ArticlePediatric research2026
Elevated maternal testosterone induces sex-specific neurodevelopmental changes and ASD-related behavioral phenotypes in rat offspring.
Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Bridging medicine and education for global developmental delay: a cluster sampling study on screening, diagnosis, and intervention in preschool children.Frontiers in public health · 2026Article
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Abstract
objectiveElevated maternal testosterone (T) during pregnancy disrupts neurodevelopment and behavior in offspring, mimicking features of autism spectrum disorder (ASD).
methodsIn a rat study, dams received daily T injections (0.5 mg/kg) from gestational days 12-20, doubling maternal plasma T to mimic levels seen in pregnancy complications. Controls received vehicle. Offspring were assessed neonatally (postnatal day 9) for communication (ultrasonic vocalizations), neurogenesis (NeuN+ neurons), myelination (MBP+ area), and brain docosahexaenoic acid (DHA). Adolescent offspring (6-8 weeks) underwent behavioral tests for cognition (Y-maze, novel object recognition) and sociability (three-chamber test).
resultsT-exposed pups had lower birth weights and reduced vocalizations during maternal separation. Sex-specific neural changes observed: males showed reduced cortical neuron density, while females had diminished corpus callosum myelination. Both sexes exhibited decreased brain DHA. In adolescence, T offspring displayed cognitive deficits (impaired spatial/recognition memory) and social impairments (reduced sociability and social novelty preference).
conclusionThe study highlights maternal T as a risk factor for neurodevelopmental disorders, with sex-specific effects on brain structure and function. Reduced brain DHA suggests a mechanistic link, implicating lipid metabolism in T-associated neurodevelopmental disruptions. These findings support further exploration of DHA supplementation as a therapeutic strategy to mitigate adverse outcomes in high-risk pregnancies. IMPACT: Elevated maternal testosterone (T) during pregnancy induces ASD-like neurobehavioral deficits (e.g., impaired communication, social/cognitive dysfunction) and sex-specific neural alterations in offspring. Prenatal T differentially impacts male vs. female brain structure: T-exposed males show cortical neuron loss, while females exhibit myelination deficits in the corpus callosum. First to connect maternal T-driven offspring brain docosahexaenoic acid (DHA) reduction to neurodevelopmental impairment. Supports prenatal DHA supplementation as a strategy to mitigate neurodevelopmental risks in high-T pregnancies. Informs policies addressing rising neurodevelopmental disorder rates linked to maternal metabolic/endocrine imbalances.
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