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Dry AMD News

Posted by Ilena Di Toro | Posted on January 14, 2020

It is a given that everyone wants to be able to see. If a person’s vision isn’t the best, eyeglasses, or contacts lenses can improve vision. If cataracts or glaucoma are present, surgery can ameliorate the situation. Unfortunately, there are vision diseases that lenses or surgery can’t correct and one of them is Dry Age-Related Macular Degeneration (AMD).

Dry AMD is the leading cause of blindness in persons age 65 and older and it affects 11 million people in the U.S. alone. The disease progresses slowly and there are no therapies available for this disease. Part of the reason for that is the pathophysiology of the disease isn’t fully understood. Still, that doesn’t mean that there isn’t research going on in order to develop treatments.

Genetics
One area of focus are genetics, specifically looking to see what processes turn the genes on or off that lead to Dry AMD. Scientists are looking to develop mouse models of Dry AMD and will test them to see what is going on at the genetic level. They want to see if it is possible to manipulate or even replace specific genes to prevent the disease from occurring in the first place.

Inflammation Suppression
Inflammation is the culprit in many conditions, such as rheumatoid arthritis, fibromyalgia, just to name a few. It also plays a role in Dry AMD. There are a number of drugs that are being looked at for their part in suppressing inflammation. Since mutations in the complement pathway of the immune system increase the risk of developing Dry AMD, inflammation suppression drugs are being investigated as treatment options. One such drug is ARC1905, also known as Latanprost, which currently being used to treat pressure in the eye due to glaucoma.

Neuroprotection
“Neuroprotection, even in glaucoma, hasn’t been shown to work,” said Peter K. Kaiser, MD, chairman of ophthalmology research at the Cleveland Clinic’s Cole Eye Institute. “In macular degeneration, all of the studies to date have been disappointing.” Okay, if studies of neuroprotection were a bust, why mention it? Because there is one study that involves anti-amyloid therapy. Beta-amyloid is a component of the brain plaque, which is found in persons with Alzheimer’s Disease. The reason for exploring this avenue is to decelerate or block the development of drusen, pigment abnormalities and geographic atrophy, all of which lead to Dry AMD.

Aging and Lipoproteins
What do Dry AMD and cardiovascular disease have in common? They are both most likely to occur over the age of 50. Christine A. Curcio, PhD, professor of ophthalmology at the University of Alabama in Birmingham saw parallels between the formation of drusen in Bruch’s membrane and lipids forming in cardiovascular vessel walls. She studied the drusen and found that they resembled dietary components. Her research has shown that the Retinal Pigment Epithelial (RPE) takes the cholesterol-rich lipoprotein from plasma to meet the metabolic requirements of the retina. The RPE takes what it needs for the photoreceptors and gets rid of what’s left over by recycling back to the Bruch’s membrane. Over time the membrane thickens and it gets hard to clear. The lipoproteins form a layer on the surface of the RPE that Dr. Curcio calls it an “oil spill”. The lipid become toxic and over time drusen forms. So, if she is correct about the collection of lipids in Bruch’s membrane being similar to cardiovascular disease, then researchers and eventually patients might benefit from the work done in cardiovascular drug development.

Thanks to ongoing research of Dry AMD, blindness due to this disease won’t be inevitable.

Sources:

https://nei.nih.gov/content/report-dry-amd-requires-broad-systems-biology-approach-leveraging-big-data-multiple

https://www.macular.org/feature/research-code-breaker

https://www.aao.org/eyenet/article/dry-amd-research-moves-ahead-clinical-trials-new-l

https://www.alz.org/alzheimers-dementia/research_progress/treatment-horizon

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