Purchase this article with an account.
David Troilo; Using experimental models to understand emmetropization and inform clinical treatments for myopia control. Journal of Vision 2017;17(15):36-37. doi: 10.1167/17.15.36.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
The increasing prevalence of myopia observed around the world has led to estimates that half of the total population may be affected by 2050. This creates both a significant financial impact because of the cost of care and a serious public health risk because of the known association between myopia and vision-threatening conditions including several retinal pathologies, glaucoma and even cataract. The chances of developing one of these conditions increases with increasing myopia. Fortunately, there are now several evidence-based treatments using lenses or drugs known to reduce significantly the progression of myopia and the increase in axial eye length, which appears to be the principal factor responsible for associated retinal pathologies.
Experimental models of myopia using animals have informed the development of theories regarding the visual control of eye growth and refractive state that form the basis of many of the treatments currently available. Experimental animal models also provide useful paradigms for testing the mechanisms and development of new and existing treatments.
In this presentation, I will summarize some of the studies from my laboratory and others that have informed the current thinking about myopia control treatments. I will present data from several studies using our non-human primate model examining the visual control of eye growth using of novel contact lens designs that provide proof of concept that multifocal lenses can be used to reduce myopia progression. I will also present results from studies examining the use of atropine for control of eye growth, and provide some preliminary data looking at gene expression in the retina during experimentally altered eye growth, which may help provide insights into the control of eye growth and refractive state and identify potential new targets for future pharmacological interventions.
This research was supported by the National Eye Institute (R01 EY-011228), and grants from Johnson & Johnson Vision Care. The author is a consultant for Johnson & Johnson Vision Care.
This PDF is available to Subscribers Only