MODERATE PRENATAL ALCOHOL EXPOSURE: FOCUS ON THE NEUROIMMUNE AXIS

Prenatal alcohol exposure (PAE) is a major cause of fetal alcohol spectrum disorders (FASDs) and is associated with long-lasting neurodevelopmental impairments. Although alcohol can induce neuroinflammatory responses, whether neuroinflammation contributes to brain alterations induced by PAE remains largely unexplored. Using a well-established mouse model, this study investigates early neuroinflammatory-related changes in the developing brain of male and female embryos. The results suggest that early alcohol exposure is associated with impaired blood–brain barrier integrity, characterized by delayed barrier closure and dysregulation of tight junction protein expression (ZO-1, Occludin). In addition, microglial morphology and the expression of key microglial markers (Iba-1, P2RY12 and CX3CR1) are altered as early as embryonic day E17, suggesting disrupted microglial maturation and homeostasis. These findings support the central hypothesis that PAE has a major effect on the neuroimmune axis, which may contribute to the cognitive and behavioral impairments observed in fetal alcohol spectrum disorders.