NFKB1 and Alzheimer disease: The interleukin IL-6, also associated with AD, induces inflammation, inhibition of neurogenesis, and decrease of synaptic plasticity in the hippocampus by triggering neuroinflammation via STAT3, exerting cAMP response element-binding (CREB) protein downregulation by Akt inhibition or by the activation of transcription factors, which compete for a limited pool of coactivators such as STAT-1, c-Jun, and NF-κB, promoting hypocholinergic signaling [103–105].