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New Study Reveals How a Cancer Protein Could Fight Alzheimer’s

  • Jan 27
  • 2 min read

Updated: Jan 27

A microscopic 3D medical illustration depicts large, pinkish organic cells with vibrant blue and orange crystal-like structures protruding from their surfaces, set against a textured, fleshy background.

For years, scientists have puzzled over a strange medical anomaly: cancer survivors rarely develop Alzheimer’s disease, and conversely, Alzheimer’s patients are less likely to develop cancer. This "enemy of our enemy" relationship has sparked hope that one disease might hold the key to treating the other. Now, a breakthrough study published in the journal Cell may finally explain why this happens, offering a promising new avenue for dementia treatment.


Researchers at Huazhong University of Science and Technology discovered that the link lies in a specific molecule produced by tumor cells called Cystatin C. In experiments involving mice, the research team transplanted human tumors—specifically lung, colon, and prostate cancers—into mice predisposed to Alzheimer’s. The results were striking: the mice with cancer did not develop the sticky amyloid plaques that are the hallmark of Alzheimer’s disease.


The study revealed that Cystatin C acts as a "Goliath" capable of infiltrating the brain. Once it crosses the blood-brain barrier, this protein binds to amyloid plaques and triggers a signaling process involving the TREM2 receptor. This signal alerts the brain's immune cells, known as microglia, to attack and clear out the toxic plaque buildup. Consequently, the treated mice demonstrated improved memory and cognitive abilities, performing better in maze tests than their untreated counterparts.


However, experts urge caution before declaring a cure. This research is currently limited to mouse models, and the transition to human application faces significant hurdles. The relationship between these diseases is complex and multifactorial, involving various immune and metabolic changes. Furthermore, scientists note that while the blood-brain barrier weakens in early Alzheimer’s, allowing Cystatin C to enter, it is unclear if this natural process occurs early enough in humans to be protective.


Despite these caveats, the findings represent a significant conceptual advance. Rather than suggesting patients should contract cancer to avoid dementia, this research helps scientists design therapies that mimic the behavior of this cancer protein. By isolating the specific mechanism of Cystatin C and TREM2 activation, researchers hope to create a "cocktail of drugs" that could one day halt the progression of Alzheimer’s.



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Keywords: Cancer Protein Could Fight Alzheimer’s

Cancer Protein Could Fight Alzheimer’s



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