Cancer-Alzheimer’s Link: Study Reveals Protein That May Improve Brain Health
- For decades, researchers have observed a curious phenomenon: individuals with a history of cancer appear less likely to develop Alzheimer’s disease, and conversely, those with Alzheimer’s are less...
- The study, 15 years in the making, found that certain cancers release a protein called cystatin-C.
- Amyloid plaques interfere with communication between nerve cells, triggering inflammation and damage that slowly erodes memory and thinking.
For decades, researchers have observed a curious phenomenon: individuals with a history of cancer appear less likely to develop Alzheimer’s disease, and conversely, those with Alzheimer’s are less prone to cancer. Now, a growing body of research is beginning to unravel the potential biological mechanisms behind this so-called “inverse comorbidity.” A recent study published in the journal Cell, utilizing mouse models, offers a compelling clue – a protein released by cancer cells may play a protective role against the development of Alzheimer’s disease.
The study, 15 years in the making, found that certain cancers release a protein called cystatin-C. This protein travels through the bloodstream and can cross the blood-brain barrier, a protective mechanism that typically shields the brain from substances circulating in the body. Once inside the brain, cystatin-C appears to bind to small clusters of amyloid beta, a protein that forms plaques characteristic of Alzheimer’s disease, and marks them for destruction by the brain’s immune cells, called microglia.
Amyloid plaques interfere with communication between nerve cells, triggering inflammation and damage that slowly erodes memory and thinking. The researchers observed that mice implanted with human lung, prostate, or colon tumors exhibited reduced amyloid plaque buildup in their brains compared to those without tumors. In some instances, the animals even showed improved cognitive function, suggesting the change wasn’t merely visible under a microscope but translated to measurable improvements in brain function.
“They have a piece of the puzzle,” says Donald Weaver, a neurologist and chemist at the Krembil Research Institute at the University of Toronto in Canada, who was not involved in the study. “It’s not the full picture by any stretch of the imagination. But it’s an interesting piece.”
This finding builds upon epidemiological data. A 2020 meta-analysis of data from over 9.6 million people revealed an 11% decreased incidence of Alzheimer’s disease in individuals with a cancer diagnosis. However, researchers acknowledge that disentangling this relationship is complex, requiring careful control for various external factors.
Dr. Bob Arnot, an internal medicine physician, explains that this research helps clarify a pattern doctors have long observed. “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,” he said.
Interestingly, research also suggests a potential link in the opposite direction. A study from the National Cancer Institute (NCI) found that melanoma cells that metastasize to the brain produce their own amyloid beta. This locally produced amyloid beta appears to help the cancer cells survive and form metastases, highlighting a complex interplay between the two conditions.
More recently, research published in by Case Western Reserve University, University Hospitals, and the Cleveland VA Medical Center, demonstrated that restoring the brain’s energy balance, specifically levels of a molecule called NAD+, could not only prevent but also reverse Alzheimer’s disease in animal models. This research, while distinct from the cancer-related findings, underscores the potential for interventions targeting fundamental cellular processes to impact the course of Alzheimer’s.
a study from UCSF explored the potential of existing cancer drugs to treat Alzheimer’s. The research indicated that certain cancer drugs reduced both the formation of toxic protein clumps and brain degeneration, and importantly, restored memory function in animal models. This suggests that repurposing existing medications could offer a faster path to developing effective Alzheimer’s treatments.
It’s crucial to emphasize that these findings are primarily based on studies in animal models. While promising, further research is needed to determine whether the same effects occur in humans. Dr. Arnot cautioned that the study does not suggest that cancer is protective or a viable therapy, but rather that biological programs activated during cancer can inadvertently engage protective immune mechanisms in the brain.
The research highlights the importance of understanding the complex interplay between cancer and Alzheimer’s disease. While a definitive explanation remains elusive, these studies offer valuable insights into potential therapeutic targets and strategies for preventing and treating Alzheimer’s disease. The focus is shifting towards not only slowing the progression of Alzheimer’s but also potentially clearing existing harmful buildup in the brain.