Abstract

Macular edema and its further complications due to the leakage from the choroidal neovascularization in course of the age-related macular degeneration (AMD) is a leading cause of blindness among elderly individuals in developed countries. Changes in tear film proteomic composition have been reported to occur in various ophthalmic and systemic diseases. There is an evidence that the acute form of neovascular AMD may be reflected in the tear film composition. Tear film was collected with Schirmer strips from patients with neovascular AMD and sex- and age-matched control patients. Two-dimensional electrophoresis was performed followed by MALDI-TOF mass spectrometry for identification of differentially expressed proteins. Quantitative analysis of the differential electrophoretic spots was performed with Delta2D software. Altogether, 11 significantly differentially expressed proteins were identified; of those, 8 were downregulated, and 3 were upregulated in the tear film of neovascular AMD patients. The differentially expressed proteins identified in tear film were involved in signaling pathways associated with impaired protein clearance, persistent inflammation, and neovascularization. Tear film protein analysis is a novel way to screen AMD-related biomarkers.

Highlights

  • IntroductionAge-related macular degeneration (AMD) is a leading cause of blindness in elderly patients in developed countries

  • Introduction published maps and institutional affilAge-related macular degeneration (AMD) is a leading cause of blindness in elderly patients in developed countries

  • We reviewed most of the recent developments in age-related macular degeneration (AMD) proteomic research in our previous manuscript, in which we sought to determine whether the pathological process in the macula can result in tear film proteome changes [30]

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Summary

Introduction

Age-related macular degeneration (AMD) is a leading cause of blindness in elderly patients in developed countries. The incidence of AMD is expected to increase by over. AMD affects central vision by evoking metamorphopsia, reading problems, and eventually legal blindness in its end stage. AMD can be divided into wet (neovascular) and dry (atrophic) forms. Atrophic AMD progresses slowly over years, while neovascular AMD with the presence of subretinal fluid and macular edema can develop in weeks due to the progressive growth of pathological choroidal vessels. There is no established treatment protocol for atrophic AMD, but antivascular endothelial growth factor (VEGF) intravitreal injections are a treatment of choice for neovascular AMD. Our awareness of AMD etiopathology has significantly improved in the past decade, the exact mechanisms underlying the disease are still vague

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