Could gene therapy stem the damage of Parkinson's?
- Protecting brain cells early on could delay or prevent the symptoms of Parkinson's disease
- Researchers found a master regulator gene called TET2 to be overactive in the brains of Parkinson's sufferers
- Reducing TET2 activity in the brain could protect brain cells from inflammatory damage and subsequent neurodegeneration
It may be possible to protect Parkinson's patients' brains from further damage by turning off a "master regulator" gene, researchers report.
"One of the biggest challenges in treating Parkinson's, other than the lack of therapies that impede disease progression, is that the disease has already laid waste to significant portions of the brain by the time it is diagnosed," said researcher Viviane Labrie, an associate professor at the Van Andel Institute, in Grand Rapids, Michigan.
"If we can find a way to protect critical brain cells from Parkinson's-related damage early on, we could potentially delay or even prevent symptom onset," she suggested in an institute news release.
Deadly for brain cells
Labrie and her colleagues compared the brains of Parkinson's patients and people without the neurodegenerative disease and found that a master regulator gene called TET2 was overactive in the brains of those with Parkinson's. That resulted in a heightened immune response and reactivation of the cell cycle.
While restarting the cell cycle is normal for many types of cells, it's deadly for brain cells, the study authors explained.
The researchers also found that reducing TET2 activity in mouse brains protects brain cells from inflammatory damage and the resulting neurodegeneration seen in Parkinson's disease patients.
These and other findings suggest that lowering TET2 activity could provide a new way to preserve brain cells in Parkinson's patients, according to the authors of the study published in the journal Nature Neuroscience.
A complex disease
For example, reducing TET2 activity might be used after a patient has a major inflammatory event, such as an infection, to relieve residual inflammation without interfering with its normal, healthy role in the body.
"Parkinson's is a complex disease with a range of triggers. Temporarily reducing TET2 activity could be one way to interfere with multiple contributors to the disease, especially inflammatory events, and protect the brain from loss of dopamine-producing cells," Labrie said.
"More work is needed before a TET2-based intervention can be developed, but it is a new and a promising avenue that we already are exploring," she concluded.
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