IL16 and Alzheimer disease: It is notable that placebo-treated 6-month-old 3×Tg-AD mice displayed an increased transactivation of NF-κB p65 subunit, an overproduction of proinflammatory mediators, including iNOS, TNF-α, IL-1β, IL-16, and IL-5, macrophage colony-stimulating factor (M-CSF), monocyte chemotactic protein 5 (MCP-5), and reduction of the anti-inflammatory IL-10.