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Journal of Ophthalmology
Volume 2016 (2016), Article ID 2913612, 7 pages
http://dx.doi.org/10.1155/2016/2913612
Review Article

Cellular and Molecular Pathology of Age-Related Macular Degeneration: Potential Role for Proteoglycans

1School of Health and Biomedical Sciences, RMIT University, Bundoora, VIC 3083, Australia
2School of Pharmacy, The University of Queensland, Woolloongabba, QLD 4102, Australia
3Faculty of Health Sciences, University of Macau, Taipa, Macau
4Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou 510006, China
5Department of Immunology, Monash University, Melbourne, VIC 3004, Australia

Received 22 March 2016; Revised 13 June 2016; Accepted 26 June 2016

Academic Editor: Van C. Lansingh

Copyright © 2016 Othman Al Gwairi et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Age-related macular degeneration (AMD) is a retinal disease evident after the age of 50 that damages the macula in the centre of retina. It leads to a loss of central vision with retained peripheral vision but eventual blindness occurs in many cases. The initiation site of AMD development is Bruch’s membrane (BM) where multiple changes occur including the deposition of plasma derived lipids, accumulation of extracellular debris, changes in cell morphology, and viability and the formation of drusen. AMD manifests as early and late stage; the latter involves cell proliferation and neovascularization in wet AMD. Current therapies target the later hyperproliferative and invasive wet stage whilst none target early developmental stages of AMD. In the lipid deposition disease atherosclerosis modified proteoglycans bind and retain apolipoproteins in the artery wall. Chemically modified trapped lipids are immunogenic and can initiate a chronic inflammatory process manifesting as atherosclerotic plaques and subsequent artery blockages, heart attacks, or strokes. As plasma derived lipoprotein deposits are found in BM in early AMD, it is possible that they arise by a similar process within the macula. In this review we consider aspects of the pathological processes underlying AMD with a focus on the potential role of modifications to secreted proteoglycans being a cause and therefore a target for the treatment of early AMD.