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Successful tests of new treatments in mice for eye disease causing irreversible blindness in humans

A team led by Krzysztof Palczewski, Ph.D., chair of pharmacology at the Case Western Reserve University School of Medicine, has taken the first steps in treating an eye disease causing irreversible congenital blindness in millions of people worldwide by successfully testing two new treatments in mice.

Publishing in this month's open access journal PLoS Medicine, the researchers found that these treatments "provide highly effective and complementary means for restoring retinal function in this animal model of human hereditary blindness."

The disease studied is Leber congenital amaurosis (LCA), characterized by severe loss of vision at birth. Its causes are not fully understood. Researchers believe that the disease might be due to abnormal development of photoreceptor cells in the retina, extremely premature degeneration of these cells, or lack of essential metabolic ingredients necessary for vision in the cells. In a subset of these diseases, it is known that the retina stops functioning due to loss of the lecithin retinol acyl-transferase enzyme (LRAT). LRAT is required for regeneration of a pigment necessary for the eye to detect light.

LCA can be caused by mutations in the gene encoding RPE65, a key protein involved in the production and recycling of 11-cis-retinal in the eye. Currently, there is no treatment for LCA, although previous studies in mice have successfully tested the injection of a virus carrying the normal gene for RPE65, and, separately, oral administration of a vitamin A-like compound.

In the current paper, Palczewski (formerly of the University of Washington) examined the effect of combining the two treatments in blind mice that did not have the LRAT enzyme. They report that gene therapy carrying the LRAT gene significantly restored electroretinographic (ERG) responses and pupillary light responses. Pharmacological intervention with orally administered drugs also caused long-lasting restoration of retinal functi
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Contact: George Stamatis
George.Stamatis@case.edu
216-368-3635
Case Western Reserve University
1-Nov-2005


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