High-Sensitivity C-Reactive Protein, Other Markers of Inflammation, and the Incidence of Macular Degeneration in Women

Abstract

Recent evidence suggests that inflammation and abnormalities of innate immunity play a role in the pathogenesis of age-related macular degeneration (AMD),¹ the leading cause of blindness among older adults.² A strong association between a common variant of the gene for complement factor H (CFH) and AMD has recently imparted considerable weight to this hypothesis.^3-9 These data coincide with the view that low-grade inflammation plays a more general role in the aging process itself,¹⁰ as well as in other age-related disorders.¹¹ Patterns of AMD progression^12,13 viewed in the context of the development of an increasingly proinflammatory status with age¹⁰ suggest the possibility that this disease may develop via at least 2 somewhat discrete steps. The first involves the accumulation of extracellular debris beneath the retina at varying rates among individuals, which may plausibly be relatedto up-regulation of immunoinflammatory responses and the development of AMD.¹⁴ The second step, which occurs in only a subset, leads to neovascular lesions and/or geographic atrophy. In the case of neovascular AMD, this process involves an overt inflammatory/neovascular response originating from the choroidal vasculature.^12,15