Fig. 9
Schematic summary of this study. A Strategy of liver-specific adiponectin gene delivery using recombinant AAV as a treatment for Alzheimer’s disease. Intravenous injection of AAV2/8-APNTri which carries APN mutant (C39S) under the ApoE enhancer and hAAT promoter overexpresses trimeric adiponectin in the liver. Increasing circulatory trimeric APN which crosses the blood–brain barrier to inhibits microglia-mediated neuroinflammation. B Molecular mechanism of the model. AβO stimulates nuclear translocation of NF-κB through binding of toll-like receptors (TLRs) or CD36. Trimeric adiponectin binds to adiponectin receptor 1 (AdipoR1) and activates AMPK to suppress NF-κB nuclear translocation. This decreases the mRNA transcriptions and the levels of NLRP3, ASC, pro-caspase 1, IL-1β, and IL-18