British researchers have discovered common protein fragments in people with Alzheimer’s disease and people with glaucoma. This discovery may change how both diseases are treated.
These protein fragments are called amyloid-beta. In people with Alzheimer’s disease, amyloid beta fragments form plaques in the brain. In people with glaucoma, amyloid beta fragments seem to cause the death of cells in the retina.
The University College of London study focused on testing drugs that blocked pathways normally traveled by the amyloid beta fragments. In animal testing, the drugs reduced eye damage and helped preserve the lives of cells in the retina. The researchers have been working on blocking amyloid beta pathways using rats that were bred specifically to develop glaucoma. Just one treatment prolonged cell life; combining different drug therapies had an even more beneficial effect.
Ophthalmologists are changing the way they think about glaucoma. Until recently, abnormally high fluid pressure in the eye was thought of as the main cause of the disease. However, almost half of all patients with glaucoma have normal or near-normal fluid pressure in the eye. Pressure has been downgraded from a cause to a risk factor. It seems that these amyloid beta protein fragments are a major culprit in glaucoma development. In laboratory tests, adding amyloid beta fragments to cultured retina cells lead to cell death.
There is a glaucoma-like retinal cell death in people with Alzheimer’s disease — this common link started researchers on the search for amyloid beta protein fragments.
Glaucoma is a leading cause of blindness in the United States. Further studies on the amyloid beta protein fragments are planned, in the hopes of discovering new treatments for glaucoma. Experts can imagine a future vaccine that could be injected into the eye to prevent the formation of the dangerous protein fragments. For now, researchers will focus on making amyloid beta fragments — rather than eye fluid pressure — the focus of treatment.