NFKB1 and bacterial infectious disease: Cytoplasmic NF-κB is activated and NF-κB signaling is induced via a wide range of physiological stressors including Aβ40, Aβ42 and other ~40–42 amino acid amyloid peptides, bacterial infection, elevations in ambient reactive oxygen species (ROS), hypoxia, ionizing radiation, neurotoxic metals, pro-inflammatory chemokines and cytokines, viral infection, and other forms of physiological stress [63,66,67,68,69,70,77].