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Extending that line of thought, it is tempting to hypothesize that RPE cells die faster in the central retina, causing the AMD phenotypes to be reached sooner in the central retina than in the periphery, but no data currently exists regarding the size, number, and position of RPE cells in aging human retinas that can be conclusively tied to retinal pathologies (Boulton and Dayhaw-Barker, 2) suggesting that whatever mechanism is at work, central RPE cells have profiles that suggest greater metabolic stress in the center of the retina vs

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7) during a prolonged allyl-ITC exposure

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