Prenatal Origins of ASD: The When, What, and How of ASD Development.
autism
brain specific
broadly expressed
gene
prenatal
proliferation
regulatory
synapse
Journal
Trends in neurosciences
ISSN: 1878-108X
Titre abrégé: Trends Neurosci
Pays: England
ID NLM: 7808616
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
24
09
2019
revised:
28
01
2020
accepted:
04
03
2020
entrez:
1
5
2020
pubmed:
1
5
2020
medline:
19
8
2021
Statut:
ppublish
Résumé
Autism spectrum disorder (ASD) is a largely heritable, multistage prenatal disorder that impacts a child's ability to perceive and react to social information. Most ASD risk genes are expressed prenatally in many ASD-relevant brain regions and fall into two categories: broadly expressed regulatory genes that are expressed in the brain and other organs, and brain-specific genes. In trimesters one to three (Epoch-1), one set of broadly expressed (the majority) and brain-specific risk genes disrupts cell proliferation, neurogenesis, migration, and cell fate, while in trimester three and early postnatally (Epoch-2) another set (the majority being brain specific) disrupts neurite outgrowth, synaptogenesis, and the 'wiring' of the cortex. A proposed model is that upstream, highly interconnected regulatory ASD gene mutations disrupt transcriptional programs or signaling pathways resulting in dysregulation of downstream processes such as proliferation, neurogenesis, synaptogenesis, and neural activity. Dysregulation of signaling pathways is correlated with ASD social symptom severity. Since the majority of ASD risk genes are broadly expressed, many ASD individuals may benefit by being treated as having a broader medical disorder. An important future direction is the noninvasive study of ASD cell biology.
Identifiants
pubmed: 32353336
pii: S0166-2236(20)30051-5
doi: 10.1016/j.tins.2020.03.005
pmc: PMC7373219
mid: NIHMS1585369
pii:
doi:
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Review
Langues
eng
Sous-ensembles de citation
IM
Pagination
326-342Subventions
Organisme : NIDCD NIH HHS
ID : R01 DC016385
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH110558
Pays : United States
Informations de copyright
Copyright © 2020 The Authors. Published by Elsevier Ltd.. All rights reserved.
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