A rationale for increased synthesis of beta-amyloid peptide percursor (APP) protein in Alzheimer's disease (AD) is developed in which Interleukin-1 (IL-1) plays a key role. This cytokine is elevated in AD, its receptors are on APP mRNA positive cells and it promotes APP gene expression. Potential involvement of the protease inhibitor (PI) activity of certain APP proteins in the activation process for IL-1 and Nerve Growth Factor (NGF) are proposed. The possibility of feedback loops among IL-1, APP and NGF and the implications for neuronal survival and function are discussed.