Macular degeneration in rhesus monkey (Macaca mulatta)

El-Mofty, Aly A.M.; Gouras, Peter; Eisner, Georg; Balazs, Endre A.

doi:10.1016/0014-4835(78)90027-1

Cited by 37 publications

(19 citation statements)

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“…Encouraged by the earlier findings of ElMofty et al [6,7] in a small sample at the CPRC, we concentrated our efforts on the aged segment of this closed primate popula tion. We confirmed the high incidence of clin ically detectable macular pathology in aged rhesus monkeys at an incidence much higher than previously observed in large surveys.…”

Section: Discussionmentioning

confidence: 99%

“…A much greater incidence of maculopathy in primates was reported by El-Mofty et al [6,7] who studied 162 seminatural free-ranging rhesus monkeys of all ages in the closed colo ny at the Caribbean Primate Research Center (CPRC) of the University of Puerto Rico. In their small sample of older adults ranging from 16 to 21 years of age, 83% of the animals showed pigmentary alterations or drusen-like changes.…”

Section: Introductionmentioning

confidence: 97%

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Degenerative Changes in Maculas of Rhesus Monkeys

Engel¹,

Dawson

Ulshafer³

et al. 1988

Ophthalmologica

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In the hope of identifying an animal model for age-related macular degeneration (AMD) we undertook a pilot investigation of aged rhesus monkeys. Twenty-nine monkeys from a seminatural colony were examined at the Caribbean Primate Research Center. Macular drusen were found in 74% of the monkey eyes. Alterations of the retinal pigment epithelium within the macula were noted in 45% of the eyes. Fluorescein angiography in selected animals revealed window defects consistent with drusen. None of this sample showed the exudative form of AMD or disciform scarring. One typical monkey underwent special studies including measurement of visual resolution by electrophysiological study of the retinal and visual cortex. Application of human criteria to this animal supported the diagnosis of early AMD. Histopathologic study of one eye by transmission electron microscopy confirmed the presence of drusen with nearly identical ultrastructural features to those found in the human pigment epithelium in AMD.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 97%

Degenerative Changes in Maculas of Rhesus Monkeys

Engel¹,

Dawson

Ulshafer³

et al. 1988

Ophthalmologica

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“…Macula is found only in primates and birds, and the animal model for macular degeneration is currently limited to monkeys [11][12][13][14]. Thus the monkey model is extremely important for understanding the mechanisms and etiology underlying macular degenerative diseases in humans [15,16].…”

Section: Introductionmentioning

confidence: 99%

Molecular Cloning of ELOVL4 Gene from Cynomolgus Monkey (Macaca fascicularis).

et al. 2003

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ELOVL4, elongation factor of very long chain fatty acids-4, is known to be responsible for autosomal dominant macular degeneration and Stargardt-like macular degeneration. In this study, we cloned the monkey homologue of ELOVL4 and determined the cellular and tissue distribution of the gene product. Sequence analysis of the monkey ELOVL4 gene revealed a high degree of homology between human and monkey. The cloned full-length cDNA of monkey ELOVL4 encoded 314 amino acids, the same length as human and two amino acids longer than mouse. The monkey ELOVL4 conserved the characteristics typical of the super family of ELO enzymes involved in the metabolism of membrane-bound fatty acid elongation. Real-time quantitative PCR demonstrated that the monkey ELOVL4 gene was highly expressed in restricted tissue-specific fashion, not only in the retina but also in the skin (90% of retina) and thymus (111% of retina). Immunohistochemical analysis detected signals predominantly in the photoreceptor layer of the monkey retina.

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“…Funduscopic examination of these animals revealed macular drusen in approximately half of animals older than 9 years and all animals older than 25 years. 20,21,[29][30][31] Histology and ultrastructural studies confirmed the presence of small and large drusen within the Bruch's membrane and beneath the RPE. 19 A small breeding colony derived from these animals was established at the University of Florida in 1994 and so exhibits similar findings.…”

Section: Adult-onset Macular Degeneration In Rhesus Monkeys (Macaca Mmentioning

confidence: 84%

REVIEW PAPER: Animals as Models of Age-Related Macular Degeneration

Zeiss

2010

Vet Pathol

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Age-related macular degeneration (AMD) is a degenerative condition that begins in Bruch's membrane and progresses to involve the retinal pigment epithelium and ultimately the overlying photoreceptors. The only required etiologic factor is age, and AMD is regarded as the leading cause of blindness in individuals older than 65 years. AMD results from variable contributions of age, environment, and genetic predisposition. Many loci are linked to AMD; in the majority of cases, the disease is associated with polymorphisms within these genes, rather than mutations that ablate gene function. The etiologic complexity of AMD is reflected by the paucity of animal models that entirely replicate the human disease. This review compares the salient anatomy of the primate and rodent retina, particularly in the light of AMD pathology. It next discusses prevailing hypotheses explaining how AMD may develop. These include the role of complement activation and macrophage chemotaxis in AMD, molecular mechanisms of choroidal neovascularization, and the roles of oxidative damage and lipid metabolism. Finally, the article gives an overview of spontaneous and induced nonhuman primate models and describes relevant mouse models in the context of each pathogenetic mechanism. KeywordsBruch's membrane, choriocapillaris, complement, degeneration, macula, retinal pigment epithelium Age-related macular degeneration (AMD) is a progressive condition of the retinal pigment epithelium (RPE), its supporting basement membrane, and the overlying photoreceptor layer. It affects the macula, the central area of the retina responsible for high-acuity daylight vision. Among individuals older than 65 years, AMD is regarded as the leading cause of blindness in the industrialized world. 39AMD has no single cause and results from variable contributions of age, genetic predisposition, and environment. Established epidemiologic risk factors include cigarette smoking, diet, female sex, Caucasian race, and a family history of AMD.52,60,61 Because AMD is rare in individuals younger than 55 years, the only required risk factor is age, which implicates the multitude of cellular changes that accompany normal aging in the pathogenesis of AMD. The challenge is to identify how these are altered to tip the process toward overt disease.With age, most people accumulate small, well-demarcated deposits of extracellular material beneath the RPE. 5,45 These are known as small, hard drusen and are not pathogenic. However, if these deposits enlarge, they become associated with regional RPE loss and eventual degeneration of overlying photoreceptors. These changes are funduscopically visible, and their progression is used to classify lesions along the continuum of early to late dry AMD. 18 The pathogenetic mechanisms of this process center on inflammation, oxidative damage, and RPE senescence 45 and are predominantly modeled in the mouse.In the minority of cases, late AMD is accompanied by growth of blood vessels from the choroid through Bruch's membrane toward the retina. ...

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Macular degeneration in rhesus monkey (Macaca mulatta)

Cited by 37 publications

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Degenerative Changes in Maculas of Rhesus Monkeys

Degenerative Changes in Maculas of Rhesus Monkeys

Molecular Cloning of ELOVL4 Gene from Cynomolgus Monkey (Macaca fascicularis).

REVIEW PAPER: Animals as Models of Age-Related Macular Degeneration

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