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M. Neuringer, P. Wallace, A. Billingslea, J. Gold, R.G. Weleber; Incidence of Drusen-like Changes in a Rhesus Monkey Colony: Effects of Age, Gender and Dietary Carotenoids . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4949.
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Purpose. To survey the prevalence of drusenoid ophthalmoscopic changes in a population of rhesus monkeys as a function of age and gender, and to examine the influence of life-long absence of dietary carotenoids. Methods. Number and severity of drusen-like spots were evaluated in color fundus stereophotographs and fluorescein angiograms of 150 rhesus monkeys from 1 to 32 years of age, including 120 over 16 years old (equivalent to 48 human years). In addition, we examined 49 rhesus monkeys reared and maintained on semipurified diets lacking the carotenoids lutein and zeaxanthin and therefore having no macular pigment. Results. Drusen-like bodies were not seen at 0-8 years and occurred in 12.5% of monkeys 9-12 years old. Prevalence was high thereafter, ranging from 46 - 64% from 13-32 years. Number and size were judged as mild in all cases up to 16 years, but increasing numbers of animals had moderate or severe changes from age 17 onward (10% at 17-20, 20% at 21-24). Females had 4 times more cases than males from 9-16 years. Severity was also greater in females, with moderate to severe cases occurring only in females at 17-24 years. In animals reared on diets lacking carotenoids, drusen were common at a much earlier age, appearing in 42% of those 5-8 years old and 46% of those 9-12, with 16% showing changes of moderate severity, and females showing more than twice the prevalence at 9-16 years. Two animals were identified with a pattern of numerous large hard drusen resembling the human syndrome of dominant drusen. Conclusions. Drusen-like changes are common in aging rhesus monkeys, particularly females, and occur significantly earlier in monkeys lacking dietary carotenoids. Histopathological studies will be necessary to determine the underlying anatomical changes. Previous studies in these and other carotenoid deprived monkeys showed increases in transmission defects seen in fluorescein angiograms, and showed that some punctate defects were due to lipoidal degeneration of RPE cells.
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