Glaucoma Could Be Treated With Alzheimer's Drugs

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The development of the devastating neurodegenerative condition, Alzheimer's disease, is strongly associated with amyloid- (A) deposition, neuronal apoptosis, and cell loss. Here, we provide evidence that implicates these same mechanisms in the retinal disease glaucoma, a major cause of irreversible blindness worldwide, previously associated simply with the effects of intraocular pressure. We show that A colocalizes with apoptotic retinal ganglion cells (RGC) in experimental glaucoma and induces significant RGC apoptosis in vivo in a dose- and time-dependent manner. We demonstrate that targeting different components of the A formation and aggregation pathway can effectively reduce glaucomatous RGC apoptosis in vivo, and finally, that combining treatments (triple therapy) is more effective than monotherapy. Our work suggests that targeting the A pathway provides a therapeutic avenue in glaucoma management. Furthermore, our work demonstrates that the combination of agents affecting multiple stages in the A pathway may be the most effective strategy in A-related diseases.

In this study led by Dr Francesca Cordeiro of the Institute of Ophthalmology at University College London, scientists found evidence of a similar process involving amyloid beta proteins in the development of glaucoma, a disease where the optic nerve is damaged. Until now the only clue to the development of glaucoma has been elevated pressure inside the eye, but some people with normal eye pressure can also get it and lose their sight, so for some time scientists have wondered what else could be happening.

Cordeiro and colleagues examined retinas where the retinal ganglion cells (RGC) in the optic nerve had died off (a key feature of glaucoma) and noticed they were accompanied by plaques of amyloid beta protein similar to the ones in brains of people with Alzheimer's Disease. They were also able to induce RGC "apoptosis" (cell death) using various timed doses of amyloid beta proteins in the lab. The team then tested the effects of drugs normally used to treat Alzheimer's Disease on the rate of development of glaucoma in rats. They used three different drugs, each targetting a different part or stage of the growth of amyloid beta protein plaques. Each drug slowed down RGC apoptosis to some extent, but using all of them together (triple therapy) was more effective.



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