Inflammatory processes, typically stress-related, have been implicated in late-life depression, anxiety, insomnia, cognitive decline, and Alzheimer’s disease (1). Aging is accompanied by a two- to fourfold increase in plasma/serum levels of inflammatory mediators such as cytokines and acute phase proteins. In addition, chronic inflammatory processes are implicated in diverse health outcomes associated with aging, such as atherosclerosis, insulin resistance, diabetes, and metabolic syndrome. Furthermore, there is some evidence that aging is associated with a dysregulated cytokine response following stimulation. Consistent with this research, inflammatory mediators are strong predictors of mortality independent of other known risk factors and comorbidity in elderly cohorts. For example, IL-6, a proinflammatory factor whose concentration generally increases in the blood with age, has been linked with Alzheimer’s disease, depression, osteoporosis, rheumatoid arthritis, cardiovascular disease, and some forms of cancer, and it is prospectively associated with general disability and mortality in large population-based studies (2, 3). Anti-inflammatory cytokines interleukin-4 (IL-4) and interleukin-10 (IL-10) may actually confer a protective role for the immune system, involving phagocytosis of dying neurons and processing of beta-amyloid and microglia that have been implicated in late-life neuropsychiatric disorders. These cytokines may be particularly important in conferring increased resilience to the inflammatory response. However, prevalence of geriatric depression is higher among those with insomnia, medically ill patients in medical settings, and in long-term care. Additional stress-inducing circumstances of acute or chronic medical illness, insomnia, or chronic pain may also be associated with depression that is relevant for this patient.