For instance, a decreased nicotinamide adenine dinucleotide (NAD+) level with compromised cellular bioenergetics and DNA repair contributes to the pathogenesis of AD, while supplementation with nicotinamide riboside (NR) normalizes NAD+ concentration, subsequently reduces cytosolic DNA and the cGAS-STING signaling, and thereby inhibiting IFN-1-related neuroinflammation, indicating a new direction for the treatment of AD[9]. This evidence concerns the gene CGAS and Alzheimer disease.