Two key gene mutations may explain three out of every four cases of age-related macular degeneration (AMD), a major cause of vision loss and blindness in the elderly, scientists say.

The discovery potentially brings doctors closer to therapies that could help prevent or treat the sight-robbing disease.

"It is difficult to project when such therapies might be available, but these results will further increase interest in AMD and the amount of effort and money spent looking for therapies," said Dr. Albert O. Edwards, president of the Institute for Retina Research at Presbyterian Hospital in Dallas. He was not involved in the study, which was conducted by a team from Columbia University in New York City.

An estimated 50 million people worldwide have lost sight because of macular degeneration, which causes the deterioration of the macula, a part of the retina.

"You lose your central vision, so you really can't see in front of you, you can't read properly, you can't drive, you can't watch TV," said study co-author Rando Allikmets, a Columbia professor of ophthalmology. "The worst-case scenario is that you end up legally blind."

Researchers estimate that about a third of the U.S. population will develop some form of macular degeneration by the time they're 75. In some cases, there is no treatment.

Last year, a team of researchers linked a specific gene variation to macular degeneration, which can be inherited. The new findings suggest that a variation of another gene, known as Factor B, works with a variation in the initial gene, known as Factor H, to cause the disorder.

Normally, both genes play major roles in keeping the body's immune system in balance: Factor B helps activate inflammation, while Factor H helps stop it. Based on the genetic analysis of 1,300 people, the researchers reported Sunday in an online edition of the journal Nature Genetics that specific variations in the genes may account for about three-quarters of all cases of age-related macular degeneration.

That finding means that "we can now target the beginning of the disease," Allikmets said.

He stressed, however, that even people with the Factor B and H variants aren't always destined to develop macular degeneration. "You have to have a trigger that gets this thing into motion," Allikmets said. "We don't know specific triggers at this point. That's one of the things that we have to figure out."

For now, the study suggests that the immune system plays a crucial role in the development of macular degeneration, knowledge that could lead to better treatments to either improve people with the disease or stop them from getting worse, Edwards said.

According to Allikmets, future research may turn up other crucial genes, helping doctors screen patients and figure out who's at increased risk of developing the condition. Then preventive treatment could be launched.

"But we have to find out how to do that," he said.