By focusing on the protein regarded as likely responsible for late-onset Parkinson’s disease, scientists at the National Institutes of Health's National Institute of Neurological Disorders and Stroke (NINDS) recently succeeded in further pinpointing certain mutations that trigger the neurological condition.
Laboratory studies revealed that the protein, LRRK2, is vital to the existence of neurons containing dopamine, suggesting the possibility of modifying treatment in humans, an NIH release said. LRRK1 and LRRK2 are related proteins, and whereas a mutation in LRRK2 alone can spur Parkinson’s in humans, it was not found to be so with mice – possibly due to altered roles of the protein in the rodents’ short lifespans, the release said.
“Parkinson’s-linked mutations such as LRRK2 have subtle effects that do not produce symptoms until late in life. Understanding the normal function of these types of genes will help us figure out what has gone wrong to cause disease,” Jie Shen, the study’s senior author, said in the release “Our findings show that LRRK is critical for the survival of the populations of neurons affected by Parkinson’s disease.”
Shen directs the NINDS Morris K. Udall Center of Excellence for Parkinson’s Disease at Brigham and Women’s Hospital in Boston. She and her team are continuing their work with mice to further analyze long-term changes of Parkinson’s, the release said.