Maternal Immune Activation Effects on Neurodevelopmental Disorders
Summary
Maternal immune activation (MIA) refers to the stimulation of a gestational parent’s immune system by infection or other inflammatory stimuli during pregnancy. A wealth of epidemiological and pre-clinical studies has linked MIA to an elevated risk of neurodevelopmental disorders in the offspring, notably autism spectrum disorder and schizophrenia. Experimental models in rodents and non-human primates have shown that maternal inflammatory signals cross the placenta and alter foetal brain development through changes in cytokine networks, microglial function and neural progenitor dynamics. Central mediators such as interleukin-6 (IL-6) drive transcriptional and epigenetic programmes in the embryonic brain, disrupting neuronal differentiation, synaptic formation and neural circuit maturation. Emerging human studies, including advanced imaging and in vitro approaches, corroborate these findings by demonstrating associations between maternal inflammatory markers and alterations in white matter integrity, cortical organisation and cognitive trajectories in early life. The convergent evidence points to sex-specific vulnerabilities, long-term behavioural consequences and potential windows for therapeutic intervention during gestation or early postnatal development.
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Maternal Immune Activation Effects on Neurodevelopmental Disorders publication trend
The graph below shows the total number of articles in maternal immune activation effects on neurodevelopmental disorders across all publications each year (not limited to Nature Index journals).
Technical terms
Maternal immune activation (MIA): Activation of the gestational parent’s immune system during pregnancy, often modelled by infection or inflammatory agents.
Cytokine: A small secreted protein released by immune cells that modulates cell signalling and inflammatory responses.
Interleukin-6 (IL-6): A pro-inflammatory cytokine implicated in mediating the effects of MIA on foetal brain development.
Organoid: A three-dimensional culture of stem cell-derived tissue that recapitulates aspects of organ architecture and cell diversity.
Radial glia: Neural progenitor cells in the developing brain that give rise to neurons and glia and guide neuronal migration.
Long non-coding RNA (lncRNA): A class of RNA molecules longer than 200 nucleotides that do not code for protein but regulate gene expression.
STAT1 (Signal Transducer and Activator of Transcription 1): A transcription factor activated by cytokine signalling that regulates immune and inflammatory gene programmes.
References
- Maternal immune activation upregulates the AU020206-IRFs-STAT1 axis in modulating cytokine production in the brain. Theranostics (2024).
- Human brain organoid model of maternal immune activation identifies radial glia cells as selectively vulnerable. Molecular Psychiatry (2023).
- Maternal Immune Activation Alters Fetal Brain Development through Interleukin-6. Journal of Neuroscience (2007).
- Maternal Interleukin-6 concentration during pregnancy is associated with variation in frontolimbic white matter and cognitive development in early life. NeuroImage (2018).
- Increasing Role of Maternal Immune Activation in Neurodevelopmental Disorders. Frontiers in Behavioral Neuroscience (2018).
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