Cancer may trigger unexpected defense against Alzheimer’s disease, researchers say

Puzzling cancer and Alzheimer’s link explored in new study: ‘SHORT QUOTE’

A new study may help clarify a long-observed link between cancer history and reduced Alzheimer’s risk.

The research, published in the journal Cell, used mouse models to explore how the biological changes associated with cancer may affect the progression of the most common dementia type.

The findings suggest that certain cancers release a protein called cystatin-C that can travel through the bloodstream and enter the brain, an area that many Alzheimer’s treatments have difficulty reaching.

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Cystatin-C binds to harmful amyloid protein clumps linked to Alzheimer’s and activates a protein called TREM2, which acts like an on-switch for the brain’s immune cells. 

When activated, those cells begin clearing away existing amyloid plaques, a process that was associated with reduced plaque buildup and improved cognitive function, the study found.

Dr. Bob Arnot, a Vermont-based internal medicine physician, told Fox News Digital that the findings help clarify a pattern doctors have observed for years.

“Scientists have long observed a puzzling statistical pattern known as ‘inverse comorbidity’ — people with a history of cancer are less likely to develop Alzheimer’s disease, and people with Alzheimer’s are less likely to develop cancer,” said Arnot, who was not involved in the study.

The findings suggest that biological signals tied to certain cancers may slow or reverse key features of Alzheimer’s disease.

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Arnot said the research is notable because it identifies a specific biological pathway that could be targeted for future Alzheimer’s treatments.

“This approach targets existing amyloid plaques, not just early prevention. That distinction could be critical for patients who already have established disease,” he said.

Arnot cautioned that the findings do not mean cancer itself is protective.

“This study does not suggest that cancer is protective, desirable or a viable therapy,” he said. “Instead, it reveals that biological programs activated during cancer can inadvertently engage protective immune mechanisms in the brain.”

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The research suggests that future treatments could focus not just on slowing Alzheimer’s, but also on clearing harmful buildup in the brain, Arnot added.

The results were based on experiments in animal models, and further research is needed to determine whether the same effects occur in humans, the researchers noted.