A new generation of drugs being developed for Alzheimer's disease may also have a role in preventing the leading cause of irreversible blindness, scientists said yesterday.

They have demonstrated for the first time that proteins involved in Alzheimer's disease are also implicated in glaucoma.

A pilot patient trial of the new drugs is planned at the end of this year or early in 2008.

Around 80,000 people in Scotland live with glaucoma, with the prevalence rising from 1%-2% of the over 40s, to 5% of the over 75s.

UK-wide, more than 500,000 people suffer to varying degrees, and worldwide, as many as 65 million people may be affected. The incidence within African Caribbean groups is significantly higher than in whites.

Previous links between glaucoma and Alzheimer's included the development of glaucoma-like retinal cell death in Alzheimer's patients.

People with Alzheimer's are much more likely to have glaucoma than the general population. In one group, 25% of patients were found to be developing the eye disease.

Now for the first time scientists have identified the other side of the coin. The amyloid-beta protein characteristic of plaques found in Alzheimer's may be causing the retinal cell death that causes glaucoma. The clue was that in some cases reduction in intra-ocular pressure - the standard treatment for glaucoma - does not work.

Glaucoma is associated with increased pressure in the eye, but up to one-third of patients continue to lose vision even when this is well controlled. Up to 30% of these difficult-to-treat patients will go blind.

Scientists at University College, London, spotted the connection after developing a new method of detecting nerve cell damage at the back of the eye.

DARC (Detection of Apoptosing Retinal Cells) uses a fluorescent marker to highlight the dying nerve cells.

The technique demonstrated that exposure to beta-amyloid triggered glaucoma in experimental rats.

When the animals were treated with a combination of drugs that prevent the build up of beta-amyloid protein, nerve cell death and glaucoma progression were halted, the researchers report in the journal Proceedings of the National Academy of Sciences.

Dr Francesca Cordeiro, from University College London, who led the Wellcome Trust-funded study, said: "When these animals are treated with beta-amyloid drugs the number of cells that are dying goes right down over a period of 16 weeks.

"It doesn't restore sight, but it stops them losing vision in the first place. You must remember that to lose vision, 30% of the retinal nerve cells have to be dead.

"Our aim, definitely, is to stop people going blind from this disease."

At present, glaucoma is not normally treated until symptoms of the disease appear. By identifying at-risk patients and spotting the early death of retinal cells, it might be possible to halt the disease before any loss of sight occurs, said Dr Cordeiro.

Anyone who has a first-degree relative with glaucoma is already offered free eyesight tests.

Treatment with the drugs could also prevent further loss of sight in glaucoma patients who have started losing vision.

The compounds used to treat the rats are of a type still being investigated as therapies for Alzheimer's. One such drug, the monoclonal antibody Bapineuzumab, is currently undergoing patient trials in Ireland and the US.

Researchers will examine patients for early signs of the disease and administer beta-amyloid drugs to those affected. If the results are positive, larger scale trials are likely to follow.

At present glaucoma care accounts for approximately 30-40% of all outpatient visits in ophthalmology departments.