Yes, not everyone thinks this is a big deal.
You are correct that a number of mutated forms of LRRK2 are precursors to PD. It was assumed that "wild type" LRRK2 was benign and not a factor. Except that may have changed...
"A recently published research article in Science Translational Medicine titled “LRRK2 activation in idiopathic Parkinson’s disease” (Di Maio et al., 2018) sought to investigate whether the wild-type (normal, as opposed to mutated) LRRK2 plays a role in idiopathic PD. What they found is stunning. By developing two new tests to determine the activation state of LRRK2 under different conditions, the research scientists revealed a series of connections that may lead to breakthrough PD therapies. In short, there might be a new way to help treat all people with PD."
Essentially, both the mutated LRRK2 and the "wild type" (unmutated) LRRK2 both "have the same downstream pathogenic effects"
Therefore this is potentially relevant for all PD folks not just the 2% with the most common form of the mutated gene.
Now the race is on.
'Denali Therapeutics -- a San Francisco-based biotech -- presented data from its Phase I LRRK2 trial to more than 300 Parkinson's researchers and industry professionals. As reported in the story, Denali's Phase I study, which investigated the drug in healthy volunteers, sought to answer two important questions:"Can the LRRK2 drug block the LRRK2 enough that it might work in Parkinson's patients? Can it do so without serious side effects, particularly in the lungs, or related to blood pressure? The answer to both questions appears to be yes."
