A Glucocorticoid-Sensitive Hippocampal Gene Network Moderates the Impact of Early-Life Adversity on Mental Health Outcomes.


Journal

Biological psychiatry
ISSN: 1873-2402
Titre abrégé: Biol Psychiatry
Pays: United States
ID NLM: 0213264

Informations de publication

Date de publication:
01 Jan 2024
Historique:
received: 03 11 2022
revised: 15 04 2023
accepted: 20 06 2023
medline: 1 12 2023
pubmed: 6 7 2023
entrez: 5 7 2023
Statut: ppublish

Résumé

Early stress increases the risk for psychiatric disorders. Glucocorticoids are stress mediators that regulate transcriptional activity and morphology in the hippocampus, which is implicated in the pathophysiology of multiple psychiatric conditions. We aimed to establish the relevance of hippocampal glucocorticoid-induced transcriptional activity as a mediator of the effects of early life on later psychopathology in humans. RNA sequencing was performed with anterior and posterior hippocampal dentate gyrus from adult female macaques (n = 12/group) that were chronically treated with betamethasone (glucocorticoid receptor agonist) or vehicle. Coexpression network analysis identified a preserved gene network in the posterior hippocampal dentate gyrus that was strongly associated with glucocorticoid exposure. The single nucleotide polymorphisms in the genes in this network were used to create an expression-based polygenic score in humans. The expression-based polygenic score significantly moderated the association between early adversity and psychotic disorders in adulthood (UK Biobank, women, n = 44,519) and on child peer relations (ALSPAC [Avon Longitudinal Study of Parents and Children], girls, n = 1666 for 9-year-olds and n = 1594 for 11-year-olds), an endophenotype for later psychosis. Analyses revealed that this network was enriched for glucocorticoid-induced epigenetic remodeling in human hippocampal cells. We also found a significant association between single nucleotide polymorphisms from the expression-based polygenic score and adult brain gray matter density. We provide an approach for the use of transcriptomic data from animal models together with human data to study the impact of environmental influences on mental health. The results are consistent with the hypothesis that hippocampal glucocorticoid-related transcriptional activity mediates the effects of early adversity on neural mechanisms implicated in psychiatric disorders.

Sections du résumé

BACKGROUND BACKGROUND
Early stress increases the risk for psychiatric disorders. Glucocorticoids are stress mediators that regulate transcriptional activity and morphology in the hippocampus, which is implicated in the pathophysiology of multiple psychiatric conditions. We aimed to establish the relevance of hippocampal glucocorticoid-induced transcriptional activity as a mediator of the effects of early life on later psychopathology in humans.
METHODS METHODS
RNA sequencing was performed with anterior and posterior hippocampal dentate gyrus from adult female macaques (n = 12/group) that were chronically treated with betamethasone (glucocorticoid receptor agonist) or vehicle. Coexpression network analysis identified a preserved gene network in the posterior hippocampal dentate gyrus that was strongly associated with glucocorticoid exposure. The single nucleotide polymorphisms in the genes in this network were used to create an expression-based polygenic score in humans.
RESULTS RESULTS
The expression-based polygenic score significantly moderated the association between early adversity and psychotic disorders in adulthood (UK Biobank, women, n = 44,519) and on child peer relations (ALSPAC [Avon Longitudinal Study of Parents and Children], girls, n = 1666 for 9-year-olds and n = 1594 for 11-year-olds), an endophenotype for later psychosis. Analyses revealed that this network was enriched for glucocorticoid-induced epigenetic remodeling in human hippocampal cells. We also found a significant association between single nucleotide polymorphisms from the expression-based polygenic score and adult brain gray matter density.
CONCLUSIONS CONCLUSIONS
We provide an approach for the use of transcriptomic data from animal models together with human data to study the impact of environmental influences on mental health. The results are consistent with the hypothesis that hippocampal glucocorticoid-related transcriptional activity mediates the effects of early adversity on neural mechanisms implicated in psychiatric disorders.

Identifiants

pubmed: 37406925
pii: S0006-3223(23)01401-4
doi: 10.1016/j.biopsych.2023.06.028
pii:
doi:

Substances chimiques

Glucocorticoids 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

48-61

Informations de copyright

Copyright © 2023 Society of Biological Psychiatry. Published by Elsevier Inc. All rights reserved.

Auteurs

Danusa Mar Arcego (DM)

Douglas Research Centre, Department of Psychiatry, Faculty of Medicine, McGill University, Montreal, Quebec, Canada; Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada. Electronic address: danusa.mararcego@douglas.mcgill.ca.

Jan-Paul Buschdorf (JP)

Translational Neuroscience Program, Singapore Institute for Clinical Sciences, Singapore, Republic of Singapore.

Nicholas O'Toole (N)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada.

Zihan Wang (Z)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada.

Barbara Barth (B)

Douglas Research Centre, Department of Psychiatry, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.

Irina Pokhvisneva (I)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada.

Nirmala Arul Rayan (NA)

Genome Institute of Singapore, Singapore, Republic of Singapore.

Sachin Patel (S)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada.

Euclides José de Mendonça Filho (EJ)

Douglas Research Centre, Department of Psychiatry, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.

Patrick Lee (P)

Translational Neuroscience Program, Singapore Institute for Clinical Sciences, Singapore, Republic of Singapore.

Jennifer Tan (J)

Translational Neuroscience Program, Singapore Institute for Clinical Sciences, Singapore, Republic of Singapore.

Ming Xuan Koh (MX)

Translational Neuroscience Program, Singapore Institute for Clinical Sciences, Singapore, Republic of Singapore.

Chu Ming Sim (CM)

Translational Neuroscience Program, Singapore Institute for Clinical Sciences, Singapore, Republic of Singapore.

Carine Parent (C)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada.

Randriely Merscher Sobreira de Lima (RMS)

Douglas Research Centre, Department of Psychiatry, Faculty of Medicine, McGill University, Montreal, Quebec, Canada.

Andrew Clappison (A)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada.

Kieran J O'Donnell (KJ)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada; Yale Child Study Center, Yale School of Medicine, Yale University, New Haven, Connecticut.

Carla Dalmaz (C)

Department of Biochemistry, Universidade Federal do Rio Grande do Sul, Porto Alegre, Rio Grande do Sul, Brazil.

Janine Arloth (J)

Department Genes and Environment, Max Planck Institute of Psychiatry, Munich, Germany; Institute of Computational Biology, Helmholtz Zentrum München, Neuherberg, Germany.

Nadine Provençal (N)

Faculty of Health Sciences, Simon Fraser University, Burnaby, British Columbia, Canada; BC Children's Hospital Research Institute, Vancouver, British Columbia, Canada.

Elisabeth B Binder (EB)

Department Genes and Environment, Max Planck Institute of Psychiatry, Munich, Germany.

Josie Diorio (J)

Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada.

Patrícia Pelufo Silveira (PP)

Douglas Research Centre, Department of Psychiatry, Faculty of Medicine, McGill University, Montreal, Quebec, Canada; Ludmer Centre for Neuroinformatics and Mental Health, Douglas Research Centre, McGill University, Montreal, Quebec, Canada; Department of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Republic of Singapore.

Michael J Meaney (MJ)

Douglas Research Centre, Department of Psychiatry, Faculty of Medicine, McGill University, Montreal, Quebec, Canada; Translational Neuroscience Program, Singapore Institute for Clinical Sciences, Singapore, Republic of Singapore; Brain Body Initiative, Agency for Science, Technology and Research (A∗STAR), Singapore, Republic of Singapore; Department of Paediatrics, Yong Loo Lin School of Medicine, National University of Singapore, Republic of Singapore.

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