Researchers have discovered that mutations in the gene GIGYF2 appear to be directly linked to the development of Parkinson's in people with a family history of the disease.
According to the findings of the study, published online Thursday in the American Journal of Human Genetics, the gene is one of only a handful linked to Parkinson's, which has no known cause or cure. This new gene could hold the key to developing new treatments for Parkinson's.
Parkinson's is a progressive and often debilitating movement disorder that affects millions of people around the world.
Although less than a quarter of all cases of Parkinson's are familial, researchers believe genes like GIGYF2 can provide clues to the mechanisms behind Parkinson's and could point to new treatments for the more common and sporadic forms of the disease.
"These findings may ultimately help open the door to the development of new therapeutic -- and possibly even preventive -- strategies that target the underlying cause of Parkinson's disease, improving the quality of life of the many people worldwide who are affected by this devastating disorder," said senior author Robert J. Smith at Rhode Island Hospital.
Their research also revealed an intriguing secondary finding --the possible association between Parkinson's and insulin and the related hormone known as insulin-like growth factor (IGF). This joins a small but growing body of research linking insulin and IGFto Parkinson's disease and other neurodegenerative disorders, such as Alzheimer's.
"A better understanding of the link between insulin or IGF and Parkinson's may lead us to new treatment strategies for Parkinson's and also new insights into the connection between diabetes and nervous system disorders," Smith said.
Parkinson's is one of the most common neurodegenerative disorders, second only to Alzheimer's, affecting between one and two percent of the population above age 60. The disease occurs when certain nerve cells in the part of the brain that controls muscle movement either die or become impaired.





