Parkinson’s disease (PD) affects 1 percent of the population over 65, and the question of how it develops still remains unanswered. One of the more recently studied risk factors for Parkinson’s comes from inside the body.
As we age, our genetic material is harmed by molecules called reactive oxygen species (ROS). Think of them as sizzling sticks of dynamite with a short fuse, latching onto strands of DNA and damaging them with a chemical reaction. One of the only ways to thwart their plot is with the body’s disaster response team: proteins that repair broken DNA before it causes any additional damage to our body. Mutations in these proteins mean that damaged DNA goes unfixed, and that ROS are free to wreak havoc on the brain and body — leading to neurodegenerative diseases like Parkinson’s.
A recent study looked at three different mutations in DNA repair proteins to see if these mutations were linked with a higher PD risk. The researchers isolated DNA from 97 Parkinson’s patients and 102 healthy controls to see if there was a relationship between the mutations they had and their health status. They found no relationship between two of the mutations and Parkinson’s, but a mutation in the XRCC1 gene made it two to three times more likely that a patient would have PD. The higher incidence of XRCC1 mutations in Parkinson’s patients compared to controls indicates that this mutation could be a risk factor for PD, and if studied further, could provide more information about how dysfunctional DNA repair can lead to brain damage and disease.
Parkinson’s has several potential risk factors, and many of them are extrinsic: cigarette smoke, heavy metal exposure, or pesticides. The study of DNA damage and repair reveals that PD risk factors can have a significant impact even at the molecular level. Understanding the deadly dance between ROS, DNA, and repair mechanisms may reveal more about how Parkinson’s gets its hooks into the brain and body.