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The Pathogenesis of Autism

Autism is well known as a complex developmental disorder with a seemingly confusing and uncertain pathogenesis. The definitive mechanisms that promote autism are poorly understood and mostly unknown, yet available theories do appear to focus on the disruption of normal cerebral development and its s...

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Detalles Bibliográficos
Autor principal: Watts, Timothy John
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Libertas Academica 2008
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160002/
https://www.ncbi.nlm.nih.gov/pubmed/21876658
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author Watts, Timothy John
author_facet Watts, Timothy John
author_sort Watts, Timothy John
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description Autism is well known as a complex developmental disorder with a seemingly confusing and uncertain pathogenesis. The definitive mechanisms that promote autism are poorly understood and mostly unknown, yet available theories do appear to focus on the disruption of normal cerebral development and its subsequent implications on the functional brain unit. This mini-review aims solely to discuss and evaluate the most prominent current theories regarding the pathogenesis of autism. The main conclusion is that although there is not a clear pathway of mechanisms directed towards a simple pathogenesis and an established link to autism on the symptomatic level; there are however several important theories (neural connectivity, neural migration, excitatory-inhibitory neural activity, dendritic morphology, neuroimmune; calcium signalling and mirror neurone) which appear to offer an explanation to how autism develops. It seems probable that autism’s neurodevelopmental defect is ‘multi-domain’ in origin (rather than a single anomaly) and is hence distributed across numerous levels of study (genetic, immunopathogenic, etc.). A more definitive understanding of the pathogenesis could facilitate the development of better treatments for this complex psychiatric disorder.
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spelling pubmed-31600022011-08-29 The Pathogenesis of Autism Watts, Timothy John Clin Med Pathol Review Autism is well known as a complex developmental disorder with a seemingly confusing and uncertain pathogenesis. The definitive mechanisms that promote autism are poorly understood and mostly unknown, yet available theories do appear to focus on the disruption of normal cerebral development and its subsequent implications on the functional brain unit. This mini-review aims solely to discuss and evaluate the most prominent current theories regarding the pathogenesis of autism. The main conclusion is that although there is not a clear pathway of mechanisms directed towards a simple pathogenesis and an established link to autism on the symptomatic level; there are however several important theories (neural connectivity, neural migration, excitatory-inhibitory neural activity, dendritic morphology, neuroimmune; calcium signalling and mirror neurone) which appear to offer an explanation to how autism develops. It seems probable that autism’s neurodevelopmental defect is ‘multi-domain’ in origin (rather than a single anomaly) and is hence distributed across numerous levels of study (genetic, immunopathogenic, etc.). A more definitive understanding of the pathogenesis could facilitate the development of better treatments for this complex psychiatric disorder. Libertas Academica 2008-09-18 /pmc/articles/PMC3160002/ /pubmed/21876658 Text en © the author(s), publisher and licensee Libertas Academica Ltd. http://creativecommons.org/licenses/by/3.0 This article is an open-access article distributed under the terms and conditions of the Creative Commons Attribution license http://creativecommons.org/licenses/by/3.0/).
spellingShingle Review
Watts, Timothy John
The Pathogenesis of Autism
title The Pathogenesis of Autism
title_full The Pathogenesis of Autism
title_fullStr The Pathogenesis of Autism
title_full_unstemmed The Pathogenesis of Autism
title_short The Pathogenesis of Autism
title_sort pathogenesis of autism
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3160002/
https://www.ncbi.nlm.nih.gov/pubmed/21876658
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