Alzheimer's Protein Implicated in Glaucoma

Amyloid-beta appears to destroy retinal cells and may be new treatment target, experts say.

By Ed Edelson
HealthDay Reporter
Tuesday, August 7, 2007; 12:00 AM

Copyright © 2007 ScoutNews, LLC. All rights reserved.

TUESDAY, Aug. 7 (HealthDay News) -- The same protein fragments that form plaques in the brains of people with Alzheimer's disease appear to cause the death of retinal cells in glaucoma, the potentially blinding eye disease, British researchers report.

In animal studies, drugs that blocked key molecular pathways for the protein fragments -- called amyloid-beta -- reduced eye damage and preserved the lives of retinal cells, said lead researcher Dr. M. Francesca Cordeiro, assistant professor of retinoneural degeneration at University College London.

Several methods of blocking those molecular pathways were tried in tests of rats bred to develop glaucoma, she explained.

"Just one treatment has prolonged the lives of retinal cells," Cordeiro noted. "Combining all the treatments together had a greater effect."

Confirmation of the eye-damaging role of amyloid-beta in further studies could open the way to new treatments for glaucoma, a leading cause of blindness in the United States.

It might also solve a puzzle that has led to a recent and revolutionary change in how ophthalmologists view the condition.

Until only a few years ago, glaucoma was officially described as the death of retinal cells caused by abnormally high pressure of the fluid in the eye. Even today, treatment is typically aimed at reducing this intraocular pressure.

But there has been growing awareness that a large percentage of glaucoma patients, perhaps more than half, have normal or near-normal intraocular pressure. In fact, the American Academy of Ophthalmology has removed mention of intraocular pressure as the cause of glaucoma and now describes pressure as just a major risk factor.

One of the clues pointing toward a causal role for amyloid-beta was the discovery of glaucoma-like retinal cell death in people with Alzheimer's disease, Cordeiro said. Laboratory work also revealed an accumulation of amyloid-beta in dying retinal cells, and adding the protein to cultured retinal cells induced their death.

"This is a very powerful idea," Cordeiro said. "We are really lacking non-pressure [based] treatments in glaucoma. Our research also gives an opportunity for treatment of Alzheimer's disease, using eyes as an entry point to the body."