Abstract
Glaucoma is an optic neurological disorder and the leading cause of irreversible blindness worldwide, with primary open angle glaucoma (POAG) as its most prevalent form. An early diagnosis of the disease is crucial to prevent loss of vision. Mechanisms behind glaucoma pathogenesis are not completely understood, but disease related alterations in the serological autoantibody profile indicate an immunologic component. These changes in immunoreactivity may serve as potential biomarkers for glaucoma diagnostics. We aimed to identify novel disease related autoantibodies targeting antigens in the trabecular meshwork as biomarkers to support early detection of POAG. We used serological proteome analysis (SERPA) for initial autoantibody profiling in a discovery sample set. The identified autoantibodies were validated by protein microarray analysis in a larger cohort with 60 POAG patients and 45 control subjects. In this study, we discovered CALD1, PGAM1, and VDAC2 as new biomarker candidates. With the use of artificial neural networks, the panel of these candidates and the already known markers HSPD1 and VIM was able to classify subjects into POAG patients and non-glaucomatous controls with a sensitivity of 81% and a specificity of 93%. These results suggest the benefit of these potential autoantibody biomarkers for utilization in glaucoma diagnostics.
Highlights
Glaucoma describes a group of optic neuropathies and is the leading cause of irreversible blindness
Experienced ophthalmic medical staff can evaluate glaucomatous damages of the optic nerve and even the diagnosis often is a matter of subjective interpretation
To help the medical staff with the assessment of glaucoma and to provide a fast and objective test that can be included in routine examinations, reliable biomarkers need to be established in easy monitorable body fluids, such as tear or serum
Summary
Glaucoma describes a group of optic neuropathies and is the leading cause of irreversible blindness. The TM in POAG is characterized by an extensive accumulation of extracellular matrix [4], the reorganization of the actin cytoskeleton [5, 6] and Autoantibody Biomarker Discovery in POAG a decreased cellularity. This causes an overall increase of tissue rigidity leading to diminishing capability to adapt to changing IOP levels. Malfunction of the AH outflow facility causes an increase of IOP above physiological levels, inducing mechanical stress to the optic nerve head. Molecular mechanisms behind pathological changes in the TM are not fully understood
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