Two of the leading causes of blindness are diabetic retinopathy and age-related macular degeneration (AMD). Recent research has found that by activating a particular blood vessel protein, these two conditions can potentially be prevented and even reversed, greatly reducing any risk of permanent blindness. Diabetic retinopathy is the most common cause of blindness for young and middle-aged individuals (“working age”), while AMD is the most common cause of blindness for people over age 65.
The protein in question, known as Robo4, was activated in mice suffering from diabetic retinopathy and mice with AMD. Robo4 worked in preventing damage in many of the mice by “inhibiting abnormal blood vessel growth and by stabilizing blood vessels to prevent leakage. Abnormal blood vessel growth and leakage are two primary factors in both age-related macular degeneration (AMD) and diabetic retinopathy.”
Dr. Dean Li of the University of Utah School of Medicine, and lead researcher for this study, thinks the potential for Robo4 goes beyond diabetic retinopathy and AMD as well. “Many diseases are caused by injury or inflammation destabilizing blood vessels and causing them to leak fluid into adjacent tissues as well,” says Li. One recently popularized example of this is Severe Acute Respiratory Syndrome (SARS). This is only hypothesizing on Li’s part though, as the study focused exclusively on retinopathy and AMD.
This is new research and new results that have been found in this study, and further testing on humans is necessary to confirm the potential of activating the Robo4 protein and the subsequent development of commercial drugs that could perform this task (a process that takes at least a few years due to testing and regulations). The results are very promising though, as thousands of diabetic retinopathy and AMD cases that are likely to lead to blindness at present, could be reversed or hindered sufficiently to prevent this from occurring.
Source: Defeat Diabetes Foundation: Nelson, Chris. Li, Dean. University of Utah Health Sciences press release. March 2008.