Keeping an eye on glaucoma

The tyrosinase/L-dopa pathway modifies glaucoma in a murine model.

Written byJonathan Weitzman
| 1 min read

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Glaucoma is the leading cause of irreversible blindness and affects millions worldwide. Patients with primary congenital glaucoma (PCG) often have mutations in the cytochrome P450 family 1, subfamily B, polypeptide 1 (CYP1B1) gene. In the March 7 Science, Richard Libby and colleagues report the characterization of a Cyp1b1-/- knockout mouse as a model for PCG (Science, 299:1578-1581, March 7, 2003).

The mice had developmental eye defects similar to those seen in human patients. Genetic and histological analysis revealed a role for the tyrosinase gene as a genetic modifier. Tyrosinase also modifies the anterior segment dysgenesis phenotypes observed in mice lacking the Foxc1 gene that has also been implicated in PCG. Tyrosinase converts tyrosine to L-dopa, and the ocular phenotypes of the knockout mice could be relieved by the administration of L-dopa.

This study suggests that L-dopa should be tested as a possible therapeutic for treating glaucoma patients.

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