ABSTRACT

Aging is associated with declines in multiple cognitive domains, including episodic and working memory, attention, processing speed, and executive functioning (e.g., Buckner, 2004; Hedden & Gabrieli, 2004). Compared with younger individuals, healthy elderly do less well on measures of delayed recall (Davis et al., 2003) and recognition (Huh, Kramer, Gazzaley, & Delis, 2006) and mental flexibility (Wecker, Kramer, Hallam, & Delis, 2005). On average, these cognitive declines begin in the late 20s and decrease at a consistent rate across adulthood (Salthouse, 2004). Age-related difficulties with cognitive function can have a significant negative impact on quality of life of older adults, and also increase risk for dementia (Barberger-Gateau, Fabrigoule, Helmer, Rouch, & Dartigues, 1999; De Lepeleire et al., 2004), injury (Sattin, 1992), hospitalization, and death (Bennett, 1996). From the perspectives of prevention and intervention, it is thus important to identify early risk factors for age-related cognitive decline. In this regard, morphometric evidence shows age-related reductions in the volume of multiple brain structures that have been demonstrated to parallel functional declines. For example, although not all findings are consistent, there is growing evidence that atrophy of the hippocampus and prefrontal cortex is associated with a decline in memory performance and executive functioning (Burgmans et al., 2009; DeCarli et al., 2005; de Leon et al., 1997; Raz, Williamson, Gunning-Dixon, Head, & Acker, 2000; Van Petten, 2004) and predicts incident dementia in the elderly (den Heijer et al., 2006; Burgmans et al., 2009). Indeed, recent evidence from a longitudinal 45-month follow-up of healthy elderly suggests that decreased hippocampal volume predicts memory decline, and decreased cortical gray matter volume predicts concomitant declines in executive function (Kramer et al., 2007). Although the biological bases for age-related regional atrophy remain unclear, growing evidence shows that a number of factors associated with increased risk for cardiovascular disease (CVD) may predict and possibly contribute to this atrophy and thus cognitive decline. Over the past decade, converging evidence suggests that systemic inflammation is one of these factors (Ziv & Schwartz, 2008). The current chapter examines evidence that age-related increases in peripheral markers of systemic inflammation, a known risk factor for incident CVD, predict accelerated cognitive aging.