Double trouble.
Researchers have found a link between glaucoma and Alzheimer's disease.


Enemy of Brain and Eye

A new study reveals a surprising link between two scourges of old age. The work suggests that plaques similar to those found in the brains of people with Alzheimer's disease (AD) may be responsible for the nerve damage of glaucoma. The research also provides evidence that drugs used to treat AD might also work against glaucoma.

The cause of glaucoma, a degenerative eye disease that produces elevated pressure within the eyeball, is unknown. Researchers have long assumed that increased intraocular pressure damages retinal ganglion cells (RGCs), the nerve cells that transmit signals to the brain. But ophthalmologists have found that glaucoma often continues to worsen even after the pressure has been controlled with drugs. Meanwhile, several recent studies have found that in glaucoma patients, RGCs produce more of a protein called β-amyloid that makes up the brain plaques in AD. Other research has found that AD patients are much more likely to have RGC damage and loss of vision.

To further investigate this link, a team led by ophthalmologist Francesca Cordeiro of University College London artificially induced glaucoma in rats. The team found an increase in β-amyloid in RGCs, especially in cells that had died. In a second experiment, the researchers injected a β-amyloid subunit that is toxic to the central nervous system into the eyes of rats without glaucoma. The greater the dose, the more RGCs died.

Finally, Cordeiro and her co-workers administered to rats with glaucoma three different treatments that block plaque formation, including one currently used to treat AD. Although each reduced plaque buildup and RGC death, combining all three produced the biggest effect, the team reports online this week in the Proceedings of the National Academy of Sciences. The authors conclude that drugs directed against β-amyloid might be effective against glaucoma, which currently is treated by lowering intraocular pressure. Cordeiro says that β-amyloid plaque formation may be a "shared pathway" that causes AD and glaucoma.

Hideaki Hara, a glaucoma researcher at Gifu Pharmaceutical University in Japan, says that the new findings confirm the suspected link between AD and glaucoma. But Pervin Iseri, a neurologist at Kocaeli University in Umuttepe, Turkey, says that β-amyloid might still turn out to be an indirect cause of RGC death. Iseri adds that further studies are necessary to show that there is a "direct effect as well as a link between the mechanisms behind glaucoma and Alzheimer's disease."

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