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V. Zubaty, E. Spoerl, A. Boehm, K. Geiger, L. Pillunat; Increased Advanced Glycation End-Products (AGEs) in Trabecular Meshwork of Patients With Primary and Secondary Glaucoma. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1607. doi: https://doi.org/.
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Advanced glycation end products (AGEs) have been implicated in degenerative diseases, associated with age-related tissue alterations, neurodegenerative and diabetic pathology. This study investigated the anterior chamber angle of human eyes for AGE expression in patients with primary or secondary glaucoma by immunohistochemistry.
Immunohistochemistry (IHC) using the monoclonal anti-AGE- 6D12 and polyclonal anti-RAGE were performed on sections of paraffin-embedded tissues of 53 trabeculectomy specimens from patients with primary open angle glaucoma (28 male, 25 female patients, mean age 67.0 +/- 20.0 years). Ten corneal transplant donor eyes without glaucoma were used as controls together with 15 eyes with a diagnosis of secondary glaucoma. Statistical evaluation was performed using the Chi-square test.
In comparison to normal control eyes, trabeculectoy specimens showed significantly higher expression of AGEs in their anterior chamber angle (P<0.0001), while the difference between controls and secondary glaucoma was barely significant. Additionally, trabeculectomy specimen from patients with primary open angle glaucoma showed significantly more AGE-deposits than the anterior chamber angle of patients with secondary glaucoma (P<0,001). In normal donor eyes, the extent of AGE-deposition in the retina was dependent on age, while the anterior chamber angle remained mostly free of AGEs. Eyes with secondary glaucoma showed low to moderate deposits of AGEs within the anterior chamber angle mostly associated with the basis of the iris and the channel of Schlemm, but only small deposits (grade 0-2) in the superficial trabecular meshwork and in the sclera. Deposits in the retina and in the optic nerve conformed to earlier reports.
Our results support the assumption that some of the passage inhibition of aqueous humor in glaucoma may be related to the effects of advanced aging with the possible consequence of altered rigidity within the trabecular meshwork which, in turn, may further worsen the drainage of aqueous humor.
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