Abstract

Geographic atrophy (GA) secondary to age-related macular degeneration (AMD) is characterized by irreversible loss of macular retinal tissue and retinal pigment epithelium (RPE) cells. Several studies have revealed that accumulation of Alu RNA in RPE cell causes RPE cell degeneration in AMD. In the present study, systemic Alu RNA expression levels were determined in 33 subjects with GA and 40 control subjects using a proprietary Alu RNA quantification method. It was observed that the expression level of Alu RNA was not significantly different between GA and Control groups (median = 21.3 in both GA and Control groups, P = 0.251). In addition, the systemic level of Alu RNA was not associated with subject characteristics, such as GA lesion size and SNP profiles of complement factors associated with increased risk of AMD. In conclusion, the usability of systemic Alu RNA expression level as a biomarker of GA secondary to AMD could not be established in this study.

Highlights

  • Age-related macular degeneration (AMD) is one of leading causes of blindness in elderly people in the United States [1]

  • A total of 73 subjects were enrolled for the study; 33 subjects were enrolled in geographic atrophy (GA) group and 40 were enrolled in Control group

  • This is the first study to analyze the relationship between the systemic expression levels of Alu RNA and GA secondary to AMD

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Summary

Introduction

Age-related macular degeneration (AMD) is one of leading causes of blindness in elderly people in the United States [1]. In early and intermediate AMD, drusen, protein, and extra-cellular deposits between the retinal pigment epithelium (RPE) and Bruch’s membrane are observed [2]. Many patients with intermediate AMD progress to the advanced stage. In advanced AMD, geographic atrophy (GA) and/or choroidal neovascularization (CNV) are observed [2]. GA secondary to AMD, is characterized by an irreversible loss of macular retinal tissue and RPE cells, and is a cause of central visual function loss. No treatment is available to prevent or reverse visual function loss secondary to GA [3,4,5]

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