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.

Image credit: iStock

We live in a world where facts and fiction get blurred
In times of uncertainty you need journalism you can trust. For 14 free days, you can have access to a world of in-depth analyses, investigative journalism, top opinions and a range of features. Journalism strengthens democracy. Invest in the future today. Thereafter you will be billed R75 per month. You can cancel anytime and if you cancel within 14 days you won't be billed. 
Subscribe to News24
Voting Booth
Zama zama crackdown: What are your thoughts on West Village residents taking the law into their own hands?
Please select an option Oops! Something went wrong, please try again later.
Authorities should bring in the army already
10% - 2489 votes
Illegal miners can't be scapegoated for all crime
52% - 12640 votes
What else did we expect without no proper policing
34% - 8187 votes
Vigilante groups are also part of the problem
3% - 811 votes
Rand - Dollar
Rand - Pound
Rand - Euro
Rand - Aus dollar
Rand - Yen
Brent Crude
Top 40
All Share
Resource 10
Industrial 25
Financial 15
All JSE data delayed by at least 15 minutes Iress logo
Editorial feedback and complaints

Contact the public editor with feedback for our journalists, complaints, queries or suggestions about articles on News24.