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The genetic relationship between handedness and neurodevelopmental disorders()
Handedness and brain asymmetry have been linked to neurodevelopmental disorders such as dyslexia and schizophrenia. The genetic nature of this correlation is not understood. Recent discoveries have shown handedness is determined in part by the biological pathways that establish left/right (LR) body...
Autores principales: | , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier Science Ltd
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969300/ https://www.ncbi.nlm.nih.gov/pubmed/24275328 http://dx.doi.org/10.1016/j.molmed.2013.10.008 |
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author | Brandler, William M. Paracchini, Silvia |
author_facet | Brandler, William M. Paracchini, Silvia |
author_sort | Brandler, William M. |
collection | PubMed |
description | Handedness and brain asymmetry have been linked to neurodevelopmental disorders such as dyslexia and schizophrenia. The genetic nature of this correlation is not understood. Recent discoveries have shown handedness is determined in part by the biological pathways that establish left/right (LR) body asymmetry during development. Cilia play a key role in this process, and candidate genes for dyslexia have also been recently shown to be involved in cilia formation. Defective cilia result not only in LR body asymmetry phenotypes but also brain midline phenotypes such as an absent corpus callosum. These findings suggest that the mechanisms for establishing LR asymmetry in the body are reused for brain midline development, which in turn influences traits such as handedness and reading ability. |
format | Online Article Text |
id | pubmed-3969300 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Elsevier Science Ltd |
record_format | MEDLINE/PubMed |
spelling | pubmed-39693002014-03-31 The genetic relationship between handedness and neurodevelopmental disorders() Brandler, William M. Paracchini, Silvia Trends Mol Med Review Handedness and brain asymmetry have been linked to neurodevelopmental disorders such as dyslexia and schizophrenia. The genetic nature of this correlation is not understood. Recent discoveries have shown handedness is determined in part by the biological pathways that establish left/right (LR) body asymmetry during development. Cilia play a key role in this process, and candidate genes for dyslexia have also been recently shown to be involved in cilia formation. Defective cilia result not only in LR body asymmetry phenotypes but also brain midline phenotypes such as an absent corpus callosum. These findings suggest that the mechanisms for establishing LR asymmetry in the body are reused for brain midline development, which in turn influences traits such as handedness and reading ability. Elsevier Science Ltd 2014-02 /pmc/articles/PMC3969300/ /pubmed/24275328 http://dx.doi.org/10.1016/j.molmed.2013.10.008 Text en © 2013 The Authors http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Review Brandler, William M. Paracchini, Silvia The genetic relationship between handedness and neurodevelopmental disorders() |
title | The genetic relationship between handedness and neurodevelopmental disorders() |
title_full | The genetic relationship between handedness and neurodevelopmental disorders() |
title_fullStr | The genetic relationship between handedness and neurodevelopmental disorders() |
title_full_unstemmed | The genetic relationship between handedness and neurodevelopmental disorders() |
title_short | The genetic relationship between handedness and neurodevelopmental disorders() |
title_sort | genetic relationship between handedness and neurodevelopmental disorders() |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3969300/ https://www.ncbi.nlm.nih.gov/pubmed/24275328 http://dx.doi.org/10.1016/j.molmed.2013.10.008 |
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