A study out of the University of Ottawa Faculty of Medicine has shown the immune system to play a larger role in the pathogenesis and progression of Parkinson’s Disease (PD) than previously thought – a discovery that opens the doors to potential new therapeutics.
Parkinson’s affects 10 million people worldwide, caused by a loss of specific brain cells leading to progressive decline of motor control.
The gene most commonly implicated in PD, LRRK2, had already been linked to the immune system. The gene is expressed as a protein in many immune cells, including those in the brain (microglia). When this gene mutates, it modifies the ability of the microglia to carry out phagocytosis (ingesting materials in the body, such as microorganisms). The resulting neurodegeneration indicates that these excessively phagocytic microglia can be toxic to those cells known to progressively die in PD.
Traditionally, research into PD has focused on the neurons themselves. However, the uOttawa study, published recently in journal PNAS, unlocks the potential to also study the role of immune signalling in PD—or, how immune cells are triggered to carry out their various roles in the immune system. Exploring immune signaling may add to the roster of potential therapeutic targets in the disease.
“Our findings should alert the field to explore the role of immune signalling in PD and neurodegeneration,” says lead author Dr. Kwang Soo Kim, postdoctoral fellow in the Department of Cellular and Molecular Medicine at the time of the paper’s writing. “This is currently happening in the Alzheimer's field as many Alzheimer's-associated genes are only expressed in microglia.”
“LRRK2 mutations are also implicated in Crohn's disease and leprosy, both immune-related disorders,” explains Dr. Paul Marcogliese, co-first author of the paper with Dr. Kim. “Our work begs the field to examine immune signalling to potentially discover therapeutics that could at a minimum slow the progression of this devastating disease.”
Main photo credit: Freepik
