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ERIC Number: EJ860513
Record Type: Journal
Publication Date: 2007
Pages: 10
Abstractor: As Provided
Reference Count: 116
ISBN: N/A
ISSN: ISSN-1080-4013
Genes, Language Development, and Language Disorders
Smith, Shelley D.
Mental Retardation and Developmental Disabilities Research Reviews, v13 n1 p96-105 2007
Genetic factors are important contributors to language and learning disorders, and discovery of the underlying genes can help delineate the basic neurological pathways that are involved. This information, in turn, can help define disorders and their perceptual and processing deficits. Initial molecular genetic studies of dyslexia, for example, appear to converge on defects in neuronal and axonal migration. Further study of individuals with abnormalities of these genes may lead to the recognition of characteristic cognitive deficits attributable to the neurological dysfunction. Such abnormalities may affect other disorders as well, and studies of co-morbidity of dyslexia with attention deficit disorder and speech sound disorder are helping to define the scope of these genes and show the etiological and cognitive commonalities between these conditions. The genetic contributions to specific language impairment (SLI) are not as well defined at this time, but similar molecular approaches are being applied to identify genes that influence SLI and comorbid disorders. While there is co-morbidity of SLI with dyslexia, it appears that most of the common genetic effects may be with the language characteristics of autism spectrum disorders rather than with dyslexia and related disorders. Identification of these genes and their neurological and cognitive effects should lay out a functional network of interacting genes and pathways that subserve language development. Understanding these processes can form the basis for refined procedures for diagnosis and treatment. (Contains 2 tables.)
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Publication Type: Journal Articles; Reports - Research
Education Level: N/A
Audience: N/A
Language: English
Sponsor: N/A
Authoring Institution: N/A