Inflammation is a natural and highly regulated response that provides protection and promotes healing when infection or injury occurs. However, if left unregulated, these same processes can cause further tissue injury and damage. It is unclear to what extent acute or chronic inflammation influences the pace of aging. Also unknown is whether age-related changes in inflammatory responses reflect a “normal” deterioration of cells or are the result of disease processes, or if psychological factors such as stress could promote the development of chronic inflammation or exacerbate its effects.
Inflammatory processes, particularly those resulting in chronic inflammation, have been implicated in a number of chronic diseases and conditions of aging, including cardiovascular disease, osteoarthritis, osteoporosis, Alzheimer’s disease, insulin resistance and diabetes, muscle wasting, and frailty. However, the precise role of inflammation in each of these conditions is not well understood. NIA-supported researchers are working to describe more fully the underlying biology connecting the mediators of inflammation with these disease processes, including:
- How inflammatory mediators—molecules that coordinate the inflammatory response at the cellular level—change with age, and how these changes contribute to disease
- How “normal” age-related cellular changes may trigger an inflammatory response
- How chronic or acute inflammation resulting from disease or dysfunction contributes to—or protects against—further cellular dysfunction
Ultimately, NIA-supported investigators hope to apply an improved understanding of inflammatory processes and their cellular mechanisms to develop more precisely targeted anti-inflammatory interventions.