Age-Related Macular Degeneration (AMD)

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In age-related macular degeneration, the nerve cells are destroyed in the macula – the point of sharpest vision on the retina. This is caused by deposits beneath the retina as a result of local disturbances in retina metabolism.
Age-related macular degeneration – dangerous, but almost unknown
The best-case scenario is that, as you grow older, you become more experienced, knowledgeable, wise – and farsighted. However, an estimated 196 million people globally live with age-related macular degeneration, 10.4 million of whom (5,3%) have moderate or severe distance vision impairment or blindness from more severe forms of the condition.1 This dangerous disease is almost unknown to the general public. Yet it is the most common cause of severe visual impairment and blindness among people over the age of 65 in developed countries. The incidence of age-related macular degeneration will go on growing dramatically as societies continue to age. Women are more frequently affected than men.
The initial symptoms of macular degeneration
The first sign of age-related macular degeneration can be when straight lines suddenly look bent. The disease usually starts in one eye, but the second is also highly likely to be affected later. Further indications of macular degeneration can emerge when reading, for example. Where the patient fixes his/her eyes, the letters become blurred, and only an indistinct blob can still be seen. This blob grows in size over time, with the result that sufferers can, for example, see a clock but not what time it is. Or they can recognize a person's outline but not his/her facial features.
Different forms of the disease
"Dry" age-related macular degeneration (AMD) is the most common form of the disease. It only progresses slowly, so that the patients' loss of vision remains limited. The "wet" form of macular degeneration (about 10 to 15 percent of all AMD cases) causes much more serious restrictions of vision. It is caused by tissue fluid and blood seeping from pathologically changed blood vessels into the macula, leading to edemas (swellings caused by fluid accumulations). In addition, new, diseased blood vessels form in the choroid under the retina, so that thickness of the retina is an important parameter of how active the disease is. As a result, the nerve cells of the retina gradually die off, and central vision can be lost within just a few years. If there is hemorrhaging, it may even be lost completely at once.
An active substance against wet AMD
More and more medicines that inhibit a specific growth factor known as VEGF (vascular endothelial growth factor) are used today in the treatment of wet age-related macular degeneration. This messenger substance usually stimulates the formation of new blood vessels.
VEGF inhibition is also the basic mechanism used by an new active substance developed by Bayer and the U.S. firm Regeneron Pharmaceuticals. This substance can prevent blindness in people with wet age-related macular degeneration (AMD). It is a protein that is injected into the eye. There, it inhibits not only VEGF, but also another messenger substance involved in the abnormal formation of new blood vessels and its fateful consequences. Progressive blindness can be stopped in this way. And not only that: because the substance causes existing edemas and pathologically formed new blood vessels in the choroid to recede, some of the photoreceptor cells that have not yet been completely destroyed can be saved – and visual acuity can even improve in some patients.
In 2013, Bayer's anti-VEGF therapy was first approved for the treatment of wet age-related macular degeneration (wet AMD) in Canada. It is now approved in many countries around the world, including the United States, Europe and Japan for wet AMD.
Sources:
1 WHO, World Report on Vision, 2019, Page 4
https://www.who.int/publications-detail/world-report-on-vision
Advice for patients
Each body reacts differently to medicines. Therefore it is impossible to tell which medicine works best for you. Please consult your physician.