Mouse studies reveal that cystatin-C, a protein released by certain tumors, penetrates the blood-brain barrier and activates microglia cells to break down amyloid-beta plaques characteristic of Alzheimer's disease. This discovery emerges from observations that cancer patients rarely develop Alzheimer's, suggesting tumor-derived factors may provide neuroprotection. The finding builds on decades of epidemiological evidence showing an inverse relationship between cancer and neurodegenerative diseases, though the mechanisms remained unclear until now. Cystatin-C appears to reprogram brain-resident immune cells into a more aggressive plaque-clearing phenotype, potentially offering a novel therapeutic pathway. However, significant hurdles remain before clinical application. The protein's effectiveness in human brains, optimal dosing strategies, and long-term safety profiles are unknown. Additionally, synthetic production of therapeutic-grade cystatin-C would need to avoid cancer-promoting properties while preserving neuroprotective effects. This represents early-stage mechanistic research that could eventually inform Alzheimer's treatment strategies, but translation to human therapy requires extensive validation and likely years of additional research to address safety and efficacy questions.