Scientists may have uncovered why cancer survivors face a significantly lower risk of developing dementia, according to groundbreaking research published in the journal Cell. Researchers at Huazhong University of Science and Technology in China identified a protein called cystatin C, released by cancer cells during tumor growth, that appears to destroy amyloid plaques in the brain. These abnormal protein clumps are strongly linked to dementia development, and the discovery could revolutionize treatment approaches for the condition.
Multiple studies over the past two decades have consistently shown that a cancer diagnosis reduces dementia risk by approximately 25 percent. The newly identified protein can cross the blood-brain barrier and trigger reactions that break down the harmful deposits associated with cognitive decline, according to the research team.
Understanding the Cancer-Dementia Connection
The research began with scientists transplanting human lung, prostate, and bowel cancer samples into mice genetically bred to have high dementia risk. None of the mice developed the brain plaques typically associated with the condition. The team then spent years analyzing thousands of proteins released by cancer cells to identify which one provided this protective effect.
During subsequent testing, researchers found that cystatin C binds directly to brain plaques. This binding activates immune cells in the brain to launch an attack that breaks up the deposits. Mice with dementia-like symptoms that received injections of the cystatin C protein showed measurable improvements in memory and learning abilities.
Implications for Dementia Treatment
The findings carry significant weight for the approximately 900,000 people living with dementia in the UK alone. Current treatments include cholinesterase inhibitors that boost brain chemicals vital for memory, but these medications only ease symptoms rather than cure the disease. Newer drugs like lecanemab and donanemab can slow disease progression in early stages, but they remain unavailable on the NHS due to cost concerns, limited effectiveness, and potential side effects including brain bleeds.
Professor Elio Riboli, a cancer epidemiology expert at Imperial College London, called the research very interesting and noted it could lead to new drugs that increase cystatin C levels to potentially prevent dementia. Additionally, the discovery might explain one of the biological mechanisms behind the reduced dementia risk observed in cancer survivors, according to Professor Riboli.
Other Cancer Proteins Under Investigation
Cystatin C is not the only cancer-related protein showing promise against dementia. A team at Bristol University is investigating PIN1, a protein that stimulates tumor development and growth. Their research suggests that higher PIN1 activity in driving cancer growth correlates with increased brain protection against cognitive failure linked to amyloid plaques and tau proteins.
Meanwhile, the same Bristol researchers are examining whether an enzyme called PI3K may reduce dementia risk. In cancer patients, this enzyme operates at high activity levels, aiding malignant cell proliferation. However, in dementia patients without cancer history, PI3K activity is significantly reduced. Scientists believe cancer stimulates PI3K activity, which then protects the brain by preventing harmful deposit formation.
The Reverse Relationship
In contrast, evidence indicates that people who develop dementia are substantially less likely to subsequently develop cancer. A 2017 study published in Neuropsychiatry examined 25,000 Alzheimer’s disease patients in Taiwan and found they were nearly 20 percent less likely to develop any form of cancer compared to those without dementia. Other research has estimated the reduction in cancer risk among dementia patients as high as 60 percent.
The prevailing theory suggests that brain cell destruction occurring with dementia suppresses the same enzymes that would otherwise promote cancer growth. This inverse relationship strengthens the evidence for shared biological pathways between the two conditions.
Professor Riboli cautioned that cystatin C likely represents just one piece of a larger puzzle and may not even be the primary protective factor. However, he acknowledged that the study demonstrates cancer proteins may have powerful protective effects against amyloid plaque formation, potentially opening new avenues for dementia prevention and treatment research. Further studies in humans are now planned to confirm whether the same mechanisms observed in animal models apply to people.
