Journal article
D. Beversdorf, H. Stevens, K. Margolis, J. A. Van de Water
Current pharmaceutical design, 2019
Current pharmaceutical design, 2019
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APA
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Beversdorf, D., Stevens, H., Margolis, K., & de Water, J. A. V. (2019). Prenatal stress and maternal immune dysregulation in autism spectrum disorders- potential points for intervention. Current Pharmaceutical Design.
Chicago/Turabian
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Beversdorf, D., H. Stevens, K. Margolis, and J. A. Van de Water. “Prenatal Stress and Maternal Immune Dysregulation in Autism Spectrum Disorders- Potential Points for Intervention.” Current pharmaceutical design (2019).
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Beversdorf, D., et al. “Prenatal Stress and Maternal Immune Dysregulation in Autism Spectrum Disorders- Potential Points for Intervention.” Current Pharmaceutical Design, 2019.
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@article{d2019a,
title = {Prenatal stress and maternal immune dysregulation in autism spectrum disorders- potential points for intervention.},
year = {2019},
journal = {Current pharmaceutical design},
author = {Beversdorf, D. and Stevens, H. and Margolis, K. and de Water, J. A. Van}
}
Abstract
BACKGROUND Genetics are a major etiological contributor to autism spectrum disorder (ASD). Environmental factors, however, also appear to contribute. ASD pathophysiology due to gene x environment is also beginning to be explored. One reason to focus on environmental factors is that they may allow opportunities for intervention or prevention.
METHODS AND RESULTS Herein, we review two such factors that have been associated with a significant proportion of ASD risk, prenatal stress exposure and maternal immune dysregulation. Maternal stress susceptibility appears to interact with prenatal stress exposure to affect offspring neurodevelopment. We also explore how maternal stress may interact with the microbiome in the neurodevelopmental setting. Additionally, understanding of the impact of maternal immune dysfunction on ASD has recently been advanced by recognition of specific fetal brain proteins targeted by maternal autoantibodies, and identification of unique mid-gestational maternal immune profiles. This might also be interrelated with maternal stress exposure. Animal models have been developed to explore pathophysiology targeting each of these factors.
CONCLUSIONS We are beginning to understand the behavioral, pharmacopathological, and epigenetic effects related to these interactions, and we are beginning to explore potential mitigating factors. Continued growth in understanding of these mechanisms may ultimately allow for the identification of multiple potential targets for prevention or intervention for this subset of environmental-associated ASD cases.
