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.

Benitez-burraco, A., Lattanzi, W., Murphy, E., Language impairments in asd resulting from a failed domestication of the human brain, <<FRONTIERS IN NEUROSCIENCE>>, 2016; 10 (AUG): 373-395. [doi:10.3389/fnins.2016.00373] [http://hdl.handle.net/10807/98486]

Language impairments in asd resulting from a failed domestication of the human brain

Benitez-Burraco, Antonio
Primo
;
Lattanzi, Wanda
Secondo
;
2016

Abstract

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.
Inglese
Benitez-burraco, A., Lattanzi, W., Murphy, E., Language impairments in asd resulting from a failed domestication of the human brain, <<FRONTIERS IN NEUROSCIENCE>>, 2016; 10 (AUG): 373-395. [doi:10.3389/fnins.2016.00373] [http://hdl.handle.net/10807/98486]
File in questo prodotto:
File Dimensione Formato  
2016_Language impairment ASD.pdf

accesso aperto

Tipologia file ?: Versione Editoriale (PDF)
Licenza: Creative commons
Dimensione 2.66 MB
Formato Adobe PDF
2.66 MB Adobe PDF Visualizza/Apri

I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.

Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/10807/98486
Citazioni
  • ???jsp.display-item.citation.pmc??? 14
  • Scopus 39
  • ???jsp.display-item.citation.isi??? 35
social impact