Neurobiology of infantile autism
Autor(a) principal: | |
---|---|
Data de Publicação: | 2021 |
Outros Autores: | |
Tipo de documento: | Artigo |
Idioma: | por |
Título da fonte: | Research, Society and Development |
Texto Completo: | https://rsdjournal.org/index.php/rsd/article/view/11495 |
Resumo: | Objective: to discuss the neurobiological characteristics of Autism Spectrum Disorder (ASD) in children. Methodology: a narrative review was conducted based on articles from the last 10 years (2010-2020) published on the databases PsycINFO, Medline, PubMed, SciELO, LILACS and Periódicos CAPES. The descriptors used are “Infantile Autism”, “Autism Disorder”, “Childhood”, “Vital Cycle”, “Child Neurodevelopment”, “Neurobiology”, “Neuroscience”, “Neuroanatomy”, “Autism Spectrum Disorder” and the Boolean “AND”. The material was entirely read, categorized, and subsequently, critically analyzed. Results and discussion: among ASD individuals there is a decrease in connectivity between the medial prefrontal cortex and the posterior cingulate cortex; this decrease is related to a reduced social function when compared to healthy children. Similar alteration was found regarding the frontoparietal network which related to the repetitive behaviors observed in the disorder. There also is a hypothesis concerning cerebellar dysfunction and more specifically, that the Tuberous Sclerosis Complex 1 (TSC 1) deletion – gene that encodes the hamartin protein – in the Purkinje cells reflects on the social and behavioral deficits among ASD individuals. Furthermore, it is suggested that the disorder phenotype is associated with a disturbance in the networks that connect the cerebellum to the medial prefrontal cortex also due to a higher activation in the last region. Conclusion: there still is no satisfactory and pathognomonic conclusion regarding the neurobiology of ASD in children. The most common neurofunctional alterations in ASD are related to cerebellar networks and Purkinje cells. |
id |
UNIFEI_7b9ccd004eacbc8fb7ae5d071e1379df |
---|---|
oai_identifier_str |
oai:ojs.pkp.sfu.ca:article/11495 |
network_acronym_str |
UNIFEI |
network_name_str |
Research, Society and Development |
repository_id_str |
|
spelling |
Neurobiology of infantile autism Neurobiología del autismo infantil Neurobiologia do autismo infantilNeurobiologyAutistic disorderNeurodevelopmental disordersAutism spectrum disorder.NeurobiologíaTranstorno autísticoTrastornos del neurodesarrolloTrastorno del espectro autista.NeurobiologiaTranstorno autísticoTranstornos do neurodesenvolvimentoTranstorno do espectro autista. Objective: to discuss the neurobiological characteristics of Autism Spectrum Disorder (ASD) in children. Methodology: a narrative review was conducted based on articles from the last 10 years (2010-2020) published on the databases PsycINFO, Medline, PubMed, SciELO, LILACS and Periódicos CAPES. The descriptors used are “Infantile Autism”, “Autism Disorder”, “Childhood”, “Vital Cycle”, “Child Neurodevelopment”, “Neurobiology”, “Neuroscience”, “Neuroanatomy”, “Autism Spectrum Disorder” and the Boolean “AND”. The material was entirely read, categorized, and subsequently, critically analyzed. Results and discussion: among ASD individuals there is a decrease in connectivity between the medial prefrontal cortex and the posterior cingulate cortex; this decrease is related to a reduced social function when compared to healthy children. Similar alteration was found regarding the frontoparietal network which related to the repetitive behaviors observed in the disorder. There also is a hypothesis concerning cerebellar dysfunction and more specifically, that the Tuberous Sclerosis Complex 1 (TSC 1) deletion – gene that encodes the hamartin protein – in the Purkinje cells reflects on the social and behavioral deficits among ASD individuals. Furthermore, it is suggested that the disorder phenotype is associated with a disturbance in the networks that connect the cerebellum to the medial prefrontal cortex also due to a higher activation in the last region. Conclusion: there still is no satisfactory and pathognomonic conclusion regarding the neurobiology of ASD in children. The most common neurofunctional alterations in ASD are related to cerebellar networks and Purkinje cells.Objetivo: discutir las características neurobiológicas del Trastorno del Espectro Autista (TEA) en niños. Metodología: se realizó una revisión narrativa con artículos de los últimos 10 años (2010-2020), en las bases de datos PsycINFO, Medline, PubMed, SciELO, LILACS y CAPES. Se utilizaron los descriptores "Autismo infantil", "Trastorno autista", "Infancia", "Ciclo de vida", "Neurodesarrollo infantil", "Neurobiología", "Neurociencia", "Neuroanatomía", "Neurofisiología", “Trastorno del Espectro Autista” y el booleano "Y". Todos estos materiales fueron leídos íntegramente, categorizados y analizados críticamente. Resultados y discusión: en individuos con TEA, hay una disminución en la conectividad entre la corteza prefrontal medial y la corteza cingulada posterior; esta disminución está relacionada con una función social más baja en comparación con los niños normales. Se encontró un cambio similar con relación a la red frontoparietal, en relación con las conductas repetitivas observadas en el trastorno. También existe la hipótesis relacionada con una disfunción cerebelosa y, más específicamente, que la deleción de Proteína 1 del Complejo de la Esclerosis Tuberosa (TSC1), un gen que codifica la proteína hamartina, en las células de Purkinje, refleja los déficits sociales y del comportamiento en los individuos con TEA. Además, se sugiere que el fenotipo del trastorno se asocia con una alteración en los circuitos que conectan el cerebelo con la corteza prefrontal medial y también con una mayor activación de esta última región. Conclusión: aún no existe una conclusión satisfactoria y patognomónica sobre neurobiología del TEA en niños; los cambios neurofuncionales más comunes están relacionados con las redes cerebelosas y las células de Purkinje.Objetivo: discutir as características neurobiológicas do Transtorno do Espectro Autista (TEA) em crianças. Metodologia: foi realizada uma revisão narrativa com artigos dos últimos 10 anos (2010-2020), nas bases de dados PsycINFO, Medline, PubMed, SciELO, LILACS e Periódicos CAPES. Utilizaram-se como descritores “Autismo Infantil”, “Transtorno Autista”, “Infância”, “Ciclo Vital”, “Neurodesenvolvimento Infantil”, “Neurobiologia”, “Neurociências”, “Neuroanatomia”, “Neurofisiologia”, “Transtorno do Espectro Autista” e o Booleano “AND”. Todos estes materiais foram lidos na íntegra, categorizados e, posteriormente, analisados criticamente. Resultados e discussão: em indivíduos com TEA, há uma diminuição da conectividade entre o córtex pré-frontal medial e o córtex cingulado posterior; esta diminuição está relacionada a uma função social inferior quando comparada com crianças normais. Alteração semelhante foi encontrada em relação à rede frontoparietal relacionando-se aos comportamentos repetitivos observados no transtorno. Há, também, a hipótese relacionada a uma disfunção cerebelar e, mais especificamente, que a deleção da Proteína 1 do Complexo Esclerose Tuberosa (TSC1) – gene que codifica a proteína hamartina – nas células de Purkinje, reflita nos déficits sociais e comportamentais em indivíduos com TEA. Além disso, é sugerido que o fenótipo do transtorno esteja associado a uma perturbação nos circuitos que conectam o cerebelo ao córtex pré-frontal medial e, também, a uma maior ativação desta última região. Conclusão: ainda não se tem uma conclusão satisfatória e patognomônica da neurobiologia do TEA em crianças; as alterações neurofuncionais mais comuns no TEA estão relacionadas às redes cerebelares e às Células de Purkinje.Research, Society and Development2021-01-04info:eu-repo/semantics/articleinfo:eu-repo/semantics/publishedVersionapplication/pdfhttps://rsdjournal.org/index.php/rsd/article/view/1149510.33448/rsd-v10i1.11495Research, Society and Development; Vol. 10 No. 1; e11910111495Research, Society and Development; Vol. 10 Núm. 1; e11910111495Research, Society and Development; v. 10 n. 1; e119101114952525-3409reponame:Research, Society and Developmentinstname:Universidade Federal de Itajubá (UNIFEI)instacron:UNIFEIporhttps://rsdjournal.org/index.php/rsd/article/view/11495/10316Copyright (c) 2021 Cecília Rezende de Almeida Oliveira; José Carlos Souzahttps://creativecommons.org/licenses/by/4.0info:eu-repo/semantics/openAccessOliveira, Cecília Rezende de Almeida Souza, José Carlos 2021-02-20T21:19:23Zoai:ojs.pkp.sfu.ca:article/11495Revistahttps://rsdjournal.org/index.php/rsd/indexPUBhttps://rsdjournal.org/index.php/rsd/oairsd.articles@gmail.com2525-34092525-3409opendoar:2024-01-17T09:33:18.435101Research, Society and Development - Universidade Federal de Itajubá (UNIFEI)false |
dc.title.none.fl_str_mv |
Neurobiology of infantile autism Neurobiología del autismo infantil Neurobiologia do autismo infantil |
title |
Neurobiology of infantile autism |
spellingShingle |
Neurobiology of infantile autism Oliveira, Cecília Rezende de Almeida Neurobiology Autistic disorder Neurodevelopmental disorders Autism spectrum disorder. Neurobiología Transtorno autístico Trastornos del neurodesarrollo Trastorno del espectro autista. Neurobiologia Transtorno autístico Transtornos do neurodesenvolvimento Transtorno do espectro autista. |
title_short |
Neurobiology of infantile autism |
title_full |
Neurobiology of infantile autism |
title_fullStr |
Neurobiology of infantile autism |
title_full_unstemmed |
Neurobiology of infantile autism |
title_sort |
Neurobiology of infantile autism |
author |
Oliveira, Cecília Rezende de Almeida |
author_facet |
Oliveira, Cecília Rezende de Almeida Souza, José Carlos |
author_role |
author |
author2 |
Souza, José Carlos |
author2_role |
author |
dc.contributor.author.fl_str_mv |
Oliveira, Cecília Rezende de Almeida Souza, José Carlos |
dc.subject.por.fl_str_mv |
Neurobiology Autistic disorder Neurodevelopmental disorders Autism spectrum disorder. Neurobiología Transtorno autístico Trastornos del neurodesarrollo Trastorno del espectro autista. Neurobiologia Transtorno autístico Transtornos do neurodesenvolvimento Transtorno do espectro autista. |
topic |
Neurobiology Autistic disorder Neurodevelopmental disorders Autism spectrum disorder. Neurobiología Transtorno autístico Trastornos del neurodesarrollo Trastorno del espectro autista. Neurobiologia Transtorno autístico Transtornos do neurodesenvolvimento Transtorno do espectro autista. |
description |
Objective: to discuss the neurobiological characteristics of Autism Spectrum Disorder (ASD) in children. Methodology: a narrative review was conducted based on articles from the last 10 years (2010-2020) published on the databases PsycINFO, Medline, PubMed, SciELO, LILACS and Periódicos CAPES. The descriptors used are “Infantile Autism”, “Autism Disorder”, “Childhood”, “Vital Cycle”, “Child Neurodevelopment”, “Neurobiology”, “Neuroscience”, “Neuroanatomy”, “Autism Spectrum Disorder” and the Boolean “AND”. The material was entirely read, categorized, and subsequently, critically analyzed. Results and discussion: among ASD individuals there is a decrease in connectivity between the medial prefrontal cortex and the posterior cingulate cortex; this decrease is related to a reduced social function when compared to healthy children. Similar alteration was found regarding the frontoparietal network which related to the repetitive behaviors observed in the disorder. There also is a hypothesis concerning cerebellar dysfunction and more specifically, that the Tuberous Sclerosis Complex 1 (TSC 1) deletion – gene that encodes the hamartin protein – in the Purkinje cells reflects on the social and behavioral deficits among ASD individuals. Furthermore, it is suggested that the disorder phenotype is associated with a disturbance in the networks that connect the cerebellum to the medial prefrontal cortex also due to a higher activation in the last region. Conclusion: there still is no satisfactory and pathognomonic conclusion regarding the neurobiology of ASD in children. The most common neurofunctional alterations in ASD are related to cerebellar networks and Purkinje cells. |
publishDate |
2021 |
dc.date.none.fl_str_mv |
2021-01-04 |
dc.type.driver.fl_str_mv |
info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion |
format |
article |
status_str |
publishedVersion |
dc.identifier.uri.fl_str_mv |
https://rsdjournal.org/index.php/rsd/article/view/11495 10.33448/rsd-v10i1.11495 |
url |
https://rsdjournal.org/index.php/rsd/article/view/11495 |
identifier_str_mv |
10.33448/rsd-v10i1.11495 |
dc.language.iso.fl_str_mv |
por |
language |
por |
dc.relation.none.fl_str_mv |
https://rsdjournal.org/index.php/rsd/article/view/11495/10316 |
dc.rights.driver.fl_str_mv |
Copyright (c) 2021 Cecília Rezende de Almeida Oliveira; José Carlos Souza https://creativecommons.org/licenses/by/4.0 info:eu-repo/semantics/openAccess |
rights_invalid_str_mv |
Copyright (c) 2021 Cecília Rezende de Almeida Oliveira; José Carlos Souza https://creativecommons.org/licenses/by/4.0 |
eu_rights_str_mv |
openAccess |
dc.format.none.fl_str_mv |
application/pdf |
dc.publisher.none.fl_str_mv |
Research, Society and Development |
publisher.none.fl_str_mv |
Research, Society and Development |
dc.source.none.fl_str_mv |
Research, Society and Development; Vol. 10 No. 1; e11910111495 Research, Society and Development; Vol. 10 Núm. 1; e11910111495 Research, Society and Development; v. 10 n. 1; e11910111495 2525-3409 reponame:Research, Society and Development instname:Universidade Federal de Itajubá (UNIFEI) instacron:UNIFEI |
instname_str |
Universidade Federal de Itajubá (UNIFEI) |
instacron_str |
UNIFEI |
institution |
UNIFEI |
reponame_str |
Research, Society and Development |
collection |
Research, Society and Development |
repository.name.fl_str_mv |
Research, Society and Development - Universidade Federal de Itajubá (UNIFEI) |
repository.mail.fl_str_mv |
rsd.articles@gmail.com |
_version_ |
1797052782767767552 |