Aug 2026· Pregnancy· Vol 2· 0 citations· 163 references
Medicine
TL;DR
Evidence suggesting how prenatal exposures to alcohol, cocaine, Zika virus, rubella virus, Toxoplasma gondii, influenza, and traumatic brain injury can impact fetal brain development is examined.
Abstract
Abstract The maternal environment plays a pivotal role in fetal neurodevelopment, but adverse conditions during pregnancy may disrupt key developmental processes. Conditions such as intoxication, infection, or trauma during pregnancy have been associated with impaired fetal oxygenation, altered immune signaling, and disrupted placental function, which may contribute to long‐term neurodevelopmental alterations. This review examines evidence suggesting how prenatal exposures to alcohol, cocaine, Zika virus, rubella virus, Toxoplasma gondii, influenza, and traumatic brain injury can impact fetal brain development. These exposures often intersect with negative social determinants of health, increasing the risk for adverse outcomes. We focus on cellular and molecular mechanisms that contribute to outcomes such as microcephaly, cognitive impairment, and neurodevelopmental disorders, including schizophrenia and autism spectrum disorder. Although clinical epidemiology studies and preclinical investigations provide novel insights, major gaps in knowledge about how real‐world exposures affect fetal outcomes remain. This review integrates comprehensive research and epidemiological evidence of risk to emphasize the need for inclusive studies and targeted prevention strategies to protect fetal brain development.
PURPOSE OF REVIEW
This review examines how prenatal inflammation may contribute to psychiatric and neurodevelopmental disorders, with a focus on maternal immune activation, microglial programming, and epigenetic mechanisms.
RECENT FINDINGS
Recent studies have found that inflammation during pregnancy is associated wit...
Alexandra U. Zezulin, Jonathan Posner· Current Opinion in Psychiatr...· 0 citations
Overall, current evidence does not support a significant increase in ASD risk, and clinical guidelines should remain unchanged, given the known risks of alternative therapies, particularly non-steroidal anti-inflammatory drugs during pregnancy.
R. Hasanain, Hayder M. Al-kuraishy, Mustafa M. Shokr et al.· Neurotoxicology· 0 citations
Recent evidence suggests that prenatal environmental factors, particularly maternal infection or maternal immune activation (MIA), may influence the progression of brain aging and lifetime risk for neurodegenerative disorders. The hypothesis is that even a short-lived inflammatory event during pregnancy may leave a las...
Kabir Shehu, O. Onimisi, H. Bunza et al.· Experimental Neurology· 0 citations
Investigating how prenatal exposures, particularly prenatal stress and psychopharmacological exposure, shape fetal neurodevelopment via the placenta-brain axis sheds light on the mechanisms by which environmental stimuli like maternal stress or pharmacology could lead to lasting changes in prenatal health and subsequen...
C. Cruceanu· International Journal of Neu...· 0 citations
Epidemiological evidence suggests that developmental arsenic (As) exposure increases behavioral abnormalities in offspring. However, how placental neuroendocrine function and sex-specific responses contribute to these effects remains poorly understood. Here, we demonstrate that maternal As exposure induces trophoblasti...
Fang Chen, Xie He, Hui Qin et al.· Environmental Science and Te...· 0 citations
Abstract Background Long-term consequences of traumatic brain injury (TBI) include dysregulated stress and inflammatory signaling and neurocognitive decline. Epidemiological evidence indicates increased psychiatric vulnerability in the offspring of parents with TBI, with greater abnormalities in sons. The mechanisms in...
Z. Khan, Ling-Sha Ju, N. Gravenstein et al.· International Journal of Neu...· 0 citations
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