Alcohol abuse and binge drinking are common during adolescence - a maturational period characterized by heightened hippocampal neuroplasticity and neurogenesis. Preclinical rodent models of adolescent binge drinking (i.e., adolescent intermittent ethanol [AIE]) find unique vulnerability of adolescent hippocampal neurogenesis with reductions persisting into adulthood after ethanol cessation. Recent discoveries implicate increased neuroimmune signaling and decreased neurotrophic support through epigenetic mechanisms in the persistent AIE-induced loss of neurogenesis. Importantly, interventions aimed at rectifying the increased neuroimmune signaling and neurotrophic-epigenetic modifications through physical activity, anti-inflammatory drugs, and histone deacetylase inhibitors protect and recover the loss of neurogenesis and cognitive deficits. The mechanisms underlying the persistent AIE-induced loss of adult hippocampal neurogenesis could contribute to broader neurodegeneration, loss of hippocampal neuroplasticity, and cognitive dysfunction.

中文翻译：

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青少年间歇性乙醇暴露后海马神经发生持续丧失的神经免疫和表观遗传机制。

酗酒和酗酒在青春期很常见——这是一个以海马神经可塑性和神经发生增强为特征的成熟期。青少年狂饮（即青少年间歇性酒精 [AIE]）的临床前啮齿动物模型发现青少年海马神经发生的独特脆弱性，酒精停止后持续到成年期减少。最近的发现表明，在持续的 AIE 诱导的神经发生丧失中，通过表观遗传机制增加了神经免疫信号并减少了神经营养支持。重要的是，旨在通过体育活动、抗炎药和组蛋白去乙酰化酶抑制剂纠正增加的神经免疫信号传导和神经营养表观遗传修饰的干预措施可以保护和恢复神经发生和认知缺陷的丧失。