Researchers link beta-amyloid protein to glaucomatous cell death

The deposition of beta-amyloid protein, which is strongly associated with the development of senile plaques and neuronal apoptosis in patients with Alzheimer's disease, may also be a contributing factor involved in the retinal ganglion cell apoptosis characteristic of glaucoma, according to an experimental study by researchers in the United Kingdom.

The study results suggest that a combined therapy targeting different components of the beta-amyloid pathway could be a new avenue for treating glaucoma, the authors noted.

M. Francesca Cordeiro, MD, and colleagues at the University College London Institute of Ophthalmology used a novel imaging technology to investigate the possible role of beta-amyloid in a rat model of glaucoma.

The researchers found that the beta-amyloid protein colocalizes with apoptotic retinal ganglion cells. It also induced significant cell death in vivo, according to the study.

In addition, the researchers evaluated whether three therapies, which are known to target the beta-amyloid protein in patients with Alzheimer's disease, could also potentially be used to prevent glaucomatous cell death. They found that simultaneously reducing beta-amyloid formation with inhibitors, clearing beta-amyloid deposition with antibodies and inhibiting beta-amyloid aggregation and neurotoxic effects with Congo red resulted in a greater than 80% reduction in retinal ganglion cell apoptosis, according to the study.

"At present in the field of glaucoma, there is a clear lack of therapies that target the actual causative cellular processes of glaucoma," the authors said. "Targeting [beta-amyloid] specifically in the eye will provide a localized therapy limiting generalized side effects associated with systemic administration."

The study is published online ahead of print on the Web site of the Proceedings of the National Academy of Sciences.