Male autism spectrum disorder is linked to prenatal BPA
A study in Nature Communications links prenatal bisphenol A exposure to increased autism symptoms in males, particularly with low aromatase activity, suggesting potential interventions with 10-hydroxy-2-decenoic acid.
Read original articleThe study published in Nature Communications investigates the relationship between prenatal exposure to bisphenol A (BPA) and autism spectrum disorder (ASD) in males, focusing on the role of brain aromatase disruption. The research, conducted on a cohort from the Barwon Infant Study, found that higher maternal BPA levels during pregnancy correlated with increased ASD symptoms in male children, particularly those with low genetic activity of the aromatase enzyme. The study demonstrated that BPA exposure led to changes in the methylation of the aromatase gene, which in turn affected brain-derived neurotrophic factor levels. In animal models, male mice exposed to BPA exhibited ASD-like behaviors and brain abnormalities, which were alleviated by administering 10-hydroxy-2-decenoic acid (10HDA), a compound that appears to reverse some of the neurodevelopmental impacts of BPA. The findings suggest that prenatal BPA exposure may impair aromatase function, contributing to ASD-related behaviors and brain changes in males, and that postnatal interventions with 10HDA could potentially mitigate these effects.
- Prenatal BPA exposure is linked to increased ASD symptoms in males with low aromatase activity.
- BPA disrupts aromatase function, leading to neurodevelopmental changes and ASD-like behaviors in male mice.
- 10HDA may reverse some negative effects of BPA exposure on brain development.
- The study highlights the importance of environmental factors in the development of ASD.
- Genetic predisposition plays a role in the impact of BPA on ASD symptoms.
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