
Cancer tumors secrete Cystatin-C protein that crosses blood-brain barrier and activates brain immune cells to degrade Alzheimer’s plaques, explaining why cancer survivors show 40% lower Alzheimer’s rates. Mouse studies show purified Cystatin-C reversed memory deficits and cleared existing brain plaques, unlike current drugs that only slow progression.
⚖️ PROFESSIONAL IMPACT
- Mouse models demonstrated Cystatin-C activated microglial degradation of pre-existing amyloid plaques, reversing cognitive deficits in water maze memory tests.
- Discovery explains inverse epidemiological relationship between cancer survival and Alzheimer’s development observed across population studies for decades.
- Purified Cystatin-C crossed blood-brain barrier and bound TREM2 receptors, distinguishing mechanism from current amyloid-lowering therapeutics that prevent new plaque formation.
- Findings establish novel therapeutic pathway targeting plaque degradation rather than prevention, potentially applicable to patients with established Alzheimer’s pathology.
🎯 ACTION ITEMS
- Monitor emerging Cystatin-C trials for potential Alzheimer’s therapeutic applications.
- Review cancer survivor patients for cognitive protection patterns in longitudinal care.
- Document family history of both conditions when counseling on Alzheimer’s risk factors.
- Educate patients that inverse relationship remains observational, not indicating cancer as prevention strategy.
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