AD brains displayed increased abundance of proteins associated with PLCB events (e.g., inositol 1,4,5-trisphosphate receptor type 1, and adenylate cyclase type 9) and pro-inflammatory activity such as the activation of complement cascade and the NF-κB pathway (e.g., plasminogen, protein kinase C delta type, ATP-dependent RNA helicase DDX1, and 5-azacytidine-induced protein 2). This evidence concerns the gene NFKB1 and Alzheimer disease.