Inflammation in dry age-related macular degeneration

To summarize the current information regarding the role of immune and inflammatory response in the pathogenesis of dry age-related macular degeneration (ARMD).

A Pubmed search was conducted of the period January 1999 to 2005. Relevant information in the literature on the role of inflammation in early dry ARMD was reviewed.

Some important evidence for inflammation in early ARMD consists in the isolation of immunoglobulins, complement proteins, cytokines and activated microglia, in retinal pigment epithelium (RPE) cells and drusen. Pivotal mechanisms in early ARMD include the accumulation of debris and proteins along the RPE surface, followed by immune-complex deposition and complement activation. In contrast, the role of other plasma enzymes such as kallikrein-kinin-bradykinin, the Hageman factor, peptides and coagulation proteins in drusen formation and ARMD has yet to be determined.

A clear role for inflammatory mediators and cells has been established in recent years. Future studies should elucidate further mechanisms in ARMD development.