Purpose: To review the evidence that exists concerning the pathogenesis of lesions in late age-related macular disease (AMD).
Design: Review of the literature.
Methods: A review of both experimental evidence and clinical observations that address these problems.
Results: There is good evidence that choroidal neovascularization (CNV) is due to a change in the balance of growth factors derived from the retinal pigment epithelial basolateral plasma membrane domain (retinal pigment epithelium). Retinal angiomatous proliferation may also have a similar pathogenesis involving the apical domain. Detachment of the retinal pigment epithelium is likely to be a consequence of increased resistance of the Bruch membrane to water flow due to deposition of lipids. Geographic atrophy is preceded by accumulation of autofluorescent material in the retinal pigment epithelium and possible causal relationships between the two have been demonstrated.
Conclusion: There is increasing understanding concerning the sequence of events that lead to those lesions causing loss of central vision in AMD. Therapeutic approaches that address the underlying mechanisms are more likely to succeed than current treatment options. Such an approach has already been initiated in the management of choroidal neovascularization.