Sex Differences in the Amygdala Resting-State Connectome of Children With Autism Spectrum Disorder.


Journal

Biological psychiatry. Cognitive neuroscience and neuroimaging
ISSN: 2451-9030
Titre abrégé: Biol Psychiatry Cogn Neurosci Neuroimaging
Pays: United States
ID NLM: 101671285

Informations de publication

Date de publication:
03 2020
Historique:
received: 27 02 2019
revised: 12 08 2019
accepted: 13 08 2019
pubmed: 30 9 2019
medline: 13 3 2021
entrez: 30 9 2019
Statut: ppublish

Résumé

Multifactorial liability models predict greater dissimilarity in the neural phenotype of autism spectrum disorder (ASD) in female individuals than in male individuals, while gender incoherence and extreme male brain models predict attenuated sex differences in ASD. The amygdala is an informative target to explore these models because it is implicated in both the neurobiology of ASD and sex differences in typical development. This study investigated amygdala resting-state functional connectivity in a cohort of 116 children with ASD (36 female) and 58 typically developing children (27 female) 2 to 7 years of age during natural sleep. First, multivariate distance matrix regression assessed global sex and diagnostic differences across the amygdala connectome. Second, univariate general linear models identified regions with mean connectivity differences. Multivariate distance matrix regression revealed greater differences between typically developing children and those with ASD in females than in males, consistent with multifactorial liability models, and attenuated sex differences in the left amygdala connectome of children with ASD in a pattern consistent with the gender incoherence model. Univariate analysis identified similar sex differences in dorsomedial and ventral prefrontal cortices, lingual gyrus, and posterior cingulate cortex, but also noted that lower amygdala connectivity with superior temporal sulcus is observed across sexes. This study provides evidence that compared with sex-matched control subjects, ASD manifests differently in the brain at the time of diagnosis and prior to the influence of compensatory mechanisms in male and female children, consistent with multifactorial liability models, and that ASD is associated with reduced sex differences in a pattern consistent with gender incoherence models.

Sections du résumé

BACKGROUND
Multifactorial liability models predict greater dissimilarity in the neural phenotype of autism spectrum disorder (ASD) in female individuals than in male individuals, while gender incoherence and extreme male brain models predict attenuated sex differences in ASD. The amygdala is an informative target to explore these models because it is implicated in both the neurobiology of ASD and sex differences in typical development.
METHODS
This study investigated amygdala resting-state functional connectivity in a cohort of 116 children with ASD (36 female) and 58 typically developing children (27 female) 2 to 7 years of age during natural sleep. First, multivariate distance matrix regression assessed global sex and diagnostic differences across the amygdala connectome. Second, univariate general linear models identified regions with mean connectivity differences.
RESULTS
Multivariate distance matrix regression revealed greater differences between typically developing children and those with ASD in females than in males, consistent with multifactorial liability models, and attenuated sex differences in the left amygdala connectome of children with ASD in a pattern consistent with the gender incoherence model. Univariate analysis identified similar sex differences in dorsomedial and ventral prefrontal cortices, lingual gyrus, and posterior cingulate cortex, but also noted that lower amygdala connectivity with superior temporal sulcus is observed across sexes.
CONCLUSIONS
This study provides evidence that compared with sex-matched control subjects, ASD manifests differently in the brain at the time of diagnosis and prior to the influence of compensatory mechanisms in male and female children, consistent with multifactorial liability models, and that ASD is associated with reduced sex differences in a pattern consistent with gender incoherence models.

Identifiants

pubmed: 31563470
pii: S2451-9022(19)30220-4
doi: 10.1016/j.bpsc.2019.08.004
pmc: PMC7033019
mid: NIHMS1538115
pii:
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

320-329

Subventions

Organisme : NIMH NIH HHS
ID : T32 MH073124
Pays : United States
Organisme : NIMH NIH HHS
ID : L30 MH114419
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH103284
Pays : United States
Organisme : NICHD NIH HHS
ID : P50 HD093079
Pays : United States
Organisme : NICHD NIH HHS
ID : U54 HD079125
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH106518
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH104438
Pays : United States
Organisme : NIMH NIH HHS
ID : R01 MH103371
Pays : United States

Informations de copyright

Copyright © 2019 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

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Auteurs

Joshua K Lee (JK)

MIND Institute, University of California Davis School of Medicine, Sacramento, California; Department of Psychiatry and Behavioral Sciences, University of California Davis School of Medicine, Sacramento, California. Electronic address: jkilee@ucdavis.edu.

David G Amaral (DG)

MIND Institute, University of California Davis School of Medicine, Sacramento, California; Department of Psychiatry and Behavioral Sciences, University of California Davis School of Medicine, Sacramento, California.

Marjorie Solomon (M)

MIND Institute, University of California Davis School of Medicine, Sacramento, California; Department of Psychiatry and Behavioral Sciences, University of California Davis School of Medicine, Sacramento, California.

Sally J Rogers (SJ)

MIND Institute, University of California Davis School of Medicine, Sacramento, California; Department of Psychiatry and Behavioral Sciences, University of California Davis School of Medicine, Sacramento, California.

Sally Ozonoff (S)

MIND Institute, University of California Davis School of Medicine, Sacramento, California; Department of Psychiatry and Behavioral Sciences, University of California Davis School of Medicine, Sacramento, California.

Christine Wu Nordahl (CW)

MIND Institute, University of California Davis School of Medicine, Sacramento, California; Department of Psychiatry and Behavioral Sciences, University of California Davis School of Medicine, Sacramento, California. Electronic address: cnordahl@ucdavis.edu.

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