Although a number of genetic variations have been identified that confer susceptibility to ARMD and responsiveness to treatments, it is not yet possible to accurately predict either the risk or the best treatment for an individual. Further research is required to understand the effect of these genes upon the disease process and so enable the therapeutic targeting of defective genes.
A number of studies are testing whether drugs that modulate immune reactions in the retina may inhibit or reverse the drusen changes of early ARMD.
Research is ongoing into the culturing of retinal pigment epithelium cells to replace those beneath the retina that have worn out.
The retina of eyes with atrophic ARMD has reduced levels of the enzyme DICER1ribonuclease type3. This normally breaks down dsRNA derived from non-encoding (Alu) DNA and the accumulation of these cytotoxic sequences may trigger apoptosis (death) in retinal pigment epithelial cells. Clinical trials will start late 2011 to see whether targetted supression of Alu RNA by increasing DICER1 or anti-sense Alu RNA in the retina will inhibit ARMD.
The CABERNET study is investigating whether attaching of a small plaque of radioactive strontium-90 to the back of the eye reduces the number of Lucentis injections required to treat a neovascular membrane.
Fenretinide interferes with vitamin A chemistry in photoreceptor cells and may reduce the build-up of cellular waste in the retina. A two year clinical trial suggests it may reduce the likelihood of progressing to wet macular degeneration.