Components of this inflammatory pathway are known to contribute to AD, in part through overexpression of IL-1α and promotion of 42-amino acid amyloid β 42 (Aβ42) peptide generation; in turn IL-1α and amyloid β induce transcription of the proinflammatory prostaglandin synthase cyclooxygenase-2 (COX-2) gene and stimulate apoptotic brain cell death and neural tissue degeneration (Mrak and Griffin, 2001). The gene discussed is IL1A; the disease is Alzheimer disease.