Control of IOP early in the disease process has been shown to delay and even arrest glaucoma progression and the resultant visual field loss.15, 16 The diagnosis of glaucoma requires a detailed examination of optic disc structure and visual field, assessing both structure and function of the eye. biomarker for glaucoma. studies on neuroretinal cells and porcine retinal explants proven a protecting effect of antibodies (eg, anti-GFAP) on RGC, which seems to be the result of reduced stress levels in the retina. We conclude the absence of some autoantibodies in glaucoma individuals reflects a loss of the protecting potential of natural autoimmunity and may thus encourage neurodegenerative processes. Concluding, autoantibody profiles resemble useful biomarkers for analysis, progression and severity of glaucoma. Long term longitudinal studies will help to improve early detection and enable better monitoring of disease progression. Introduction The term glaucoma subsumes a group of optic neuropathies that share characteristic morphological changes within the retinal nerve dietary fiber layer and the AM-2099 optic nerve head which are associated with a sluggish and progressive retinal ganglion cell (RGC) death and visual field loss.1 Glaucoma is the most common cause for irreversible blindness and the second leading cause of blindness worldwide.2 The most frequent glaucoma form in the Western world is the main open-angle glaucoma (POAG).3, 4 Although the risk for POAG increases with the elevation of intraocular pressure (IOP) and an elevated IOP is the most common known risk element for glaucoma, most individuals with ocular hypertension will not develop glaucoma.5 It is assumed that risk reasons others than IOP are mainly involved in the onset of the condition, especially depicted in glaucoma patients with statistically Rabbit Polyclonal to SIN3B normal pressure levels less than 21?mm?Hg, the so called normal pressure glaucoma (NTG).6 Beside age, sex, and ethnicity,7 events such as oxidative stress,8 systemic and ocular vascular factors,9 elevated glutamate concentration10 or nitric oxide levels,11 or an autoimmune component12, 13 are considered possible risk factors. It is also likely that a combination of multiple risk factors increases the possibility of developing glaucoma and may influence its severity and additional phenotypic characteristics.14 By now, elevated IOP is the only risk element that can be treated, for example, with medications or glaucoma surgery. Control of IOP early in the disease process has been shown to delay and even arrest glaucoma progression and the resultant visual field loss.15, 16 The analysis of glaucoma requires a detailed examination of optic disc structure and visual field, assessing both structure and function of the eye. Regrettably, most potential screening tests have an estimated specificity of approximately 85%17 resulting in an insufficient predictive power. Hence, most individuals have suffered from glaucoma for over 10 years without knowing and as many as half of RGC and their axons can be lost before 1st pathological changes can be recognized.18, 19 Several AM-2099 epidemiological studies have shown that at least half of glaucoma individuals remain undiagnosed in developed countries20 and nine out of 10 worldwide.7 Especially the early analysis of the disease has an important part, since so far the threat of blindness can only be prevented by timely treatment through lowering the IOP. This underlines the strong demand for more diagnostic options and disease or treatment monitoring, for example, by use of biomarkers. A biomarker is definitely defined as a characteristic that is objectively measured and evaluated as an indication of normal biological processes, pathogenic processes, or pharmacologic reactions to a restorative intervention, and offers useful applications in disease detection and AM-2099 monitoring of health status.21 Recognition of potential glaucoma biomarkers from clinical studies By now, several proteomic markers, for example, crystallins,22, 23 warmth shock protein 60 (HSP 60) and HSP 90, myotrophin, apolipoprotein B and apolipoprotein E, endothelial leukocyte adhesion molecule-1, myoblast determination protein 1, myogenin, vasodilator-stimulated phosphoprotein, ankyrin-224 and transthyretin,25.