In a mouse model that expresses the constitutively active STING variant N153S, researchers observed degeneration of DA neurons, a lower density of dopaminergic axon terminals and the concentration of dopamine in the striatum, α-syn pathology and a lower density of synaptic puncta, and neuroinflammation.45 Moreover, the histological evidence shows that the cGAS–STING pathway appears to be activated in endothelial and neural cells in multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, and ALS. This evidence concerns the gene STING1 and Alzheimer disease.