ArticleMolecular psychiatry2021
Behavioral, neuroanatomical, and molecular correlates of resilience and susceptibility to maternal immune activation.
Article in Molecular psychiatry, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 80 papers.
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Who cites it
80 citing papers in PubMed, 132 citations in OpenAlex.
- Maternal immune activation disrupts epigenomic and functional maturation of cortical excitatory neurons.Molecular psychiatry · 2026Article
- Maternal immune activation in mice recapitulates features of attention-deficit/hyperactivity disorder (ADHD) in susceptible offspring.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026Article
- An emerging theoretical lens post global epidemic and turmoil: Psychological immunity.Dialogues in health · 2026Review
- Astroglial disinhibition of cortical circuits disrupts cognition via kynurenic acid in mice.Nature communications · 2026Article
- Prenatal maternal immune activation triggers lasting cell-specific transcriptomic dysregulation in the amygdala of primate offspring.Molecular psychiatry · 2026Article
- Maternal Immune Activation Leads to Mitochondrial Dysfunction and a Social Deficit in Offspring That Is Reversed by Nicotinamide Riboside.Nutrients · 2026Article
- Maternal immune activation with high molecular weight poly (I:C) induces selective depressive-like phenotype in adult offspring.Translational psychiatry · 2026Article
- Prenatal immune activation and adult Poly(I:C) re-challenge promote neuroimmune priming and AD-related behavioural, cellular and molecular alterations in wild-type mice.Frontiers in immunology · 2026Article
- The dopaminergic system in neurodevelopment: preclinical models of neurodevelopmental disorders and susceptibility to neurodegeneration.Frontiers in cellular neuroscience · 2026Review
- Microglial activity during postnatal development is required for infantile amnesia in mice.PLoS biology · 2026Article
- Microglial plasticity across development mediates infantile amnesia.bioRxiv : the preprint server for biology · 2025Article
- Inflammatory status along the brain-liver axis in animals vulnerable to prenatal stress: sex-related implications for stress-induced comorbidities.Translational psychiatry · 2025Article
- The role of maternal infections in neurodevelopmental psychiatric disorders: focus on the P2X7/NLRP3/IL-1β signalling pathway.Journal of neuroinflammation · 2025Review
- Recapitulation and reversal of neuropsychiatric phenotypes in a mouse model of human endogenous retrovirus type W expression.Molecular psychiatry · 2025Article
- Emerging Epigenetic Therapeutics and Diagnostics for Autism Spectrum Disorder.Current issues in molecular biology · 2025Review
- Association between redox dysregulation and vulnerability to cognitive deficits induced by maternal immune activation.Translational psychiatry · 2025Article
- Investigating the impact of severe maternal SARS-CoV-2 infection on infant DNA methylation and neurodevelopment.Molecular psychiatry · 2025Article
- Interleukin-6 produces behavioral deficits in pre-pubescent mice independent of neuroinflammation.Brain, behavior, and immunity · 2025Article
- Dysregulation of the mTOR-FMRP pathway and synaptic plasticity in an environmental model of ASD.Molecular psychiatry · 2025Article
- Understanding, predicting, and treating depression in pregnancy to improve mothers' and offspring's mental health outcomes: The HappyMums study.Brain, behavior, & immunity - health · 2025Article
20 more citing papers are in PubMed but not listed here.
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Authors and funding
11 authors at 4 institutions in 3 countries.
Funding
Abstract
Infectious or noninfectious maternal immune activation (MIA) is an environmental risk factor for psychiatric and neurological disorders with neurodevelopmental etiologies. Whilst there is increasing evidence for significant health consequences, the effects of MIA on the offspring appear to be variable. Here, we aimed to identify and characterize subgroups of isogenic mouse offspring exposed to identical MIA, which was induced in C57BL6/N mice by administration of the viral mimetic, poly(I:C), on gestation day 12. Cluster analysis of behavioral data obtained from a first cohort containing >150 MIA and control offspring revealed that MIA offspring could be stratified into distinct subgroups that were characterized by the presence or absence of multiple behavioral dysfunctions. The two subgroups also differed in terms of their transcriptional profiles in cortical and subcortical brain regions and brain networks of structural covariance, as measured by ex vivo structural magnetic resonance imaging (MRI). In a second, independent cohort containing 50 MIA and control offspring, we identified a subgroup of MIA offspring that displayed elevated peripheral production of innate inflammatory cytokines, including IL-1β, IL-6, and TNF-α, in adulthood. This subgroup also showed significant impairments in social approach behavior and sensorimotor gating, whereas MIA offspring with a low inflammatory cytokine status did not. Taken together, our results highlight the existence of subgroups of MIA-exposed offspring that show dissociable behavioral, transcriptional, brain network, and immunological profiles even under conditions of genetic homogeneity. These data have relevance for advancing our understanding of the variable neurodevelopmental effects induced by MIA and for biomarker-guided approaches in preclinical psychiatric research.
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