To investigate whether the increased phagocytic baseline production of catecholamines in ADX rats (Figure 4) would result in activation of NFκB (Figure 1) with subsequent release of TNFα, IL-1β and IL-6 and MIP-2 by macrophages (Figures 2 and 3) in vivo, plasma from healthy and otherwise untreated AD+ or ADX animals was obtained and screened for baseline levels of proinflammatory mediators. The gene discussed is IL1B; the disease is Alzheimer disease.