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What causes dyslexia? The answer may lie in the eyes


Scientists might have found the cause behind this common learning disability.

Despite the fact that between 5 and 10 percent of the population experiences dyslexia, very little is known about the causes of this condition. Some evidence has shown that people with dyslexia rely more heavily on one hemisphere of the brain than the other, but no exact cause has been established. But new research out of the University of Rennes may indicate an exciting new link between dyslexia and light receptors in the eyes.

Dyslexia is a learning difficulty that affects reading, writing, and spelling. This new research shows that people with dyslexia have a different pattern of cone cells, the cells in the eyes responsible for red, blue, and green light. In the majority of the population, the patterns in these cells are asymmetrical, which means light is not absorbed the same way in each eye. This ultimately causes the person to develop a “dominant” eye whose reception of light is favored over the non-dominant eye.

However, people with dyslexia don’t appear to have asymmetric arrangements; rather, they have symmetrical ones. This causes their brain to process some images as mirrored. For example, “b” and “d” would appear to be the same. Because the patterns of cone cells are the same in both eyes, the brain can’t distinguish between which reception of light is more accurate.

The scientists also discovered that invisible flashing light from an LED lamp helped erase one mirror image, allowing the individual with dyslexia to see the letters properly. However, the team was unable to distinguish whether these symmetrical patterns were the direct cause of dyslexia or the result of an underlying neurological issue.

Either way, these advances do not mean the end of dyslexia, but they are a great step moving forward! These discoveries could mean new interventions for young people and will hopefully lead to new ways to help those with learning difficulties achieve their full potential.

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