Elevated maternal testosterone induces sex-specific neurodevelopmental changes and ASD-related behavioral phenotypes in rat offspring.

Researchers gave pregnant rats testosterone injections to mimic high hormone levels during pregnancy. The baby rats showed autism-like behaviors including less communication, social difficulties, and memory problems. Male and female babies were affected differently - males had fewer brain cells in thinking areas while females had problems with brain connections. All babies had lower levels of an important brain fat (DHA).

This suggests high testosterone during pregnancy might increase autism risk, and that supplements might help.

This rat study investigated how elevated maternal testosterone during pregnancy affects offspring neurodevelopment and behavior. Pregnant rats received testosterone injections that doubled maternal hormone levels, mimicking pregnancy complications. Offspring showed ASD-like features including reduced birth weight, impaired communication (fewer vocalizations), and cognitive/social deficits in adolescence. Sex-specific brain changes were observed: males had reduced cortical neurons while females showed decreased brain white matter.

Both sexes had lower brain DHA levels. The study suggests maternal testosterone exposure is a neurodevelopmental risk factor, with reduced brain DHA as a potential mechanism. Findings support investigating DHA supplementation as a preventive strategy.

Suggests monitoring maternal testosterone levels during pregnancy and investigating DHA supplementation as prevention. Supports research into hormonal risk factors for autism. May inform prenatal counseling for high-risk pregnancies with metabolic or endocrine complications.

Animal study using rats may not directly translate to humans. Sample size not reported. Single testosterone dose tested. Long-term developmental outcomes beyond adolescence not assessed. Mechanism linking testosterone to DHA reduction requires further investigation.

Elevated maternal testosterone (T) during pregnancy disrupts neurodevelopment and behavior in offspring, mimicking features of autism spectrum disorder (ASD). In 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). T-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). The 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.

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.