 Abstract neuroinflammation, caused by the activation of microglia, is a major risk factor for cognitive dysfunction. Riboflavin, vitamin B2, can reduce inflammation and oxidative stress, but its mechanism of action in microglia remains unknown. In this study, researchers found that riboflavin kinase, RFK, a key enzyme in riboflavin metabolism, was highly expressed in microglia. They also discovered that riboflavin converts to flavonmononucleotide, FMN, which then inhibits the activity of RFK and reduces inflammation. Furthermore, they developed a new type of drug delivery system called microglial nanoparticles, MNPs at FMN, that can deliver FMN directly into the brain. This drug delivery system successfully reduced inflammation and improved cognition in animal models of neurodegenerative diseases such as Alzheimer's disease. These findings suggest that riboflavin and its derivatives could be used as a novel therapeutic approach for treating neuroinflammation-related cognitive disorders. This article was authored by Mengran Zhang, Huoqing Chen, Wenlong Zhang, and others. We are article.tv, links in the description below.