中国神经再生研究(英文版)

中国神经再生研究(英文版) ›› 2026, Vol. 21 ›› Issue (8): 3479-3495.doi: 10.4103/NRR.NRR-D-25-00410

• 综述:脑损伤修复保护与再生 • 上一篇    下一篇

海马神经元功能改变与认知障碍

  

  • 出版日期:2026-08-18 发布日期:2026-04-25
  • 基金资助:
    江苏省研究生科研实践创新项目（KYCX25_3785）

Dysfunction of hippocampal cells and its role in cognitive impairment

Jingwen Ye1, #, Lihong Zhou1, #, Qiaohuizi Li1, #, Yuchen Huang1, #, Xiaoqin Wu1, Liusuyu Zhu1, Jie Zhu1, Jiahao Liu1, Dengsiyuan Gao1, Xia Chen1, *, Gang Chen1, 2, *, Ying Chen1, *   

  1. 1Department of Histology and Embryology, Medical School of Nantong University, Nantong, Jiangsu Province, China; 
    2Key Laboratory of Neuroregeneration of Jiangsu Province and the Ministry of Education, Co-innovation Center of Neuroregeneration, Nantong University; Center for Basic Medical Research, Medical School of Nantong University; Department of Anesthesiology, Affiliated Hospital of Nantong University, Nantong, Jiangsu Province, China
  • Online:2026-08-18 Published:2026-04-25
  • Contact: Ying Chen, PhD, yingchen@ntu.edu.cn; Gang Chen, PhD, chengang6626@ntu.edu.cn; Xia Chen, PhD, ylchenxia@ntu.edu.cn.
  • Supported by:
    This work was supported by Postgraduate Research & Practice Innovation Program of Jiangsu Province, No. KYCX25_3785 (to JY).
     

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摘要：

缺血性脑卒中具有较高的生存率，且相较于出血性脑卒中更常导致认知障碍。认知障碍的核心病理机制主要涉及特定脑区神经回路功能障碍及细胞损伤。文章的目的是详细阐述海马在脑卒中后认知障碍中的作用。文献回顾表明，海马区作为代谢活跃的结构，易受缺氧、低血糖等代谢状态影响。脑卒中后认知障碍相关海马细胞的功能改变主要表现为神经元凋亡、突触可塑性受损及神经发生减少。脑卒中后认知障碍的核心病理机制是一个复杂的反应级联过程，包括神经炎症激活、氧化应激爆发及线粒体功能障碍诱导的神经元凋亡。针对脑缺血后认知障碍的干预药物包括神经保护药物、中药及其提取物以及干细胞疗法，这些药物中许多具有抑制神经炎症、抑制凋亡、促进神经发生等独特优势，在脑缺血后认知障碍的预防和治疗中具有巨大潜力。然而，目前大多数研究为动物实验，临床研究相对较少。未来研究应重点关注脑缺血后认知障碍的干预策略。这些发现可为脑缺血后认知障碍的治疗提供新思路。最后，简要讨论了海马细胞功能障碍在其他与认知衰退相关的疾病中的作用。此综述旨在为研究人员提供海马在认知障碍中的作用及其干预策略的全景视图。


https://orcid.org/0000-0002-4863-2707 (Xia Chen); https://orcid.org/0000-0003-3669-5687 (Gang Chen); 

https://orcid.org/0000-0003-2363-0550 (Ying Chen)

关键词: 凋亡, 脑缺血模型, 认知衰退, 海马, 海马神经元, 线粒体功能障碍, 神经炎症, 神经保护, 神经血管单元, 卒中后认知障碍

Abstract: Ischemic stroke has a higher survival rate and is more likely to result in cognitive impairment than hemorrhagic stroke. The primary pathological mechanism underlying cognitive impairment involves dysfunction of neural circuits and damage to specific brain regions. This review aims to investigate the role of the hippocampus in cognitive impairment following a stroke. A review of the literature suggests that the hippocampus is a metabolically active structure that is easily involved in various metabolic states, such as hypoxia and hypoglycaemia. The functional changes in hippocampal cells associated with poststroke cognitive impairment mainly manifest as neuronal apoptosis, impaired synaptic plasticity, and decreased neurogenesis. The primary pathological mechanism of poststroke cognitive impairment involves a complex cascade of reactions, including neuroinflammatory activation, bursts of oxidative stress, and neuronal apoptosis induced by mitochondrial dysfunction. Interventional drugs for cognitive impairment after cerebral ischemia include neuroprotective drugs, traditional Chinese medicines and their extracts, and stem cell therapies. Many of these drugs have unique advantages, including the inhibition of neuroinflammation, the prevention of apoptosis, and the promotion of neurogenesis. They hold great potential for the prevention and treatment of cognitive impairment following cerebral ischemia. However, most current studies are animal experiments, and relatively few clinical studies exist. In future research, emphasis should be placed on interventions for cognitive impairment following cerebral ischemia. These findings offer novel perspectives for the treatment of cognitive impairment after cerebral ischemia. Finally, the role of hippocampal cell dysfunction in other diseases associated with cognitive decline is briefly discussed. The aim of this review is to provide researchers with a comprehensive overview of the role of the hippocampus in cognitive impairment and its intervention strategies. 

Key words: apoptosis, cerebral ischemia model, cognitive decline, hippocampal neurons, hippocampus, mitochondrial dysfunction, neuroinflammation, neuroprotection, neurovascular unit, poststroke cognitive impairment