This is a medical mystery that has puzzled scientists for decades – why do some people survive? cancer Is it very unlikely that I will develop dementia in the future?
Numerous studies over the past 20 years or so have found that a diagnosis of cancer (almost any type of cancer) reduces the risk of dementia by about 25 percent.
Now researchers think they may have discovered the secret to this unusual connection between two of the world’s biggest killers. Scientists at Huazhong University of Science and Technology China They identified an important protein called cystatin C, which is released by cancer cells as a byproduct of tumor growth.
The study, published in the journal Cell, shows that the protein can cross the blood-brain barrier, the cell’s protective chain that blocks access to potentially harmful substances.
Once in the brain, cystatin C appears to trigger a response that destroys abnormal protein clumps (called amyloid plaques) that are associated with the development of dementia.
This finding comes from animal studies, and it is not yet clear whether the same process occurs in humans.
But the study could provide important clues in the search for new and effective dementia treatments, says Elio Rivoli, professor of cancer epidemiology and prevention at Imperial College London, who has long studied the important interactions between cancer and dementia.
“This is a very interesting study and may explain one of the mechanisms behind why cancer survivors seem to have a lower risk of dementia,” Professor Riboli says.
Scientists have discovered that a protein released by cancer cells called cystatin C can destroy abnormal protein clumps in the brain that are associated with the development of dementia.
“It may lead to the development of new drugs.” [for dementia] It increases this protein and potentially interferes with it. ”
Approximately 900,000 people live with dementia in the UK. It kills more people than cancer or heart disease, about 75,000 people a year. It is usually caused by problems caused by a weakened immune system, such as pneumonia or difficulty swallowing.
Current drug treatments include cholinesterase inhibitors (such as Aricept), which work by increasing the activity of acetylcholine, a brain chemical essential for memory and learning.
However, while these may relieve symptoms and improve quality of life, they are not a cure. New drugs such as lecanemab and donanemab slow the progression of the disease in the early stages, when symptoms begin to appear.
However, they are not approved on the NHS due to their cost, limited effectiveness and potential side effects such as brain haemorrhage.
Understanding why cancer can prevent some people from developing dementia in the first place could be crucial in the search for better treatments.
Cancer survivors, especially those who had cancer during childhood, tend to live shorter lives (often due to toxicity to major organs caused by treatments such as chemotherapy), and some may not live long enough to develop dementia.
And people who survive cancer may be generally healthier and less likely to develop dementia by eating wisely, exercising regularly, and limiting their alcohol intake.
However, most studies take these confounders into account and still find that cancer reduces risk.
The latest study began with scientists transplanting samples of human lung, prostate and bowel cancers into mice genetically bred to be at increased risk of dementia.
None of the mice developed cerebral plaques associated with this condition.
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In a study, mice with dementia-like deposits were injected with cystatin C protein, which improved memory and learning.
The team then spent several years trying to determine which of the thousands of proteins released by cancer cells had this protective effect. They eventually narrowed it down to one: cystatin C.
In subsequent tests, the research team found that cystatin C binds to plaques in the brain. This activates immune cells in the brain, which mount an attack that destroys the plaque.
When mice with dementia-like deposits were injected with cystatin C protein, their memory and learning improved. Further studies are currently being planned.
Cystatin C is not the only cancer-based protein that holds promise for preventing dementia.
A team of scientists at the University of Bristol is currently studying the role of PIN1, a protein released by cancer cells to stimulate further development and growth of tumors.
Their research suggests that the more active the PIN1 protein, which promotes cancer growth, is, the more the brain is protected from cognitive failure associated with amyloid plaques. It also has a similar effect on tau, another protein that accumulates in brain cells and is associated with dementia.
Meanwhile, the same Bristol team is investigating whether another molecule, an enzyme called PI3K, may be a factor in reducing dementia risk.
In cancer, this enzyme is highly active and helps malignant cells grow and spread the disease.
However, in patients with dementia who do not have cancer, cancer activity rapidly declines.
Cancer is thought to stimulate the activity of PI3K, which subsequently protects the brain from dementia by preventing the formation of deposits.
However, there is also evidence that people who develop dementia are less likely to develop cancer later in life.
A 2017 Taiwanese study published in the journal Neuropsychiatry looked at 25,000 people with Alzheimer’s disease and found that they were about 20 percent less likely to develop some cancers than those without dementia.
Other studies report a reduction in cancer risk by as much as 60%.
The theory is that the destruction of brain cells that occurs in dementia means that the same enzymes that promote cancer growth are severely suppressed.
Professor Riboli warns that it may not be as simple as finding a single protein secreted by cancer to halt the progression of dementia.
“Cystatin C can’t be the only one, and in fact, it might not even be the main one,” he says.
“But this new study shows that they [cancer proteins] It may have a strong protective effect against amyloid plaque formation. ”