 Glucoserabrosidase mutations cause gossous disease, which is the most common risk factor for Parkinson's disease. Therapies to restore the enzyme's function in the brain have great promise for treating the neurological implications. To do this, researchers created a fusion protein called GKSBS, which has transferrin receptor binding moieties attached to it. This fusion protein showed significantly improved uptake and lysosomal efficiency compared to the enzyme alone. In a cellular disease model, GKSBS was able to rescue the lysosomal protome and lipid accumulation beyond known substrates. In a mouse disease model, intravenous injection of GKSBS led to a sustained reduction of glucosalcine and lowered neurofilament-light chain plasma levels. These results suggest that GKSBS could be used to treat GBA1-associated lysosomal dysfunction, providing insight into potential biomarkers and opening up a new treatment paradigm for lysosomal storage diseases. This article was authored by Alexandra Gehrlein, Vinod Udaya, Nadia Onostosi, and others.