AI Article Synopsis
- Several copy number variants have been linked to neuropsychiatric disorders and cognitive abilities, with a focus on the 15q11.2(BP1-BP2) deletion that is tied to learning disabilities and brain structure changes.
- This study expands the sample size to explore how the 15q11.2 deletion impacts dyslexia and dyscalculia, revealing it heightens the risk of these conditions and is associated with a smaller left fusiform gyrus.
- Through neuropsychological testing and brain imaging techniques, the research shows that this deletion significantly alters cognitive and neurological processes related to both dyslexia and dyscalculia.
Article Abstract
Several copy number variants have been associated with neuropsychiatric disorders and these variants have been shown to also influence cognitive abilities in carriers unaffected by psychiatric disorders. Previously, we associated the 15q11.2(BP1-BP2) deletion with specific learning disabilities and a larger corpus callosum. Here we investigate, in a much larger sample, the effect of the 15q11.2(BP1-BP2) deletion on cognitive, structural and functional correlates of dyslexia and dyscalculia. We report that the deletion confers greatest risk of the combined phenotype of dyslexia and dyscalculia. We also show that the deletion associates with a smaller left fusiform gyrus. Moreover, tailored functional magnetic resonance imaging experiments using phonological lexical decision and multiplication verification tasks demonstrate altered activation in the left fusiform and the left angular gyri in carriers. Thus, by using convergent evidence from neuropsychological testing, and structural and functional neuroimaging, we show that the 15q11.2(BP1-BP2) deletion affects cognitive, structural and functional correlates of both dyslexia and dyscalculia.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5416713 | PMC |
| http://dx.doi.org/10.1038/tp.2017.77 | DOI Listing |
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