Researchers have discovered new evidence that Parkinson’s disease may have an infectious or autoimmune origin.
The study was conducted by the NeuroGenetics Research Consortium, an international team of researchers led by Haydeh Payami, research scientist at the New York State Department of Health Wadsworth Center. The clinical directors for the study were Dr. Cyrus Zabetian, Stewart Factor and John Nutt.
In the study, researchers detected a new association with the HLA (human leukocyte antigen) region, which contains a large number of genes related to immune system function in humans.
HLA genes are essential for recognizing foreign invaders from the body’s own tissues.
Similarly, HLA molecules are supposed to recognize a body’s own tissue as itself and prevent immune reactions against them. But the system doesn’t always work perfectly.
Certain variants of the genes are associated with increased risk or protection against infectious disease, while other variants can induce autoimmune disorders in which the immune system attacks the body’s own tissues.
People who take non-steroidal anti-inflammatory drugs (NSAIDs, such as ibuprofen) have a reduced risk of developing Parkinson’s disease, which also supports an immune-related mechanism.
Pursuing the connection between Parkinson’s disease and inflammation, especially in the context of variable genetic makeup, may lead to better, more selective drugs for treating Parkinson’s disease.
“Our results also pointed to several other genes that might play a role in developing Parkinson’s disease, and these findings need to be confirmed, so we have a lot of work ahead of us,” Nature quoted Zabetian as saying.
The study appears online in Nature Genetics.