Scientists link gene to dyslexia
Discovery offers hope for treatment of dyslexia
A gene which is likely to be one of the causes of dyslexia in children has been discovered by researchers at Cardiff University.
They believe the major finding will give researchers a better understanding of what causes the brain disorder which disrupts reading and writing skills.
It is now hoped that follow-up research will also lead to the discovery of treatments which could help children susceptible to dyslexia.
The discovery was made by a team from the Department of Psychological Medicine, Wales College of Medicine.
They carried out analysis of 300 families from Wales and the West of England where at least one child suffered from the disorder.
The research team led by Professor Julie Williams and Professor Michael O'Donovan will now continue their study in order to discover more about the gene called "KIAA0319".
The research will focus on discovering exactly how the gene works within the brain to disrupt reading and writing skills.
Professor Williams said: "This is a major breakthrough and the first study to identify one gene which contributes to susceptibility to the common form of dyslexia. We would like to thank all the parents and children who took part in the study and would extend a call to new volunteers to take part in this important research."
The researchers want to hear from more families with at least one child who has dyslexia.
Professor O'Donovan said: "The finding vindicates our optimism that a disorder as apparently complicated as impaired reading ability can be amenable to molecular genetic dissection." However, he added: "Much more remains to be done before the finding is translated into therapy. To tackle the genetic origins of disorders like dyslexia, both quality of assessment and sample size are crucial. We have the tools to take care of the latter, but we are entirely dependent on the altruism of the public in offering their time and DNA".
Source: Eurekalert & othersLast reviewed: By John M. Grohol, Psy.D. on 21 Feb 2009
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