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Peter Gouras, Lena Ivert, Martha Neuringer, Julie Mattison; Not age but the rate of aging drives the pathogenesis of age related macular degeneration in primates. Invest. Ophthalmol. Vis. Sci. 2013;54(15):4595.
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To understand how the retinal pigmented epithelium (RPE) contributes to the pathogenesis of age related macular degeneration (AMD).
We have determined the prevalence of AMD, mild to severe drusen, in rhesus monkeys and compared it to data obtained similarly in humans. We have examined the macular RPE of the monkeys histologically to determine how age changes the RPE, a likely factor in the pathogenesis of AMD, i.e. the buildup of lipofuscin bodies and the depletion of melanosomes and compared it to similar data in humans (Feeney IOVS 25:195,1984).
In monkeys AMD starts at about 10 and reaches maximum at about 25 years of age. In man it starts at about 30 and reaches maximum at about75. The buildup of lipofuscin bodies and the depletion of melanosomes reflect this same difference in time scale between monkeys and man.
The faster rate of pathogenesis of AMD in monkeys is unlikely due to a faster or greater turnover of outer segments or from toxic substances in these outer segments. The rate of outer segment turnover is the same in monkeys and man. Human RPE must have mechanisms that slow the rate of aging more effectively than monkeys and this retards the pathogenesis of AMD.
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