gms | German Medical Science

VI. International Symposium on AMD – Age-Related Macular Degeneration – Emerging Concepts – Exploring known and Identifying new Pathways

11. - 12.09.2015, Baden-Baden

AMD degeneration in the monkey

Meeting Abstract

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  • Peter Gouras - New York

VI. International Symposium on AMD – Age-Related Macular Degeneration – Emerging Concepts – Exploring known and Identifying new Pathways. Baden-Baden, 11.-12.09.2015. Düsseldorf: German Medical Science GMS Publishing House; 2015. Doc15amd20

doi: 10.3205/15amd20, urn:nbn:de:0183-15amd207

Veröffentlicht: 1. Oktober 2015

© 2015 Gouras.
Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). Lizenz-Angaben siehe



Purpose: To determine the pathogenesis of age related macular degeneration in the rhesus monkey and its relationship to its human counterpart.

Methods: Rhesus monkeys have been maintained for more than 25 years by the National Institute on Aging to determine if caloric restriction increases their life span as it does for small animals. We have been examining these monkeys clinically and histologically to determine if caloric restriction influences age related ocular disease, especially maular degeneration.

Results: Monkeys develop drusenoid maculopathy and accumulate lipofuscin in and lose melanosomes from the macula much faster than humans. This occurs despite a similar rate of outer segment turnover. The macula epithelium has the most lipofuscin which diminishes progressively with retinal eccentricity. The macula epithelium has the least melanosomes which increase in number with eccentricity. Mitochondria, concentrated at the basal third of the epithelium, decrease in number and elongate with age. Caloric restriction does not alter the prevalence or severity of the degeneration.

Conclusion: The faster rate of pathogenesis of the macular degeneration in the monkey cannot be explained by outer segment turnover because the turnover rate is similar in both species. It suggests that the pathogenesis of age related macular degeneration is strongly influenced by the rate of aging of the organism, which is faster in monkey than man. This is supported by the evidence that the macular epithelium in the monkey shows a faster rate of degeneration than the more peripheral retina, i.e., greater accumulation of lipofuscin and a greater loss of melanosomes. The elongation of mitochondria in macular epithelium suggests that oxidative stress is occurring and this may be responsible for the degeneration and its accelerated course in the monkey.