Researchers bred mice in which the gene PTP-Meg2 (protein tyrosine phosphatase megakaryocyte 2) was mutated. As a result, the animals suffered from chronic intraocular pressure elevation. The research team successfully demonstrated that, in their model, the intraocular pressure elevation was associated with a loss of optic nerve fibers and retinal cells. They also observed that retinal cells were unable to function properly. They further discovered glial cells and certain components of the immune system showed a reaction in the animals’ optic nerve and retina. As both aspects may be relevant for neurodegeneration, specific and early intervention into these cellular mechanisms could inhibit glaucoma.
By making use of a genetic screening, the researchers identified new potential biomarkers for glaucoma, which in the future, may facilitate early detection. As a result, it will be possible to start therapy at an earlier stage, before the optic nerve and retina are damaged. The glaucoma-mouse model may, moreover, be used to test new therapy options. So far intraocular pressure was reduced and nerve cells were retained in the mice if they were given a drug that has been used to treat human patients.
With more than 60 million patients, Glaucoma is a leading cause of blindness worldwide. In Germany alone, there are one million patients — and the estimated number of unknown cases is likely to be much higher, due to the fact that symptoms often remain undetected during the early stage of the disease. In glaucoma patients, the optic nerve and the retinal nerve cells are damaged beyond repair.
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