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 (1): 107-125.doi: 10.4103/NRR.NRR-D-24-01019

• 综述:退行性病与再生 • 上一篇    下一篇

神经元可塑性及在阿尔茨海默病和帕金森病中的作用

  

  • 出版日期:2026-01-15 发布日期:2025-04-19

Neuronal plasticity and its role in Alzheimer’s disease and Parkinson’s disease

Israt Jahan1 , Mohammad Harun-Ur-Rashid2, *, Md. Aminul Islam1 , Farhana Sharmin3 , Soad K. Al Jaouni4 , Abdullah M. Kaki5 , Samy Selim6, *   

  1. 1 Genetic Engineering and Biotechnology Research Laboratory (GEBRL), Centre for Advanced Research in Sciences (CARS), University of Dhaka, Dhaka, Bangladesh;  2 Department of Chemistry, International University of Business Agriculture and Technology (IUBAT), Sector 10, Uttara Model Town, Dhaka, Bangladesh;  3 Department of Anatomy, Shaheed Suhrawardy Medical College, Dhaka, Bangladesh;  4 Department of Hematology/Oncology, Yousef Abdulatif Jameel Scientific Chair of Prophetic Medicine Application, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia;  5 Department of Anesthesia and Pain Medicine, Director of Pain Clinic, Faculty of Medicine, King Abdulaziz University, Jeddah, Saudi Arabia;  6 Department of Clinical Laboratory Sciences, College of Applied Medical Sciences, Jouf University, Sakaka, Saudi Arabia
  • Online:2026-01-15 Published:2025-04-19
  • Contact: Samy Selim, PhD, sabdulsalam@ju.edu.sa; Mohammad Harun-Ur-Rashid, PhD, mrashid@iubat.edu.
  • Supported by:
    This work was financially supported by King Abdulaziz University, Deanship of Scientific Research (DSR).

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摘要：

神经元可塑性是大脑在结构和功能上的适应能力，对于学习、记忆和伤后恢复至关重要。在阿尔茨海默病和帕金森病等神经退行性疾病中，这种可塑性被破坏，导致认知和运动障碍。此综述探讨了神经元可塑性的机制及其对阿尔茨海默病和帕金森病的影响。阿尔茨海默病的特点是淀粉样β蛋白（Aβ）斑块和tau缠结损害突触功能，而帕金森病涉及多巴胺能神经元的丧失，影响运动控制。增强神经元的可塑性为这些疾病提供了治疗潜力。重点关注阿尔茨海默病和帕金森病的神经元可塑性研究。数据综合确定了突触机制、神经发生和治疗策略等关键主题，将分子见解与临床应用联系起来。研究结果表明，针对突触可塑性机制（如长期延时和长期抑制）的研究大有可为。神经营养因子、先进的成像技术和分子工具（如聚类规则间隔短回文重复序列（CRISPR）和光遗传学）对于理解和增强可塑性至关重要。目前的疗法，包括多巴胺替代、脑深部刺激和生活方式干预，都显示出缓解症状和改善预后的潜力。总之，通过靶向疗法增强神经元可塑性在治疗神经退行性疾病方面大有可为。未来的研究应整合多学科方法，充分利用神经元可塑性在阿尔茨海默病和帕金森病中的治疗潜力。

https://orcid.org/0000-0003-4025-8586 (Samy Selim); https://orcid.org/0000-0003-1883-4620 (Mohammad Harun-Ur-Rashid)

关键词: 阿尔茨海默病, 长时程抑制, 长时程增强, 神经炎症, 神经元可塑性, 帕金森病, 突触可塑性

Abstract: Neuronal plasticity, the brain’s ability to adapt structurally and functionally, is essential for learning, memory, and recovery from injuries. In neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease, this plasticity is disrupted, leading to cognitive and motor deficits. This review explores the mechanisms of neuronal plasticity and its effect on Alzheimer’s disease and Parkinson’s disease. Alzheimer’s disease features amyloid-beta plaques and tau tangles that impair synaptic function, while Parkinson’s disease involves the loss of dopaminergic neurons affecting motor control. Enhancing neuronal plasticity offers therapeutic potential for these diseases. A systematic literature review was conducted using databases such as PubMed, Scopus, and Google Scholar, focusing on studies of neuronal plasticity in Alzheimer’s disease and Parkinson’s disease. Data synthesis identified key themes such as synaptic mechanisms, neurogenesis, and therapeutic strategies, linking molecular insights to clinical applications. Results highlight that targeting synaptic plasticity mechanisms, such as long-term potentiation and long-term depression, shows promise. Neurotrophic factors, advanced imaging techniques, and molecular tools (e.g., clustered regularly interspaced short palindromic repeats and optogenetics) are crucial in understanding and enhancing plasticity. Current therapies, including dopamine replacement, deep brain stimulation, and lifestyle interventions, demonstrate the potential to alleviate symptoms and improve outcomes. In conclusion, enhancing neuronal plasticity through targeted therapies holds significant promise for treating neurodegenerative diseases. Future research should integrate multidisciplinary approaches to fully harness the therapeutic potential of neuronal plasticity in Alzheimer’s disease and Parkinson’s disease.

Key words: Alzheimer’s disease, long-term depression, long-term potentiation, neuroinflammation, neuronal plasticity, Parkinson’s disease, synaptic plasticity