Downregulation of NF-κB and NLRP3 in aging wildtype and amyloid β transgenic mice

Neuroinflammation is a key component of Alzheimer's disease (AD), and it may be driven by the activation of NFκB and NLRP3 signaling pathways. AD pathology, like amyloid-β, may exacerbate the activation of these pathways. We used a nucleic acid therapeutic (nanoligomer) cocktail targeting NFκB and NLRP3 to reduce inflamamtory signaling in aged wildtype mice and a transgenic mouse model of amyloid-β pathology (APP/PS1). Short-term (3 days) treatment reversed age- and amyloid-β-related gene sigantures, supporting the idea that this nanoligomer cocktail may have the potential to improve AD-related neuroinflammation and cognitive dysfunction. RNA-seq data was generated from hippocampus samples of young C57BL/6, old C57BL/6, old nanoligomer treated C57BL/6, APP/PS1, APP/PS1 nanoligomer treated, and "non-carrier" littermate controls