a graduate student working with Farrer, said. "It's something we might rescue with the right drugs, and something we might visualize, because LRRK2 and VPS35 affect the same biological pathway. We're hoping to use PET imaging to provide a clinically relevant biomarker, which would be relevant beyond genetic forms of the disease."
Farrer said the animal studies are putting them on the path to developing drugs to treat the disease.
"Imagine if we could begin helping people at risk of Parkinson's disease as early as their 40s and 50s," he said. "We believe we're in the right key with LRRK2 and VPS35, now it's just a matter of arranging the notes."