Given the well-characterized biochemical roles of PD-associated proteins such as GBA1 and GPNMB in regulating lipid metabolism and/or dynamics and considering the commonalities and overlap in AD and PD pathophysiology, including and not limited to excess oxidative stress and sterile inflammation, it is intriguing to consider whether preventing LD accumulation in PD models and/or patients can be utilized to halt disease progression. Here, GBA1 is linked to Parkinson disease.