Información del artículo
Abstract
Introduction
Dyslexia is a learning disability in which reading (but not any other) impairment is the most prominent symptom. There seems to be a high comorbidity among dyslexia and other learning disabilities, such as SLI, SSD or ADHD.
DevelopmentThe nulear deficit in dyslexia appears to correspond to an impairment in phonological processing. Structural and functional studies in dyslexic readers converge to indicate the presence of malformations in the brain areas corresponding to the reading systems, but also a failure of these systems to function properly during reading. Genes linked (or associated) to dyslexia have been shown to be involved in neuronal migration and axon guidance during the formation of the cortex. In the developing cerebral neocortex of rats, local loss of function of most of these genes not only results in abnormal neuronal migration and neocortical and hippocampal malformations, but also in deficits related to auditory processing and learning. While the structural malformations resemble neuronal migration abnormalities observed in the brains of individuals with developmental dyslexia, processing/learning deficits also resemble deficits described in individuals affected by the disease.
ConclusionsOn the whole, dyslexia seems to be on a continuum with typical reading at different biological levels (genetic, biochemical, physiological, cognitive). Furthermore, certain elements belonging to some of these levels (mainly -some of the-genes linked or associated to the disease, but also -some of the-neuronal structures whose development is regulated by these genes) would simultaneously belong to those of other cognitive abilities, which give rise to diseases of a different nature (i.e. non-dyslexic impairments) when they are impaired
Keywords:
Animal models
Comorbidity
Dyslexia
Neurobiology
Neurogenetics
Resumen
Introducción
La dislexia es un trastorno cognitivo que lleva aparejada una competencia lectora reducida y que suele ser comórbido con otros que tienen como característica distintiva un déficit en la capacidad de aprendizaje y de adquisición de competencias específicas (fundamentalmente, trastorno específico del lenguaje, de los sonidos del habla o por déficit de atención e hiperactividad).
DesarrolloEn el caso de la dislexia, el déficit nuclear parece corresponderse con una disfunción del componente fonológico de la memoria de trabajo verbal. El cerebro de los individuos disléxicos presenta diversos tipos de malformaciones estructurales, así como patrones anómalos de actividad cerebral durante las tareas de lectura y deletreo, que conciernen, entre otras, a las áreas que integran el dispositivo de procesamiento cuya actividad se ha asociado con estas actividades en la población no disléxica. Los genes identificados hasta la fecha cuya mutación parece constituir un componente causal (o un factor de riesgo) significativo en relación con el trastorno codifican proteínas que intervienen en la regulación de la migración de determinados linajes neuronales o del proceso de axonogénesis. La disminución del grado de expresión de los correspondientes genes ortólogos produce en el cerebro de los organismos modelo del trastorno alteraciones estructurales y funcionales semejantes a las observadas en los individuos disléxicos. Dichas alteraciones originan, a su vez, déficit auditivos y cognitivos que recapitulan satisfactoriamente los descritos en dichos individuos.
ConclusionesEn conjunto, resulta plausible la hipótesis de que la dislexia vendría a ser, en diferentes niveles de complejidad biológica (genético, bioquímico, fisiológico, cognitivo), y en mayor o menor grado, un extremo del continuo de desarrollo que representa la capacidad de lectura en la población general; al mismo tiempo, algunos de los elementos que integran estos niveles (en particular —varios de—, los genes relacionados con el trastorno, así como —algunas de— las estructuras neuronales cuyo desarrollo está regulado, en buena medida, por los programas que conforman dichos genes) podrían formar parte simultáneamente de los correspondientes a otras capacidades cognitivas, cuya disfunción da lugar a trastornos de diferente naturaleza clínica.
Palabras clave:
Comorbilidad
Dislexia
Neurobiología
Neurogenética
Modelos animales
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