The hippocampus and perinatal alcohol exposure

Perinatal alcohol exposure is a significant and preventable cause of neurodevelopmental impairment, resulting in long-term changes to the structure and function of the hippocampus. This region of the brain is particularly vulnerable due to its prolonged developmental trajectory and critical role in learning, memory, and emotional regulation. This chapter provides a review of the mechanisms underlying the disruption of hippocampal development caused by alcohol exposure during the prenatal and early postnatal periods. The important mechanisms consist of disrupted neurogenesis, increased neuronal apoptosis, oxidative stress, and neuroinflammation. These all contribute to permanent changes in the circuitry of the hippocampus and its behavioral outcome. Structural and morphological abnormalities, such as reduced hippocampal volume, altered cytoarchitecture, and impaired dendritic development, are discussed in relation to functional outcomes. These changes are closely linked to deficits in hippocampus-dependent cognitive processes, including spatial learning, recognition memory, and behavioral flexibility, as demonstrated in both clinical and experimental studies. Understanding the mechanisms underlying hippocampal dysfunction provides a basis for improved prevention strategies, early diagnosis, and targeted interventions. Given that fetal alcohol spectrum disorders are entirely preventable, integrating biological insights with public health approaches is essential for reducing the long-term burden of developmental alcohol exposure.