Abstract
Preeclampsia (PE) is a severe hypertensive disorder of pregnancy that poses significant risks to both maternal health and offspring development. Increasing epidemiological evidence suggests that children born to women with PE have a higher risk of neurodevelopmental disorders (NDDs), including autism spectrum disorder (ASD), cognitive impairment, and attention-deficit/hyperactivity disorder (ADHD). However, the underlying biological mechanisms remain incompletely understood. This review aims to summarize current evidence on the association between PE and offspring neurodevelopmental outcomes, with a particular focus on the potential role of imprinted genes in epigenetic regulation. A literature search was conducted using databases including PubMed, Web of Science, and Scopus, covering studies published up to 2025. Relevant articles were identified using keywords such as "preeclampsia", "imprinted genes", "epigenetics", "DNA methylation", and "neurodevelopment". Current evidence suggests that epigenetic alterations, particularly aberrant DNA methylation of imprinted genes, may be associated with disrupted placental function and potentially influence fetal brain development through proposed mechanisms. These changes are thought to be involved in the placenta-brain axis, although most findings remain associative and are derived from a combination of human observational studies and animal models. In conclusion, imprinted genes may play an important role in the epigenetic mechanisms linking PE and offspring neurodevelopmental abnormalities. However, findings across studies remain heterogeneous and sometimes inconsistent. Therefore, further studies are required to clarify causal relationships and to translate these findings into clinical applications.