Researchers at the University of Kentucky, US, compared eyes donated by deceased AMD patients with those of healthy individuals. The healthy were found to have three times higher levels of dicer, an enzyme, in their retinas.

Low levels of dicer cause the build-up of a genetic material alu, which becomes instrumental in killing off light-sensitive retinal cells in advanced "dry" AMD, the journal Nature reported.

Jayakrishna Ambati, professor of ophthalmology in the University of Kentucky, has created two drugs that could halt the disease. One boosts levels of dicer, the other breaks down the toxic alu, according to a Kentucky University statement.

Ambati said: "When the levels of dicer decline, the control system is short-circuited and too much alu accumulates. This leads to death of the retina."

Patients with dry AMD, the most widespread variant, could be treated this year. The numbers of sufferers are expected to treble over the next 25 years.

AMD renders daily tasks like reading, driving and watching TV impossible.