Prenatal omega-3 fatty acids supplementation mitigates some schizophrenia-like deficits in offspring: A PET and MRI study in a rat model
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Updated: Jun 11, 2026
Modeling Encephalopathy of Prematurity Using Prenatal Hypoxia-ischemia with Intra-amniotic Lipopolysaccharide in Rats
Published on: November 20, 2015
Diego Romero-Miguel1, Marta Casquero-Veiga1,2,3, Nicolás Lamanna-Rama1,3,4
1Instituto de Investigación Sanitaria Gregorio Marañón, Madrid, Spain.
Insights
Prenatal omega-3 fatty acid (OM) supplementation may prevent schizophrenia-like deficits in offspring. Dietary OM intake during pregnancy ameliorated behavioral and brain abnormalities in a maternal immune stimulation model.
Area of Science:
- Neuroscience
- Developmental Psychology
- Nutritional Science
Background:
- Schizophrenia is a complex mental disorder with potential developmental origins.
- Omega-3 fatty acids (OM) are investigated for their role in brain health and psychiatric conditions.
- The preventive potential of prenatal OM supplementation against schizophrenia-like deficits is not well understood.
Purpose of the Study:
- To investigate if dietary OM supplementation during pregnancy can prevent schizophrenia-like deficits in offspring using a maternal immune stimulation (MIS) rat model.
- To assess the impact of OM on behavioral, metabolic, and structural brain changes.
Main Methods:
- Pregnant Wistar rats received PolyI:C (MIS) or Saline on gestational day 15.
- Offspring were exposed to diets enriched with OM from MIS until delivery (OM7) or throughout gestation (OM21).
- Offspring underwent behavioral tests (locomotion, anxiety, memory), PET scans for brain metabolism, and MRI for structural analysis.
Main Results:
- OM supplementation (OM7/OM21) prevented hyperlocomotion and cortical metabolic/volumetric changes in MIS-offspring.
- OM7 improved short-term memory deficits, while both OM7/OM21 prevented ventricular enlargement.
- OM21 specifically protected white matter (WM) integrity in MIS-offspring.
Conclusions:
- Prenatal dietary OM supplementation shows promise in ameliorating specific schizophrenia-like deficits induced by maternal immune stimulation.
- OM may be a viable nutritional strategy to mitigate neurodevelopmental risks associated with prenatal adversity.
- Further research is warranted to explore the clinical implications of prenatal OM for schizophrenia prevention.
Abstract:
Omega-3 fatty acids (OM) have been employed as adjunctive therapy in patients with schizophrenia, but their potential as a preventive strategy remains unclear. This study aims to evaluate whether dietary OM supplementation during pregnancy may prevent schizophrenia-like deficits in a maternal immune stimulation (MIS) model. Pregnant Wistar rats were injected with PolyI:C (i.e. MIS) or Saline on gestational day 15. They were fed with OM-enriched chow, either from MIS until delivery (OM7) or throughout gestation (OM21). Two control groups (Saline-naïve & MIS-naïve) were maintained on standard chow. In adulthood, offspring were assessed through tests for locomotion, anxiety and short- and long-term memory (STM, LTM). Brain glucose metabolism and structural in vivo neuroimaging studies were performed using PET and MRI techniques. OM7/OM21 treatments prevented the hyperlocomotion in MIS-offspring while STM deficits were only improved by OM7. Both OM7/OM21 treatments prevented certain metabolic and volumetric changes in the cortex, as well as the enlargement of the ventricles. Additionally, OM21 protected WM integrity in MIS-offspring. Altogether, our study highlights the potential of prenatal OM dietary supplementation to ameliorate some of the SCZ-like deficits observed in the MIS model.
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