GRIN2B mediates susceptibility to intelligence quotient and cognitive impairments in developmental dyslexia. (February 2015)

• Record Type: Journal Article
• Authors: Mascheretti, Sara; Facoetti, Andrea; Giorda, Roberto; Beri, Silvana; Riva, Valentina; Trezzi, Vittoria; Cellino, Maria R.; Marino, Cecilia
• Is Part Of: Psychiatric genetics. Volume 25:Number 1(2015:Feb.)
• Publication Date: 2015-02
• Subjects: Mental illness -- Genetic aspects -- Periodicals; Periodicals; 616.89042
• DOI: 10.1097/YPG.0000000000000068
• Languages: English
• ISSNs: 0955-8829

Abstract

<abstract> <title> <x xml:space="preserve">Abstract</x> </title> <sec> <title>Objective(s)</title> <p>Developmental dyslexia (DD) is a complex heritable condition associated with impairments in multiple neurocognitive domains. Substantial heritability has been reported for DD and related phenotypes, and candidate genes have been identified. Recently, a candidate gene for human cognitive processes, that is, <italic>GRIN2B</italic>, has been found to be associated significantly with working memory in a German DD sample. In this study, we explored the contribution of six <italic>GRIN2B</italic> markers to DD and key DD-related phenotypes by association analyses in a sample of Italian nuclear families. Moreover, we assessed potential gene-by-environment interactions on DD-related phenotypes.</p> </sec> <sec> <title>Materials and methods</title> <p>We carried out a family-based association study to determine whether the <italic>GRIN2B</italic> gene influences both DD as a categorical trait and its related cognitive traits in a large cohort of 466 Italian nuclear families ascertained through a proband affected by DD. Moreover, we tested the role of the selected <italic>GRIN2B</italic> markers and a set of commonly described environmental moderators using a test for G×E interaction in sib pair-based association analysis of quantitative traits in 178 Italian nuclear families.</p> </sec> <sec> <title>Results</title> <p>Evidence for a significant association was found with the categorical diagnosis of DD, performance intelligence quotient, phonemic elision, and auditory short-term memory. No significant gene-by-environment effects were found.</p> </sec> <sec> <title>Conclusion</title> <p>Our results add further evidence in support of <italic>GRIN2B</italic> contributing toward DD and deficits in DD. More specifically, our data support the view that <italic>GRIN2B</italic> influences DD as a categorical trait and its related quantitative phenotypes, thus shedding further light on the etiologic basis and the phenotypic complexity of this disorder.</p> </sec> </abstract>