Though based on mouse studies, the research bolsters the idea that humans suffering from these and other eye conditions may be able to help preserve function by adding antioxidants to their diet, and explains why this would work. The team also devised a new cell-based gene therapy technique that could eventually offer another option for arresting vision loss from these diseases.
The work, led by Scripps Research Professor Martin Friedlander, M.D., Ph.D., was reported in an advance, online edition of the Journal of Clinical Investigation on February 2, 2009. The research is also likely to apply to a range of other neurodegenerative conditions, including vision loss from Huntington's and Alzheimer's diseases and inherited retinal degenerations, such as retinitis pigmentosa.
Many forms of blinding degenerative eye conditions are tied to the abnormal proliferation of new blood vessels in the eyes, or neovascularization. Treatment of these conditions has generally focused on blocking continued neovascularization, but this typically only slows disease progression because new growth eventually wins out, leading to continued damage and vision loss.
For many of these conditions, vision loss has been definitively attributed to the blinding effect of fluid leakage and hemorrhage from newly grown blood vessels. But the cause of vision loss in certain diseases such as MacTel has been more elusive.
To better understand these eye diseases, and to develop new and better treatments, the research team examined a mouse model of these human diseases. The particular "knockout" mouse the team focused on has been used by other researchers for studying fat metabolism. The mouse model, however, also has a genetic alteration that leads to increased blood vessel growth in the eyesa fact that Friedlander and colleagues had pointed out in a previous publication. In this model, neovascularization occurs in the back of the eyes in an area of the
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| Contact: Keith McKeown kmckeown@scripps.edu 858-784-8134 Scripps Research Institute Source:Eurekalert |