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New dyslexia gene identified
posted 2005-10-30 22:27:13 latest updated 2006-05-02 14:38:39
neuroscience A gene involved in the development of the brain has now been linked to dyslexia by a team of scientists from Karolinska Institutet and Finland.

Dyslexia is a condition which involves difficulties reading and writing despite a normal intelligence and education, and one that affects 3-10 per cent of the population. The causes are thought to be partly genetic, and several possible candidate genes have been proposed. However, the biochemical mechanisms behind dyslexia remain unclear. Now, scientists at Karolinska Institutet, working alongside a team of researchers from Finland, have identified a new gene, called ROBO1, associated with dyslexia. The results of the study, which are to be published in the scientific journal PLoS Genetics, show that the gene was mutated in one dyslexic individual and had a lower expression in a group of others. ROBO1, which is localised on chromosome three, is involved in the development of neural tracts between the cerebral hemispheres. This is the first time that such a specific biochemical and developmental biological mechanism has been linked with dyslexia.

“Disrupted communication between the cerebral hemispheres could explain why an individual with a dysfunction in this gene can develop dyslexia, but we still do not know exactly how ROBO1 affects reading and writing skills,” says Professor Juha Kere of the Department of Bioscience at Novum at Karolinska Institutet’s Centre for Biotechnology.

The research group, which identified the first dyslexia-linked gene two years ago, will now go on to try to discover exactly which effects of ROBO1 are the most critical.

Published in the Public Library of Science Genetics: The Axon Guidance Receptor Gene ROBO1 is a Candidate Gene for Developmental Dyslexia. Katariina Hannula-Jouppi, Nina Kaminen-Ahola, Mikko Taipale, Ranja Eklund, Jaana Nopola-Hemmi, Helena Kääriäinen, Juha Kere. PLoS Genetics 2005 1 (4): e50

Source:
Karolinska Institutet Sabina Bossi Information and Public Relations Office


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