title: [Neurobiology and neurogenetics of dyslexia].
abstract: BACKGROUND
  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.
  
  
  METHODS
  The 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.
  
  
  CONCLUSIONS
  On 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.
authors.affiliation: Departamento de Filología Española, Área de Lingüística, Facultad de Filología, Universidad de Oviedo, Oviedo, España. abenitez@us.es
authors.forename: A
authors.initials: A
authors.lastname: Benítez-Burraco
mesh_terms: D000818:Animals; D001921:Brain / Q000002:abnormalities / Q000033:anatomy & histology / Q000503:physiopathology; D015897:Comorbidity; D003598:Cytoskeletal Proteins; D004410:Dyslexia / Q000453:epidemiology / Q000235:genetics / Q000503:physiopathology; D006801:Humans; D007859:Learning Disabilities / Q000453:epidemiology / Q000503:physiopathology; D009419:Nerve Tissue Proteins / Q000235:genetics; D009446:Neurobiology; D009687:Nuclear Proteins / Q000235:genetics; D020033:Protein Isoforms / Q000235:genetics; D011932:Reading
chemical_list: D003598:Cytoskeletal Proteins; C478878:DNAAF4 protein, human; D009419:Nerve Tissue Proteins; D009687:Nuclear Proteins; D020033:Protein Isoforms