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. Author manuscript; available in PMC: 2013 May 2.
Published in final edited form as: Prog Retin Eye Res. 2009 Dec 2;29(2):95–112. doi: 10.1016/j.preteyeres.2009.11.003

Figure 8.

Figure 8

Inflammation model of macular degeneration (updated from Anderson et al, 2002). According to the model, AMD may triggered by one or more environmental risk factors (see text) that occurs against the background of a genetic susceptibility profile conferred by variants in the CFH, CFB/C2, and/or C3 gene triad (The potential role of the ARMS2 locus in the inflammatory process, if any, remains to be clarified). This confluence of environmental and genetic risk factors gives rise to pathological changes in the RPE-choroid late in life which generates a chronic, local inflammatory response that includes complement activation and other inflammation-mediated events characterized, in part, by alterations in Bruch’s membrane, drusen formation and the accumulation of other sub-RPE deposits, bystander cell lysis, and dendritic cell involvement. Over time, these processes/events result in photoreceptor degeneration and the loss of central vision that defines the clinical entity of AMD.