Tumor-derived cystatin C enables amyloid clearance.

Li et al. described a tumor-derived neuroimmune mechanism that promotes clearance of established amyloid pathology in Alzheimer's disease. secreted cystatin C activates TREM2-dependent microglial phagocytosis, reducing plaques and improving cognition. This work introduces a context-dependent neuroimmune-modulatory strategy that shifts Alzheimer's therapy from broad immune activation toward substrate-coupled amyloid clearance.