Research into the pathophysiology of age related macular degeneration (AMD) has advanced at a rapid rate in recent years. To see the pace of progress, one need only pick up any issue of a major ophthalmic journal or attend a poster session at an ophthalmic society meeting. Efforts are under way to learn more about the ageing of Bruch’s membrane, drusen formation, and angiogenesis in choroidal neovascularisation (CNV). And it’s beginning to pay off: our understanding of these mechanisms has led to some promising new treatments, particularly in the area of angiogenesis.

In the case of CNV, much of the focus lately has been on pro-angiogenic proteins such as vascular endothelial growth factor (VEGF). Treatment strategies that target pathologically elevated levels of VEGF are easy to understand: they try to block or reduce a known stimulus for the growth of CNV. Some early successes have been reported with anti-VEGF therapies.^1,2

The waters are still muddy, though, when it comes to more fundamental, or at least earlier, steps in the process that leads an eye to develop AMD. What factors cause an ageing Bruch’s membrane to become susceptible to fissure and invasion by CNV? Why do excess lipids accumulate to form drusen in some patients but not others? What disrupts the balance of pro-angiogenic and anti-angiogenic factors in the retinochoroid …