[The molecular bases of dyslexia].
BACKGROUND
The recent identification and cloning of the first genes with a mutation linked to dyslexia is starting to allow researchers to achieve a more precise characterisation of both the disorder itself and the functioning of the neuronal circuits responsible for the ability to read and spell.


METHODS
The dyslexia-related genes that have been characterised to date appear to be involved in controlling the migration of certain neuronal lineages, as well as in regulating axonal growth. Furthermore, there seems to be a satisfactory match between their dysfunction and some of the structural and functional anomalies detected in individuals affected by the disorder. In some cases there has been a positive selection of certain modifications to their sequencing during the recent developmental history of the human kind.


CONCLUSIONS
Molecular analysis of the endophenotypes associated with dyslexia and the search for the alleles that make the individual susceptible to the disorder (apart from the search for the genes that have a direct influence in the disorder, which researchers are beginning identify) will make it possible, some time in the future, to reach a more precise characterisation of the components of the genetic regulation programme that modulates the organisation and activity of the neuronal centres related to the capacity to read. Many of these centres are likely to be common to other programmes governing the development of neuronal circuits linked to linguistic processing and the learning and acquisition of new capacities. It will also make it possible to carry out a more exact assessment of how this programme is affected by the molecular and ontogenetic context, as well as by the environment in which the individual grows up.
Benítez-Burraco
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Departamento de Filología Española, Universidad de Oviedo, Facultad de Filología, Oviedo, Asturias, Spain. abenitez@us.es
D002540:Cerebral Cortex / Q000033:anatomy & histology / Q000502:physiology; D015897:Comorbidity; D004410:Dyslexia / Q000235:genetics / Q000503:physiopathology; D006801:Humans; D007806:Language Disorders / Q000503:physiopathology; D008967:Molecular Biology; D010641:Phenotype