Potential Mechanism Connecting Preeclampsia to Autism Spectrum Disorder in Offspring: The Role of Microglial Abnormalities.

This research review looks at how preeclampsia (a serious pregnancy complication involving high blood pressure) might increase the risk of autism in children. The study suggests that preeclampsia may affect special brain cells called microglia, which help the brain develop properly. When these cells don't work correctly, it might contribute to autism development. The researchers found that children born to mothers with preeclampsia have higher chances of developing autism.

This review examines potential mechanisms linking preeclampsia (PE) during pregnancy to increased autism spectrum disorder (ASD) risk in offspring, focusing on microglial abnormalities. The authors report that prenatal PE exposure increases ASD risk, with epidemiological studies showing elevated odds ratios in affected offspring. The review highlights how microglia, the brain's resident immune cells, play crucial roles in neurodevelopment including neural stem cell proliferation and synaptic pruning. Both early-onset and late-onset preeclampsia may impact microglial function through different pathways.

Postmortem ASD studies reveal increased microglial density, altered morphology, and upregulated inflammatory markers in key brain regions including hippocampus and prefrontal cortex, suggesting microglial dysfunction as a potential mechanistic link.

Findings suggest importance of monitoring neurodevelopmental outcomes in children born to mothers with preeclampsia. Early screening and intervention may be warranted for this population. Microglial-targeted therapeutic approaches represent potential novel treatment avenues, though further research is needed to establish causal relationships and develop specific interventions.

This is a narrative review without systematic methodology details. No sample size reported and specific study quality assessment unclear. The mechanistic connections between preeclampsia, microglial abnormalities, and ASD remain largely theoretical based on available evidence.

Preeclampsia (PE) is a serious complication of pregnancy characterized by chronic inflammation and immune dysregulation, which significantly increases the risk of neurodevelopmental disorders in offspring, including the autism spectrum disorder (ASD). This review investigated the potential mechanisms linking PE to ASD, with a particular focus on the role of microglial abnormalities. Epidemiological studies have revealed that prenatal exposure to PE raised the risk of ASD, with affected offspring showing increased odds ratios. Microglia, the prime resident immune cells of the central nervous system (CNS), are critical for normal neurodevelopment, influencing processes such as neural stem cell (NSC) proliferation, synaptic pruning, and normal function of the neural circuit.

Early-onset preeclampsia (EOPE) and late-onset preeclampsia (LOPE) may have an impact on the microglia abnormality and ASD through not exactly same pathway. Postmortem studies of ASD have further revealed increased microglial density, altered microglial morphology, and upregulated inflammatory markers in key brain regions, including the hippocampus and prefrontal cortex. Understanding the complex processes and potential mechanisms between EOPE, LOPE, microglial abnormalities, and ASD pathogenesis may highlight the importance of early screening and intervention for children born to mothers with PE. Targeting microglia-mediated pathways may offer novel therapeutic strategies to reduce the risk of ASD in these vulnerable populations.