Chronic peripheral inflammation, hippocampal neurogenesis, and behavior.
Chronic peripheral inflammation, hippocampal neurogenesis, and behavior.
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DOI：
10.1016/j.bbi.2016.01.017
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发表时间：
2016-11
期刊：
影响因子：
--
通讯作者：
Wawrowsky K
中科院分区：
文献类型：
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作者：
Chesnokova V;Pechnick RN;Wawrowsky K
成年海马神经发生与记忆和学习有关，神经发生中断与认知障碍和情绪障碍有关，包括焦虑和抑郁。一些长期的外周疾病和代谢紊乱，以及正常的衰老，创造了慢性外周炎症的状态。这些病症与行为障碍有关，这些行为障碍与成年海马神经发生中断有关，例如认知障碍、学习和记忆缺陷以及抑郁和焦虑。在外周中释放的促炎细胞因子通过激活脑中的常驻小胶质细胞而参与外周免疫系统与脑的通信。活化的小胶质细胞通过抑制神经元干细胞增殖、增加神经元祖细胞的凋亡和减少新发育的神经元的存活及其整合到现有神经元回路中来减少神经发生。在这篇综述中，我们总结了不断发展的证据表明，慢性外周炎症的状态减少成人海马神经发生，这反过来又产生了慢性炎症性疾病中观察到的行为障碍。由于没有关于慢性外周炎性疾病患者神经发生的数据，我们专注于动物模型，并同时考虑人类患者认知障碍和情绪障碍的证据。
Adult hippocampal neurogenesis is involved in memory and learning, and disrupted neurogenesis is implicated in cognitive impairment and mood disorders, including anxiety and depression. Some long-term peripheral illnesses and metabolic disorders, as well as normal aging, create a state of chronic peripheral inflammation. These conditions are associated with behavioral disturbances linked to disrupted adult hippocampal neurogenesis, such as cognitive impairment, deficits in learning and memory, and depression and anxiety. Pro-inflammatory cytokines released in the periphery are involved in peripheral immune system-to-brain communication by activating resident microglia in the brain. Activated microglia reduce neurogenesis by suppressing neuronal stem cell proliferation, increasing apoptosis of neuronal progenitor cells, and decreasing survival of newly developing neurons and their integration into existing neuronal circuits. In this review, we summarize evolving evidence that the state of chronic peripheral inflammation reduces adult hippocampal neurogenesis, which, in turn, produces the behavioral disturbances observed in chronic inflammatory disorders. As there are no data available on neurogenesis in humans with chronic peripheral inflammatory disease, we focus on animal models and, in parallel, consider the evidence of cognitive disturbance and mood disorders in human patients.