U.S. researchers link gene to dyslexia

Nov 21, 2005, 15:01 GMT

New York - U.S. researchers believe they have made more progress in understanding the genetic roots of dyslexia, a learning disability that makes reading and spelling difficult.

Dyslexia is the most common neurological condition that hampers learning regardless of intelligence, educational background or the amount of money a family has. An estimated 10 to 17 per cent of the U.S. population is dyslexic.

A team of researchers at Yale University in New Haven, Connecticut, reported in the November issue of the Proceedings of the National Academy of Sciences that there is a link between the gene DCDC2 on chromosome 6 and dyslexia.

In 2002, the team verified that the location of the dyslexic gene was on the sixth chromosome. Led by Jeffrey Gruen, associate professor in Yale's paediatrics department, the team studied 153 families, all with dyslexic children for their most recent study.

The DCDC2 gene was missing several DNA building blocks in the dyslexic children studied. In 20 per cent of them, it was deleted, which Gruen said was statistically significant.

The exact function of DCDC2 is not known. But it appears to be responsible for regulating neuron activity, and successful reading is based on neural connections, Gruen said.

A separate study at the Karolinska Institute in Stockholm, Sweden confirmed the Yale study's results in two separate populations, one in Finland and the other in Germany, Gruen said.

Gruen said his study confirmed that dyslexia is genetic. Early screening tests in future will be able to identify dyslexic children before they begin school, which Gruen said was necessary to effectively prepare a dyslexic child for the classroom.

Gruen's team conducted animal studies in which they suppressed the effects of DCDC2 and discovered that without it, nerve cells in the brain laid down shorter return paths.

Further studies in humans showed that the gene is active in dyslexics when they read fluently from a book. The researchers concluded that the reading disorder is due to a malfunction of the gene and not its complete failure.

In 2003, Swedish researchers ago found the gene DYXC1 in 20 Finnish families with dyslexia. It was either interrupted or too short in the family members with the disorder and produced a faulty protein found primarily in the brain.