Abstract
Purpose: The lack of suitable animal models for (dry) age-related macular degeneration (AMD) has hampered therapeutic research into the disease, so far. In this study, pigmented rats and mice were systematically injected with various doses of sodium iodate (SI). After injection, the retinal structure and visual function were non-invasively characterized over time to obtain in-depth data on the suitability of these models for studying experimental therapies for retinal degenerative diseases, such as dry AMD. Methods: SI was injected into the tail vein (i.v.) using a series of doses (0–70 mg/kg) in adolescent C57BL/6J mice and Brown Norway rats. The retinal structure and function were assessed non-invasively at baseline (day 1) and at several time points (1–3, 5, and 10-weeks) post-injection by scanning laser ophthalmoscopy (SLO), optical coherence tomography (OCT), and electroretinography (ERG). Results: After the SI injection, retinal degeneration in mice and rats yielded similar results. The lowest dose (10 mg/kg) resulted in non-detectable structural or functional effects. An injection with 20 mg/kg SI did not result in an evident retinal degeneration as judged from the OCT data. In contrast, the ERG responses were temporarily decreased but returned to baseline within two-weeks. Higher doses (30, 40, 50, and 70 mg/kg) resulted in moderate to severe structural RPE and retinal injury and decreased the ERG amplitudes, indicating visual impairment in both mice and rat strains. Conclusions: After the SI injections, we observed dose-dependent structural and functional pathological effects on the retinal pigment epithelium (RPE) and retina in the pigmented mouse and rat strains that were used in this study. Similar effects were observed in both species. In particular, a dose of 30 mg/kg seems to be suitable for future studies on developing experimental therapies. These relatively easily induced non-inherited models may serve as useful tools for evaluating novel therapies for RPE-related retinal degenerations, such as AMD.
Highlights
Age-related macular degeneration (AMD) is one of the major causes of visual impairment in the developed world [1–5]
In the early and intermediate stages, pathological hallmarks of age-related macular degeneration (AMD) include the appearance of soft subretinal deposits and pigment alterations in the macular area of the retinal pigment epithelium (RPE)
Four mice and four rats received a single intravenous injection with 0.9% NaCl. This group served as a control group
Summary
Age-related macular degeneration (AMD) is one of the major causes of visual impairment in the developed world [1–5]. The irreversible and non-treatable vision loss that is associated with AMD is a significant social burden, with a projected number of people with the disease around 288 million in 2040 worldwide [6]. Detection and prevention are critical in increasing the likelihood of retaining good and functional vision [1]. Despite decades of research worldwide, the complex pathogenesis of AMD has not been fully elucidated yet [7]. In the early and intermediate stages, pathological hallmarks of AMD include the appearance of soft subretinal deposits and pigment alterations in the macular area of the retinal pigment epithelium (RPE).
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