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VAI researchers discover "master regulator" that may lead to Parkinson's Disease treatments

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Van Andel Institute

Parkinson’s Disease impacts the brains of more than 10 million people. It’s a nerve degenerative illness causing motor and non-motor symptoms. At Grand Rapids Van Andel Institute, researchers have discovered molecular marker that may lead to protecting the brain from inflammatory damage.

In a study published in Nature Neuroscience, Van Andel Institute researchers isolated brain neurons. In Parkinson’s Disease some of these cells die causing symptoms.

Associate professor, Dr. Viviane Labrie is the studies senior author.

“We found that in brain neurons there were DNA metholation abnormalities that affected the survival of neurons, and in another data set, we found that there was a high level of inflammatory activity in Parkinson’s Disease brains.”

Labrie and her team discovered an abnormal function of a gene called TET2. It’s a master regulator that could serve as the “switch” protecting the brain.

“Our most remarkable finding was that when we eliminated TET2 activity in a model system, we found that neurons that would otherwise die in a Parkinson’s Disease brain were fully protected from the damaging affects of inflammation. We saw that reducing TET2 activity both protected the neurons and reduced levels of inflammation in the brain.”

Labrie says the study reveals a new target that can potentially protect neurons and lower inflammation that could one day lead to a Parkinson’s Disease treatment.

Patrick joined WGVU Public Media in December, 2008 after eight years of investigative reporting at Grand Rapids' WOOD-TV8 and three years at WYTV News Channel 33 in Youngstown, Ohio. As News and Public Affairs Director, Patrick manages our daily radio news operation and public interest television programming. An award-winning reporter, Patrick has won multiple Michigan Associated Press Best Reporter/Anchor awards and is a three-time Academy of Television Arts & Sciences EMMY Award winner with 14 nominations.