Scientists have discovered a possible new way to slow the brain damage caused by Alzheimer’s disease.
The research suggests that an immune system signal called STING may become too active in the brain and contribute to memory loss.
Alzheimer’s is the most common cause of dementia and mainly affects older adults. It gradually damages brain cells, leading to problems with memory, thinking, communication and eventually the ability to carry out everyday activities.
Two major changes are commonly found in the brains of people with Alzheimer’s. One is the buildup of sticky clumps known as amyloid plaques, while the other is the formation of twisted tau tangles inside brain cells.
Researchers have long studied these plaques and tangles, but they are not the whole story. Growing evidence suggests that long-lasting inflammation in the brain also plays an important part in the disease.
A team at the University of Virginia School of Medicine has now identified STING as a possible link between this inflammation and Alzheimer’s-related brain damage. STING is part of the body’s natural immune defense system.
Under normal conditions, STING helps the immune system detect danger, including signs of viral infection and damage inside cells. It can trigger inflammation that helps the body respond to threats and remove unhealthy cells.
But too much immune activity can become harmful. The researchers found evidence that STING becomes unusually active in Alzheimer’s and may cause inflammation to continue when it should not.
This excessive immune response appears to affect microglia, the immune cells that live in the brain. Microglia normally help protect brain tissue by removing waste, damaged cells and other unwanted material.
In Alzheimer’s, however, these cells can become overactive and produce substances that increase inflammation. Instead of protecting nearby nerve cells, they may begin contributing to the damage.
The research team, led by Dr. John Lukens, studied what happened when STING activity was blocked in mouse models of Alzheimer’s disease. The treatment reduced several signs of harmful brain inflammation.
Blocking STING also reduced damage linked with both amyloid plaques and tau tangles. This is particularly interesting because many experimental Alzheimer’s treatments have focused mainly on one of these two major disease changes.
The researchers also found that microglia became less reactive around amyloid plaques when STING was blocked. Nearby brain cells appeared to be better protected from damage.
The benefits were not limited to what scientists could see in brain tissue. Mice with reduced STING activity also performed better on memory tests, suggesting that controlling this immune pathway helped preserve some brain function.
These findings raise the possibility that STING could become a target for future Alzheimer’s medicines. A treatment that reduces harmful inflammation while affecting several parts of the disease process could potentially complement medicines that directly target amyloid or other brain changes.
However, scientists need to be careful when interfering with the immune system. STING has useful roles in fighting infections and helping the body respond to damaged or abnormal cells, so blocking it too strongly could have unwanted effects.
Researchers will therefore need to determine whether STING can be controlled safely in people and whether the benefits seen in mice also occur in humans. Many treatments that look promising in animal studies do not ultimately work in patients.
The work was carried out by researchers at the University of Virginia, including scientists associated with the Harrison Family Translational Research Center at the Paul and Diane Manning Institute of Biotechnology. Jessica Thanos and other members of the team emphasized the importance of understanding how the brain’s immune system changes with aging and disease.
The research adds to a broader shift in Alzheimer’s science. Instead of viewing the disease only as a problem of plaques and tangles, scientists are increasingly studying how the immune system, inflammation and aging interact to damage the brain.
If future studies confirm the findings in people, controlling STING may offer another way to protect nerve cells and slow memory decline. For now, the discovery provides an important new clue in the search for treatments that can change the course of Alzheimer’s rather than simply manage its symptoms.
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