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Antenatal maternal depression, early life inflammation and neurodevelopment in a South African birth cohort
Petrus J W Naudé1, Carmine Pariante2, Nadia Hoffman3
1Department of Psychiatry and Mental Health, University of Cape Town, South Africa; Neuroscience Institute, University of Cape Town, South Africa.
Insights
Antenatal maternal depression is linked to elevated inflammatory markers in mothers and children. Infant interleukin-1 beta (IL-1β) at 6-10 weeks partially explains the association between maternal depression and poorer child language development at 2 years.
Area of Science:
- Neuroscience
- Immunology
- Developmental Psychology
Background:
- Maternal psychological adversity, including depression, during pregnancy is associated with impaired child neurodevelopment.
- The biological mechanisms underlying this association, particularly in early development, are not fully understood.
- This study examines the link between antenatal maternal depression, inflammatory markers, and child neurodevelopmental outcomes.
Purpose of the Study:
- To investigate the association between antenatal maternal depression and maternal/infant inflammatory markers.
- To explore the relationship between these inflammatory markers and child neurodevelopmental outcomes at 2 years.
- To identify potential biological pathways linking maternal depression to child neurodevelopment.
Main Methods:
- A subgroup of 255 mother-child pairs from a South African birth cohort study were followed from pregnancy to 2 years postpartum.
- Maternal depressive symptoms were assessed using the Beck Depression Inventory (BDI-II) during gestation.
- Maternal and child serum inflammatory markers were measured at multiple time points, and child neurodevelopment was assessed using the Bayley Scales of Infant and Toddler Development III.
Main Results:
- Antenatal depressive symptoms in mothers were associated with elevated maternal levels of interleukin-7 (IL-7), interleukin-8 (IL-8), and tumor necrosis factor-alpha (TNF-α).
- Children born to mothers with depressive symptoms exhibited elevated serum interleukin-1 beta (IL-1β) and neutrophil gelatinase-associated lipocalin (NGAL) over time.
- Elevated infant IL-1β levels at 6-10 weeks partially mediated the association between maternal depressive symptoms and poorer language scores in children at 2 years.
Conclusions:
- Early life immune alterations, indicated by elevated IL-1β, may represent a pathway through which antenatal maternal depression impacts child language development.
- Findings highlight the role of inflammation in the neurodevelopmental consequences of maternal depression.
- Intervention strategies targeting inflammation could potentially mitigate the negative effects of maternal depression on child development.
Background:
Antenatal exposure to maternal psychological adversity, including depression, increases the risk of impaired neurodevelopment in children. The underlying biological mechanisms remain unclear, especially in early life during critical windows of development and maturation. This study investigated the association of antenatal maternal depression, maternal and early life inflammatory markers and neurodevelopmental outcomes in children at 2 years of age.
Methods:
A subgroup of mothers and their children (n = 255) that were enrolled in a South African birth cohort study, the Drakenstein Child Health Study, were followed from the antenatal period through to 2 years of child age. Maternal depressive symptoms were measured by the Beck Depression Inventory (BDI-II) at 26 weeks gestation. Serum inflammatory markers [granulocyte-macrophage colony-stimulating factor (GM-CSF), interferon-γ (IFN-γ), interleukin IL-1β, IL-2, IL-4, IL-5, IL-6, IL-7, IL-8, IL-10, IL-12p70, IL-13, tumour necrosis factor-α (TNF-α), neutrophil gelatinase-associated lipocalin (NGAL) and metalloproteinase-9 (MMP-9)] were measured in mothers at enrolment and in their children at 6-10 weeks and at 2 years. Neurodevelopment was assessed at 2 years using the Bayley Scales of Infant and Toddler Development III.
Results:
Antenatal depressive symptoms (present in 25% of the mothers) were significantly associated with higher levels of IL-7 (p = 0.008), IL-8 (p = 0.019) and TNF-α (p = 0.031) in the mothers after correcting for sociodemographic and lifestyle factors. Serum IL-1β and NGAL levels were significantly elevated over time in children born to mothers with depressive symptoms compared to those without depression, after controlling for maternal and child health and sociodemographic factors. Elevated infant IL-1β at 6-10 weeks of age partially mediated the association of maternal depressive symptoms with poorer language scores at 2 years.
Conclusion:
Alterations in early life immunity, as reflected by elevated IL-1β, is a potential pathway through which antenatal maternal depressive symptoms may impact language development in young children.
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