Loss of dopaminergic neurons is a hallmark of Parkinson’s disease pathology. When dopaminergic neurons are stressed, they send out a call for help to nearby glial cells that are tasked with providing neuronal support, protection and nourishment. Under particular molecular conditions, those calls for help can over-activate the glial cells, resulting in a cascade of inflammatory signaling that eventually contributes to the degradation of these neurons over time. Working in two fruit fly models of Parkinson’s disease, researchers at the Buck Institute have characterized a novel molecular mechanism that orchestrates such a harmful cascade of inflammatory signaling and demonstrated that its disruption protects neurons as they age. The research, published in Cell Reports, provides a new framework for understanding the pathology of Parkinson’s disease and offers an alternative approach for developing preventative treatments for a neurodegenerative disorder that afflicts millions of patients worldwide.