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Language Impairments in ASD Resulting from a Failed Domestication of the Human Brain
Autism spectrum disorders (ASD) are pervasive neurodevelopmental disorders entailing social and cognitive deficits, including marked problems with language. Numerous genes have been associated with ASD, but it is unclear how language deficits arise from gene mutation or dysregulation. It is also unc...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2016
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5002430/ https://www.ncbi.nlm.nih.gov/pubmed/27621700 http://dx.doi.org/10.3389/fnins.2016.00373 |
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author | Benítez-Burraco, Antonio Lattanzi, Wanda Murphy, Elliot |
author_facet | Benítez-Burraco, Antonio Lattanzi, Wanda Murphy, Elliot |
author_sort | Benítez-Burraco, Antonio |
collection | PubMed |
description | Autism spectrum disorders (ASD) are pervasive neurodevelopmental disorders entailing social and cognitive deficits, including marked problems with language. Numerous genes have been associated with ASD, but it is unclear how language deficits arise from gene mutation or dysregulation. It is also unclear why ASD shows such high prevalence within human populations. Interestingly, the emergence of a modern faculty of language has been hypothesized to be linked to changes in the human brain/skull, but also to the process of self-domestication of the human species. It is our intention to show that people with ASD exhibit less marked domesticated traits at the morphological, physiological, and behavioral levels. We also discuss many ASD candidates represented among the genes known to be involved in the “domestication syndrome” (the constellation of traits exhibited by domesticated mammals, which seemingly results from the hypofunction of the neural crest) and among the set of genes involved in language function closely connected to them. Moreover, many of these genes show altered expression profiles in the brain of autists. In addition, some candidates for domestication and language-readiness show the same expression profile in people with ASD and chimps in different brain areas involved in language processing. Similarities regarding the brain oscillatory behavior of these areas can be expected too. We conclude that ASD may represent an abnormal ontogenetic itinerary for the human faculty of language resulting in part from changes in genes important for the “domestication syndrome” and, ultimately, from the normal functioning of the neural crest. |
format | Online Article Text |
id | pubmed-5002430 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2016 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-50024302016-09-12 Language Impairments in ASD Resulting from a Failed Domestication of the Human Brain Benítez-Burraco, Antonio Lattanzi, Wanda Murphy, Elliot Front Neurosci Neuroscience Autism spectrum disorders (ASD) are pervasive neurodevelopmental disorders entailing social and cognitive deficits, including marked problems with language. Numerous genes have been associated with ASD, but it is unclear how language deficits arise from gene mutation or dysregulation. It is also unclear why ASD shows such high prevalence within human populations. Interestingly, the emergence of a modern faculty of language has been hypothesized to be linked to changes in the human brain/skull, but also to the process of self-domestication of the human species. It is our intention to show that people with ASD exhibit less marked domesticated traits at the morphological, physiological, and behavioral levels. We also discuss many ASD candidates represented among the genes known to be involved in the “domestication syndrome” (the constellation of traits exhibited by domesticated mammals, which seemingly results from the hypofunction of the neural crest) and among the set of genes involved in language function closely connected to them. Moreover, many of these genes show altered expression profiles in the brain of autists. In addition, some candidates for domestication and language-readiness show the same expression profile in people with ASD and chimps in different brain areas involved in language processing. Similarities regarding the brain oscillatory behavior of these areas can be expected too. We conclude that ASD may represent an abnormal ontogenetic itinerary for the human faculty of language resulting in part from changes in genes important for the “domestication syndrome” and, ultimately, from the normal functioning of the neural crest. Frontiers Media S.A. 2016-08-29 /pmc/articles/PMC5002430/ /pubmed/27621700 http://dx.doi.org/10.3389/fnins.2016.00373 Text en Copyright © 2016 Benítez-Burraco, Lattanzi and Murphy. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Benítez-Burraco, Antonio Lattanzi, Wanda Murphy, Elliot Language Impairments in ASD Resulting from a Failed Domestication of the Human Brain |
title | Language Impairments in ASD Resulting from a Failed Domestication of the Human Brain |
title_full | Language Impairments in ASD Resulting from a Failed Domestication of the Human Brain |
title_fullStr | Language Impairments in ASD Resulting from a Failed Domestication of the Human Brain |
title_full_unstemmed | Language Impairments in ASD Resulting from a Failed Domestication of the Human Brain |
title_short | Language Impairments in ASD Resulting from a Failed Domestication of the Human Brain |
title_sort | language impairments in asd resulting from a failed domestication of the human brain |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5002430/ https://www.ncbi.nlm.nih.gov/pubmed/27621700 http://dx.doi.org/10.3389/fnins.2016.00373 |
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