The brain has its own immune system, which detects threats and mounts a defense. A growing body of evidence has shown that in Alzheimer’s disease, those immune cells are chronically overactivated, causing inflammation that damages the connections between brain cells.
Now, in a preclinical study using human Alzheimer’s brain cells, scientists at Scripps Research have identified a molecular switch—and potential drug target—responsible for driving that chronic inflammation.
The research, published in Cell Chemical Biology on April 23, 2026, centers on a protein called STING, which normally functions as part of the immune system’s early-warning system. In the brains of people with Alzheimer’s, the team discovered that STING undergoes a chemical modification known as S-nitrosylation (or SNO, a reaction involving sulfur, oxygen and nitrogen) that promotes its overactivation. Blocking this chemical change to STING in a mouse model of the disease decreased neuroinflammation.