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Stanford study identifies molecular mechanism that triggers Parkinson’s

Stanford's Bingwei Lu, PhD, and his colleagues have unraveled a molecular pathway though which a frequently occurring mutation may be causing Parkinson's disease. The mutation in question has been found in as many as one-third of all Parkinson's cases among Ashkenazi (European descent) Jews and North African Arabs, whose common Semitic origin places the two ethnic groups closer together, genetically speaking, then some might think.

This finding highlights the growing number of diverse roles played in every mammalian cell by a molecular entity, RNA, that was once viewed as somewhat of a cellular stepchild. The nonscientists among us who have heard of RNA tend to think of it as a collection of chemical copies that carry genetic instructions from the nucleus-bound master blueprint - our vaunted DNA-constituted genome - to the outer regions of a cell. Here, these copied instructions can be read by molecular machines that produce proteins - the muscled working-class citizens of the cell - according to DNA's specifications.

But, it turns out, RNA is doing much, much more. The Lu study highlights a pint-sized player called microRNA, which doesn't encode instructions for making proteins at all. Instead, it binds to those longer, instruction-trucking RNA molecules, rendering them at least temporarily unreadable. Thus, microRNA fine-tunes the rate of protein production within cells.

And when microRNA can't do its job, bad things can happen to good people. In the Lu study, restoring microRNA function not only relieved symptoms but actually prevented the nerve-cell death that classically defines Parkinson's disease.

Caution: Much more work needs to be done before these findings can be translated into Parkinson's treatments.This study was performed in fruit flies. At the level of the cell, these creatures are remarkable similar to humans. But there's still "plenty o' slip 'twixt the cup and the lip."

On the other hand, some of the newly implicated molecular players in the mutation-Parkinson's connection are already drug targets for entirely different diseases. So if studies in mammals bear out the Lu team's findings, it may be possible to pull these already extant compounds off the shelf and test them in humans, possibly making it easier for science to traverse the notorious "Valley of Death" that all too often separates basic research from medical payoffs.

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