Blocking a STING Switch Could Slow Alzheimer’s Brain Inflammation
Researchers pinpoint S-nitrosylation of the STING protein at cysteine 148 as a driver of chronic brain inflammation and synapse loss in Alzheimer’s. In mouse models, preventing this modification reduced inflammation and protected synapses, a result mirrored in human Alzheimer’s tissue and stem-cell models. The findings suggest a targeted therapy that dampens harmful inflammation without suppressing overall immunity, with small molecules designed to block the cysteine-148 site in development.