A team of Yale scientists have come a little closer to decoding the mystery behind dyslexia, after finding the disorder is an issue of genes, not intelligence.

Pediatric researchers at the Yale School of Medicine have linked a gene called DCDC2 on chromosome 6 to dyslexia, a neurological disorder affecting the reading and writing skills of between 10 and 17 percent of the U.S. population. Lead author Jeffrey Gruen, associate professor in the Yale School of Medicine’s Pediatrics Department, said the findings hold tremendous potential in promoting the early detection that is necessary to effectively deal with dyslexia.

“My message to children and adults with dyslexia as well as parents, teachers, principals and policy makers is that we are able to confirm by our studies that dyslexia is genetic,” he said. “Their reading difficulty is by no fault of their own. The difficulty is real.”

Gruen said that by defining the disorder as a genetic disability, future screening tests will be able to identify dyslexic children before they begin school. But he said that unless a proper infrastructure is in place to deal with early testing, the screens will be relatively useless.

“We have early-intervention programs that work,” he said. “It is essential to identify early, because in the U.S., dyslexic kids are mostly missed until middle and high school, by which time they think they can’t perform.”

Gruer’s findings rebuff common misonceptions about dyslexia, said Sally Shaywitz, professor of pediatrics and co-director of the Yale Center for the Study of Learning, Reading and Attention.

“The challenge is that dyslexics are smart people who struggle to read, and reading is a proxy for intelligence,” she said. “So people assume that if you can’t read well, you’re unmotivated or unintelligent.”

Shaywitz said that finding this gene, in addition to the other genes that are known to be linked to dyslexia, will not only lead to early identification but also to more precise approaches to correcting the learning disability earlier on.

University of Colorado, Boulder psychology professor Richard Olson said Gruen’s work is a molecular genetic advancement that has significant potential to help dyslexics.

“It will help us in the long run to identify the kids at risk,” said Olson, who is also the director of the Colorado Learning Disability Research Center. “The more we understand the biology, the more we understand how to treat the disorder and use biological therapy.”

Gruen said dyslexic children have the same capacity for learning as students without any learning disabilities.

“There is no reason that [dyslexic children] shouldn’t be able to achieve the same success as fluent readers and to pursue their passions,” he said. “But for that to happen, we have to make their educational experience a positive one.”

Gruen’s study involved 153 families from Colorado, all with dyslexic children. In 2002 his team verified, using gene linkage analysis, that the location of the dyslexic gene was on the sixth chromosome. Further studies revealed that the DCDC2 gene was deleted in 20 percent of the dyslexic children in the study, which he said is a highly statistically significant number.

DCDC2 appears to be responsible for regulating neuron activity, and successful reading is based on neural connections, Gruen said.

A separate study led by Dr. Juha Kere at the Karolinska Institute in Stockholm, Sweden provided independent confirmation of Gruen’s results in two separate populations, one in Finland and the other in Germany, Gruen said. Kere’s results, which are currently at press, give Gruen’s team’s results the validation they need to proceed with their studies.

The Yale Center for the Study of Learning, Reading and Attention performed a collaborative study on children with dyslexia, and their results showed that 17 percent of children with dyslexia have the same deletion; this was also true of 20 percent of the cases in an adult study performed by the Yale Child Health Research Center, which houses Gruen’s lab.

Gruen’s plans for the future are to further develop his results. He said he must now determine the positive predictive value, or the likelihood that if a person has the gene deletion, he or she will develop dyslexia.