Retinal Degeneration Diseases Introduction

Retinitis pigmentosa (RP) and age-related macular degeneration (AMD) are two major retinal degenerative diseases that lead to blindness. RP represents a family of genetic disorders that cause rod cell degeneration. Many of these are associated with mutations in rod-specific rhodopsin (RHO). Unlike lower vertebrates, higher vertebrates, including humans, do not regenerate significantly after injury or disease. This leads to interest in stem cell transplantation therapies to restore damaged photoreceptors. So far, there is no definitive treatment. New therapeutic approaches have been explored using various animal models based on the natural history of the disease. Iodoacetic acid (IAA) selectively destroys photoreceptors in the retina, during which the inner retina is preserved and displays the histological features seen early in human RP.

Fig. 1. Representative fundus photographs from one swine prior to IAA administration (top) and 5 weeks post-IAA 10 mg/kg IAA. (Noel JM, et al., 2012)

Service Overview

Iodoacetic acid (IAA) has been reported to cause photoreceptor degeneration in small animal models. However, differences in eye size and anatomy reduce the usefulness of these models for studying retinal rescue strategies in humans. The porcine eye is close in size to the human eye and is rich in rods and cones. This makes a rapidly induced porcine model of photoreceptor damage advantageous for many therapeutic strategies. In view of this, Ace Therapeutics has successfully developed a porcine retinal degeneration model induced by iodoacetic acid based on a deep understanding of the anatomical characteristics and functional organization of the porcine retina. This large animal model of controlled photoreceptor damage could be used to study therapeutic options to replace damaged photoreceptors.

Explore Ace Therapeutics' Minipig Models of Iodoacetic Acid-Induced Retinal Degeneration

Ace Therapeutics researchers successfully create a minipig model of retinal degeneration by intravenously administering iodoacetic acid. The follow-up period was 6 weeks. This model mimics the functional changes in patients with RP, with an initial phase of decreased nighttime vision (rod function) and a later phase of decreased daytime vision (cone function).

Model characteristics: Loss of rod cells. It represents a model of retinal damage dominated by rod cells.

Available Support Services

To validate the reliability of the model and test potential therapeutic strategies, highly qualified scientists at Ace Therapeutics evaluate retinal degeneration by methods including, but not limited to:

• Clinical examination

Slit lamp examination.

Fundus mirror photo.

• Retinal morphological and functional assessment

Multifocal ERG(mf-ERG).

Full-field ERG (ff-ERG).

Histological evaluation.

Immunohistochemical analysis.

Ace Therapeutics aims to provide global customers with a powerful tool to explore new therapies for RP and explain therapeutic mechanisms. Our scientists take a hands-on approach, working side-by-side with clients to understand their specific preclinical research requirements. If you are interested in our services or need more detailed information, please feel free to contact us. Our experienced scientists are ready to help you!

References

1. Wang W, Fernandez de Castro J, Vukmanic E, et al. Selective rod degeneration and partial cone inactivation characterize an iodoacetic acid model of Swine retinal degeneration. Invest Ophthalmol Vis Sci. 2011, 52(11):7917-23.
2. Noel JM, Fernandez de Castro JP, Demarco PJ Jr, et al. Iodoacetic acid, but not sodium iodate, creates an inducible swine model of photoreceptor damage. Exp Eye Res. 2012, 97(1):137-47.
3. Scott PA, Kaplan HJ, Sandell JH. Anatomical evidence of photoreceptor degeneration induced by iodoacetic acid in the porcine eye. Exp Eye Res. 2011, 93(4):513-27.

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