Investigators at Boston University School of Medicine (BUSM) have spotlighted the cascade of events that contributes to neuronal death in idiopathic Parkinson's disease. And they're hoping that their insights can be used as a springboard to the discovery of new drugs for the fatal and perplexing disease.
The problem, the researchers say, is that a newly discovered defect in the way PLA2g6 proteins function in turn triggers a dysfunction in calcium homeostasis that threatens the existence of cells. Being able to reproduce the defect in a genetic model of the disease, they add, other researchers can zero in on that mechanism for drug research.
There are two forms of Parkinson's, idiopathic--which is the most common--and familial.
"Idiopathic or genetic dysfunction of calcium signaling triggers a sequence of pathological events leading to autophagic dysfunction, progressive loss of dopaminergic neurons and age-dependent impairment of vital motor functions typical for Parkinson's disease," explained corresponding author Victoria Bolotina, a professor of medicine at BUSM.
Their work was published in Nature Communications and supported by research grant awards from The Michael J. Fox Foundation for Parkinson's Research, the NIH, BU and others.
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