Abstract

Glaucoma is one of the most common causes of irreversible blindness worldwide. The pathogenesis of the disease is not fully understood. Elevated intraocular pressure is still considered to be one of the most important risk factors, but cannot explain all cases of glaucoma disease. The involvement of autoimmune mechanisms may play an important role in the pathogenesis of glaucoma. Evidence to support this theory has been shown by our group in previous studies: glaucoma patients were found to develop antibody alterations against specific retina and optic nerve proteins. In the experimental autoimmune glaucoma model, we demonstrated that an immunisation with these proteins causes retinal ganglion cell loss in an autoimmune context. In spite of these results, it is still unclear whether the changes in antibody patterns have a causal connection with glaucoma development or are merely an epiphenomena of the disease. However, these changes in the natural autoimmunity offer a new approach to gain deeper insight into glaucoma pathophysiology and to develop a diagnostic approach for early diagnosis.

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