The brain has its own built in immune defenses that help detect threats and protect nerve cells. But growing evidence suggests that in Alzheimer's disease, these immune cells become stuck in a state of chronic activation. Instead of helping, they trigger ongoing inflammation that can damage the connections between brain cells.
Now, researchers at Scripps Research have identified a molecular mechanism that appears to play a key role in that process. Using human Alzheimer's brain cells and other experimental models, the team discovered a chemical change that can push the brain's immune response into overdrive. The findings, published in Cell Chemical Biology, point to a promising new target for future Alzheimer's treatments.
A Key Protein Linked to Brain Inflammation
The study focuses on a protein called STING, which normally serves as part of the body's early warning system against threats. Researchers found that in Alzheimer's disease, STING undergoes a chemical modification known as S-nitrosylation (or SNO, a reaction involving sulfur, oxygen and nitrogen). This alteration appears to make the protein excessively active, fueling harmful inflammation.
When the scientists blocked this specific chemical modification in a mouse model of Alzheimer's disease, levels of neuroinflammation dropped.
