A study of gene changes in the retina has brought closer the day when drugs may be able to stop or reverse the development of nearsightedness, or myopia, a common condition expected to affect half the world's population by 2050.

Dr. Andrei Tkatchenko, of Columbia University in New York City, NY, led a study that found that, for the most part, the development of myopia and hyperopia, or farsightedness, involves different genes and cell signaling pathways.

Prior to this, specialists typically assumed that "opposite changes in the same genes and pathways" determined how the two eye conditions developed after birth, note the authors in a paper on their work that now features in the journal PLOS Biology.

However, their findings contravene the traditional view: they offer an alternative understanding of myopia and "a framework for the development of new antimyopia drugs."

Myopia is on the rise

Myopia is a condition in which the eye focuses images in front of the retina, instead of exactly on it.

The World Health Organization (WHO) says that myopia and high myopia prevalence is rising at "an alarming rate" worldwide, with accompanying increases in risks of serious eye conditions, such as cataract, retinal damage, and glaucoma.

Dr. Tkatchenko and team cite research that suggests that by 2050, the number of people affected by myopia will reach 4.8 billion, or around half of the global population, and that the WHO ranks it among the world's "five priority health conditions."

Myopia impairs distance vision but not near vision; it usually develops because the eye grows too long.

Those with hyperopia experience the opposite: their eye is too short, causing it to focus images behind the retina.

This generally results in distant objects being clearer than near ones, but in some cases, it can result in everything looking blurred.

The molecular mechanisms were unclear

There is evidence that both genes and environmental factors, such as spending less time outdoors and more time indoors reading and using computers, can increase the risk of myopia. Before this study, however, it was not clear what the underlying molecular mechanisms were.

One way to observe the biological development of myopia or hyperopia is by altering the focal length of the eye in laboratory animals. Specialists can do this by placing a lens in front of the eye for several weeks.

Depending on the type of lens, the exposure causes the eye to develop to a length that is either too long or too short.

The scientists used this method in marmosets to study the development of myopia and hyperopia. They placed a lens in front of only one eye for up to 5 weeks and let the other eye develop normally for comparison.

'Largely distinct pathways'

Upon examining each animal's two retinas after the exposure time, the team revealed differences in gene expression between the exposed and the nonexposed eye.

A comparison between those that had an eye that developed myopia and those that developed hyperopia, however, showed that the conditions were the result of "activation or suppression of largely distinct pathways."

The researchers also found that 29 of the genes that changed expression were in the same chromosome regions that large genetic studies have linked to myopia in humans.

"Identification of these pathways provides a framework for the identification of new drug targets and for the development of more effective treatment options for myopia."

–Dr. Andrei Tkatchenko