A new study in rats, published in the Proceedings of the National Academy of Sciences, shows that a protein fragment that litters the brains of people with Alzheimer’s disease may also bear responsibility for some of the 1) ___ loss in glaucoma. Glaucoma patients typically have abnormal fluid pressure within the eye, but it remains unknown how this stress kills the nerve cells at the back of the 2) ___. While there is no current cure for glaucoma, easing eye 3) ___ with drugs or surgery helps prevent vision loss in many patients. Some glaucoma patients, however, experience vision loss even with normal eye pressure, indicating that other factors are sometimes involved. The new research suggests that one hidden assailant is 4) ___, the same protein fragment that accumulates in the brains of Alzheimer’s patients. An earlier rodent study of glaucoma had found the substance in the animals’ eyes, but other evidence of amyloid-beta in glaucoma is scarce. In the new study, glaucoma was induced in 60 rats by injecting 5) ___ into the animals’ eyes. Within weeks, amyloid-beta deposits showed up in dying retinal-nerve cells. The researchers then gave another round of eye injections to some of the rats. In one eye, the animals received a synthetic antibody that absorbs amyloid-beta. The other eye got a 6) ___. After 3 weeks, the medicated eyes showed only one-fourth as much retinal-cell death as did the untreated eyes. The effect remained 13 weeks later. Next, the scientists repeated the experiment on other rats with glaucoma, this time using a cocktail that included the 7) ___ and two other drugs with anti–amyloid-beta effects: a dye called Congo red and an enzyme deactivator called beta-secretase inhibitor. The triple combination worked even better than the antibody alone, reducing cell 8) ___ by 84%.

ANSWERS: 1) vision; 2) retina; 3) pressure; 4) amyloid-beta; 5) saline; 6) placebo; 7) antibody; 8) death

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