There is increasing evidence from basic science and human epidemiological studies that inflammation, oxidative stress, and metabolic abnormalities are associated with age-related cognitive decline and impairment. This article summarizes selected research on these topics presented at the Cognitive Aging Summit II. Speakers in this session presented evidence highlighting the roles of these processes and pathways on age-related cognitive decline, pointing to possible targets for intervention in nondemented older adults. Specific areas discussed included age differences in the production of cytokines following injury or infection, mechanisms underlying oxidative stress-induced changes in memory consolidation, insulin effects on brain signaling and memory, and the association between metabolic syndrome and cognitive decline in older adults. These presentations emphasize advances in our understanding of mechanisms and modifiers of age-related cognitive decline and provide insights into potential targets to promote cognitive health in older adults.

An accurate assessment of the impact of reserve on cognitive functioning in older individuals with brain pathology requires careful measurement of each and an assessment of the extent to which each influences the other. Studies to integrate information about molecular biology, neuropathology, behavioral aspects of cognitive decline, and cognitive resilience will be of particular importance. In addition, more work is needed to improve our understanding of the effect of systemic factors on brain health and function. It seems likely that, even in later life, the brain's plasticity may allow for a positive response to stimulation. The ultimate goal of this research is to create a validated set of variables and interventions-and to understand the biology underlying them-that are useful not only in describing an individual's cognitive state but also in identifying promising paths for treatment and prevention of cognitive decline.