To study a gene mutation identified in Parkinson's disease sufferers, researchers have developed a new mammalian model which could help in developing new drugs to treat the condition.

Until now, researchers have encountered difficulty in reproducing PD pathology in animals because of an incomplete understanding of the disease.
Recently, a mutation of the gene coding for LRRK2, a large enzyme in the brain, has emerged as the most prevalent genetic cause of PD (genetics are implicated in about 10 percent of all PD cases). When the enzyme is mutated, it becomes hyperactive, causing the death of vulnerable neurons and leading to a reduction in levels of the brain neurotransmistter dopamine.
This decrease in dopamine eventually triggers the symptoms characteristic of Parkinson's, such as tremors, instability, impaired movement, and later stage dementia.
Now, Aebischer and his team have successfully introduced mutant LRRK2 enzyme into one hemisphere of a rat brain, resulting in the same PD manifestations that occur in humans in one side of the rodent's body.
To do this, the researchers spent two years producing and optimizing a viral vector to deliver mutated, LRRK2 coding DNA into the rat brain. LRRK2 is a large and complicated enzyme and designing a vector capable of transporting its extremely long genetic code was no small feat.
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Armed with the LRRK2 model, new pharmaceuticals that inhibit the hyper-activity of the enzyme could one day prevent the destructive chain of events that leads to neurodegeneration and devastation in many with PD.
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Source-ANI