Jul 27, 2012

Tempering the Immune System to Save Vision

Science Education

Great progress is being made in identifying targets for therapies, including using the body’s own protective systems to keep the photoreceptors alive.

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Photo of a retina with dry AMD

A retina with dry AMD. The yellow spots (called drusen) accumulate and can cause damage in AMD.

The human body has highly impressive mechanisms to protect itself from harm. For example, a group of molecules known as the complement system work with antibodies to kill invading bacteria by punching holes in them and letting the internal contents leak out.

Unfortunately, these same mechanisms, if not regulated properly, can be harmful to us. It turns out that these powerful molecules are also involved in the death of retinal cells in age-related macular degeneration(AMD).

Last week, 150 retinal scientists from around the world met in Bad Goegging, Germany, for the 15th International Symposium on Retinal Degenerations to discuss a variety of research efforts and advances, and the role of the complement system was a major topic of discussion. Many of the talks focused on how we can use natural complement control mechanisms in the body to stop the damage.

In addition, there were several discussions on how to better determine the actual genetic risk for getting AMD, and how high-risk, complement-related genes affect someone’s response to Lucentis, Avastin or Eylea, the current treatments available for wet AMD.

It was in 2005 that Foundation-funded researchers first discovered that genes associated with the complement system were linked to AMD. The game-changing breakthrough was made in conjunction with the Human Genome Project, a 13-year effort to identify all the genes in the human body.  And given the complexities of the immune system, the research community continues to work hard to figure out how to manage and tweak the complement system so it doesn’t cause vision loss.

The International Symposium also included insightful talks on the role of oxidative stress in photoreceptor death in all retinal degenerations, and the studies underway to stave it off through what are known as neuroprotective therapies. Oxidative stress occurs through normal aging and wear and tear on the body, but also when the body is fighting off illness or toxins.

For example, cigarette smoke is a major contributor to oxidative stress. Eating unhealthy food can also increase it. That’s why healthy living is important for everyone, especially for those with a retinal degeneration.

Clearly, great progress is being made in identifying targets for therapies, including using the body’s own protective systems to keep the photoreceptors alive. Science never seems to move fast enough, and that is in large part due to the complexity of the human body, including systems that regulate immunity.

But thanks to the tenacity and persistence of the international research community, and by working together through meetings like the one in Bad Goegging, we’re getting there.