¹Institute of Health and Biomedical Innovation, School of Optometry, Queensland University of Technology, Brisbane, Queensland, Australia

Correspondence: B Feigl, Institute of Health and Biomedical Innovation, School of Optometry, Centre for Health and Biomedical Innovation, Queensland University of Technology, Victoria Park Road, Kelvin Grove, Queensland 4059, Australia. Tel: +61 7 3864 5739; Fax: +61 7 3864 5665; E-mail: b.feigl@qut.edu.au

Received 29 November 2005; Accepted 27 March 2006; Published online 5 May 2006.

Abstract

We review proposed models and psychophysical and electrophysiological tests performed in many studies for early age-related maculopathy (ARM). We suggest that ischaemia is the trigger for impaired retinal pigment epithelium function causing imbalance of secretion of vascular growth factors, reduced disc degradation capability and reduced metabolic activity and possible inflammatory response. This results in increased deposition of cell debris, such as drusen and thickens Bruch's membrane causing even more ischaemia of the overlying neurosensory retina. The photoreceptors are more resistant to ischaemia given their proximity to the choroid. Furthermore, being 'upstream' from the inner retinal layers, they act as an oxygen sink depriving retinal layers further from the choroid. Postreceptoral cell layers and especially parts of the inner nuclear layer that are located in the watershed zone between two sources of blood supply are preferentially vulnerable to ischaemia. Based on psychophysical and electrophysiological findings we propose that most of the function impairment in early ARM starts postreceptorally.