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06-10-2009 | Cardiometabolic | Article

Age-related macular degeneration linked to lipoprotein build-up in retina


Free abstract

MedWire News: A build-up of lipoprotein particles at the back of the retina, similar to the build-up of cholesterol in coronary arteries, may play a key role in the development and progression of the “dry” form of age-related macular degeneration, show results from a review of recent research.

Age-related macular degeneration (ARMD) is a major cause of vision loss in the elderly and exists in two forms “wet” and “dry.”

In the “wet” form, abnormal blood vessels behind the retina grow into the macula, and can separate it from the rest of the retina leading to sight-threatening complications.

The “dry” form of the disease is much more common, but until recently was poorly understood. A leading research team in this area, led by Christine Curcio (University of Alabama School of Medicine, Birmingham, USA) summarizes current knowledge in a review published in the Journal of Lipid Research.

The current focus of Curcio and colleagues is Bruch’s membrane (the innermost layer of the choroid) and the retinal pigment epithelium, in particular the boundary between the retinal pigment epithelium and Bruch’s membrane.

They believe that a build-up of lipoprotein particles in this boundary plays a major role in the development and progression of ARMD.

“We speculate that plasma lipoproteins taken up by retinal pigment epithelium are stripped of nutrients required by photoreceptors (eg, xanthophylls, cholesterol, vitamin E) and repackaged for secretion in Bruch’s membrane as large, esterified cholesterol-rich apolipoprotein B lipoproteins,” they write.

These lipoproteins naturally accumulate in Bruch’s membrane with age, but in some people may collect at the boundary between the retinal pigment epithelium and Bruch’s membrane, and form a barrier to the exchange of fluid and nutrients required for the retinal pigment epithelium to survive.

“We suggest that the formation of ARMD lesions and their aftermath may be a pathological response to the retention of a sub-endothelial apolipoprotein B lipoprotein, similar to a widely accepted model of atherosclerotic coronary artery disease,” conclude the authors.

If Curcio et al’s lipid wall hypothesis is correct, their findings will give researchers a fresh target for new imaging and diagnostic techniques, as well as another point of intervention for drug therapy.

MedWire ( is an independent clinical news service provided by Current Medicine Group, a trading division of Springer Healthcare Limited. © Springer Healthcare Ltd; 2009

By Jenny Grice