In addition, glial cultures obtained from rapid brain autopsies of AD patients stimulated with Aβ show an increased release of prointerleukin-1β (pro-IL-1β), IL-6, IL-8, TNF-β, MCP-1, macrophage inflammatory peptide-1α (MIP-1α), and macrophage colony-stimulating factor (M-CSF) [22], corroborating the inflammatory activation of glial cells as part of the physiopathology of AD. The gene discussed is CCL3; the disease is Alzheimer disease.