A study from Nagoya University reveals the impact of maternal inflammation on neurodevelopment, focusing on CD11c-positive microglia crucial for brain myelination.
Inflammation during pregnancy could impede CD11c-positive microglia proliferation, affecting neurodevelopment in infants.
CD11c-positive microglia play a vital role in myelination, essential for efficient neural signal transmission and cognitive development.
Experiments on neonatal mice showed reduced CD11c-positive microglia proliferation due to maternal inflammation, mirroring human implications found in preterm infants.
Analysis of cord blood samples revealed decreased levels of insulin-like growth factor 1, linked to impaired microglial function and delayed myelination in infants.
Maternal immune activation can lead to cognitive challenges in children, indicating long-term neurological consequences from prenatal inflammation.
Research highlights the importance of understanding the link between inflammation, CD11c-positive microglia, and cognitive outcomes in infants.
Impaired myelination due to maternal inflammation can result in neurological issues, emphasizing the need for interventions to safeguard fetal brain development.
Insights into the relationship may lead to targeted therapies mitigating the effects of maternal inflammation on neurodevelopment, potentially protecting infants from cognitive deficits.
As research progresses, interventions targeting CD11c-positive microglia could offer promising strategies to enhance cognitive outcomes in children affected by maternal inflammation.