Jahan Israt, Harun-Ur-Rashid Mohammad, Islam Md Aminul, Sharmin Farhana, Al Jaouni Soad K, Kaki Abdullah M, Selim Samy
Genetic Engineering and Biotechnology Research Laboratory (GEBRL), Centre for Advanced Research in Sciences (CARS), University of Dhaka, Dhaka, Bangladesh.
Department of Chemistry, International University of Business Agriculture and Technology (IUBAT), Sector 10, Uttara Model Town, Dhaka, Bangladesh.
Neural Regen Res. 2024 Dec 16;21(1):107-25. doi: 10.4103/NRR.NRR-D-24-01019.
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.
神经元可塑性,即大脑在结构和功能上进行适应的能力,对于学习、记忆以及损伤恢复至关重要。在诸如阿尔茨海默病和帕金森病等神经退行性疾病中,这种可塑性遭到破坏,导致认知和运动功能障碍。本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。阿尔茨海默病的特征是淀粉样β蛋白斑块和tau蛋白缠结,它们会损害突触功能,而帕金森病则涉及多巴胺能神经元的丧失,影响运动控制。增强神经元可塑性为这些疾病提供了治疗潜力。使用PubMed、Scopus和谷歌学术等数据库进行了系统的文献综述,重点关注阿尔茨海默病和帕金森病中神经元可塑性的研究。数据综合确定了诸如突触机制、神经发生和治疗策略等关键主题,将分子层面的见解与临床应用联系起来。结果表明,针对突触可塑性机制,如长时程增强和长时程抑制,具有前景。神经营养因子、先进的成像技术和分子工具(如成簇规律间隔短回文重复序列和光遗传学)对于理解和增强可塑性至关重要。目前的治疗方法,包括多巴胺替代、深部脑刺激和生活方式干预,显示出缓解症状和改善预后的潜力。总之,通过靶向治疗增强神经元可塑性在治疗神经退行性疾病方面具有重大前景。未来的研究应整合多学科方法,以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。