Studying the APP/PS1 amyloid mouse model, Hou et al. found that the induced inflammation in their brains was correlated with reduced levels of NAD+ and that treatment with an NAD+ precursor increased brain NAD+ levels, reduced the expression of proinflammatory cytokines, and decreased the activation of microglia and astrocytes, with reduced NLRP3 inflammasome expression, DNA damage, apoptosis, and cellular senescence in the AD mouse brains, dependent on the cGAS-STING [251]. Here, CGAS is linked to Alzheimer disease.