Cancer may spark surprise defense against Alzheimer’s

Study Explores Cancer-Alzheimer’s Link

A recent study published in the journal Cell sheds light on the intriguing connection between a history of cancer and a lower risk of developing Alzheimer’s disease. Using mouse models, researchers investigated how biological changes triggered by cancer might influence the progression of this common form of dementia. The findings highlight a potential protective mechanism, where proteins released by certain cancers could interfere with Alzheimer’s hallmarks, offering new insights into a long-observed but puzzling phenomenon known as inverse comorbidity.

Mechanism of Protection Uncovered

The research revealed that specific cancers produce a protein called cystatin-C, which circulates through the bloodstream and penetrates the brain—a challenging area for many Alzheimer’s treatments. Once in the brain, cystatin-C binds to harmful amyloid protein clumps associated with Alzheimer’s and activates TREM2, a protein that stimulates the brain’s immune cells. This activation prompts the cells to clear away existing amyloid plaques, resulting in reduced plaque accumulation and enhanced cognitive function in the mouse models.

Insights from Medical Experts

Dr. Bob Arnot, an internal medicine physician from Vermont who was not involved in the study, commented to Fox News Digital that these results help explain a pattern clinicians have noticed for years. He described inverse comorbidity, where individuals with cancer are less prone to Alzheimer’s, and vice versa. Arnot emphasized that the study identifies biological signals from certain cancers that may inadvertently slow or reverse key aspects of Alzheimer’s, engaging protective immune responses in the brain.

Potential for Future Treatments

The research is significant because it points to a specific pathway that could inspire new Alzheimer’s therapies, particularly those targeting established amyloid plaques rather than just prevention. However, Arnot stressed that this does not imply cancer itself is beneficial or a treatment option. Instead, it suggests focusing on mimicking these protective mechanisms to clear brain buildup. The study is based on animal models, so additional human research is essential to confirm these effects and explore therapeutic applications.

Source