Study Reveals Cancer’s Surprising Protective Effect Against Alzheimer’s Disease

A groundbreaking study published in the journal Cell has uncovered a biological mechanism that may explain why people with a history of cancer appear to have a lower risk of developing Alzheimer’s disease, a connection doctors have observed for years but never fully understood.

Researchers using mouse models discovered that certain cancers release a protein called cystatin-C that can travel through the bloodstream and penetrate the blood-brain barrier—an area many Alzheimer’s treatments struggle to reach. This protein appears to perform a crucial function once inside the brain.

“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,” explained Dr. Bob Arnot, a Vermont-based internal medicine physician not involved in the study.

The research revealed that cystatin-C binds to the harmful amyloid protein clumps associated with Alzheimer’s disease. Once bound, it activates a protein called TREM2, which effectively serves as an “on switch” for the brain’s immune cells. When activated, these cells begin clearing away existing amyloid plaques, resulting in reduced plaque buildup and improved cognitive function in the study subjects.

This finding is particularly significant because it identifies a specific biological pathway that could potentially be targeted for future Alzheimer’s treatments. Current therapies primarily focus on early prevention or slowing disease progression.

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

The Alzheimer’s treatment landscape has seen significant advances in recent years, but most approved medications aim to slow progression rather than reverse damage. More than 6 million Americans currently live with Alzheimer’s disease, and this number is projected to more than double by 2050, according to the Alzheimer’s Association.

The discovery that cancer-related biological signals might help slow or even reverse core aspects of Alzheimer’s represents a potential paradigm shift in treatment approaches. Instead of merely slowing the disease’s advance, future therapies might focus on actively clearing harmful buildup in the brain.

However, researchers and medical experts emphasize that these findings don’t suggest cancer itself is protective or beneficial.

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

The protein cystatin-C is normally produced in nearly all nucleated cells and is found in virtually all body fluids. While its connection to cancer has been previously documented, this is the first research to establish its potential role in Alzheimer’s prevention and treatment.

Healthcare experts note that the study could help explain why certain cancer survivors appear to have lower rates of Alzheimer’s disease later in life. This inverse relationship has been documented in multiple epidemiological studies but lacked a clear biological explanation until now.

It’s worth emphasizing that the current results are based on experiments in animal models. The research team acknowledges that further studies are needed to determine whether the same effects occur in humans and to explore potential therapeutic applications.

If confirmed in human studies, this research could potentially lead to new treatment approaches that mimic the protective effects of cystatin-C without the harmful aspects of cancer, offering hope to millions affected by Alzheimer’s disease worldwide.