Mechanisms of Alcohol Interference with Hippocampal Neurogenesis and its Repair Strategies

The hippocampus is the central target of alcohol-induced neurotoxicity in impairing memory function, with neurogenesis inhibition being its primary mechanism of action. Alcohol interference with hippocampal neurogenesis is closely associated with various diseases. However, limited treatment options currently exist for alcohol-induced hippocampal neuronal damage, and the therapeutic effects are unsatisfactory, placing a significant economic and mental burden on patients' families and society. This review summarises the effects of alcohol on hippocampal neurogenesis during the foetal, adolescent, and adult periods, as well as its mechanisms of action. During the foetal period, alcohol exposure may lead to a decrease in hippocampal cell numbers, impairment of hippocampal synaptic plasticity, alterations in neurodevelopmental proteins, reduced expression of various receptors, interference with neural stem cell differentiation, changes in hippocampal DNA methylation, modifications in neurotrophic factor levels, induction of neuroinflammatory responses, and slow ethanol metabolism. In adolescence, alcohol consumption can adversely affect hippocampal neurogenesis and synapse formation, disrupt metabolic processes within the hippocampus, trigger inflammatory responses, and impair the synthesis of neurotrophic factors. During adulthood, alcohol intake may lead to a reduction in hippocampal neurogenesis, and provoke neuroinflammatory responses, suppress the expression of neurotrophic factors, alter hippocampal metabolite levels, and impact cytoskeletal dynamics within the hippocampus. We also explore potential repair strategies, including pharmacological treatments, nutritional supplementation, plant extracts, and physical therapy, to promote more effective therapeutic approaches.