According to a story from Parkinson’s News Today, a recent study has found a new connection between two different features that appear in Parkinson’s disease. These features are lysosomal dysfunction and mitochondrial defects, issues that appear in neurons which lacked expression of a gene called PARK2. Mutations of this gene are present in some cases of early-onset Parkinson’s. While Parkinson’s disease as a whole is not considered rare, the early-onset form is.
About Parkinson’s Disease
Parkinson’s disease is a type of long term, progressive, degenerative illness that affects the central nervous system. Symptoms tend to develop over a period of years and primarily affect the movement ability and mental state of the patient. The cause of Parkinson’s disease remains a mystery, although there are a number of risk factors that have been identified. These factors include head injuries, pesticide exposure, and certain genetic variants and mutations. About 15 percent of patients have a close relative with the disease, suggesting some genetic connection. Symptoms include slowed movements, poor coordination, trouble walking, shaking, stiffness, abnormal posture, depression, anxiety, inhibited thinking, hallucinations, and dementia. Treatment may involve a number of medications, rehabilitation, and surgical operations. Survival rate varies, but most patients survive around a decade after getting diagnosed. To learn more about Parkinson’s disease, click here.
About the Research
PARK2 mutations are considered to be the most frequent cause of early-onset disease. The gene codes for a protein known as parkin. This protein is known to play a role in the activity of mitochondria (energy producing cellular organelles) and their interactions with lysosomes (organelles that recycle waste material).
A comparison of dopaminergic neurons with normal PARK2 function and without revealed multiple changes. When parkin was absent, the lysosome activity dropped even while proteins associated with them increased; the lysosomes were also greater in size and number. There were changes to the mitochondria as well; they tended to be nearer the nucleus and were misshapen.
After a test using a chemical on the control neurons to trigger mitochondrial stress, the researchers concluded that issues with mitochondrial function ultimately led to lysosomal buildup over time. With a link now established between mitochondrial defects and lysosome dysfunction, only continued research will reveal any possible implications for treatment.
Check out the original study here.
