阿尔茨海默病中的氧化应激:关于信号通路和治疗方法的当前知识
Rishika Dhapola1, Samir K Beura2, Prajjwal Sharma1
1Advanced Pharmacology and Neuroscience Laboratoty, Department of Pharmacology, School of Health Sciences, Central University of Punjab, Ghudda, Bathinda, Punjab, 151401, India.
Molecular biology reports
|January 2, 2024
概括
氧化压力通过破坏神经元和加剧蛋白质聚合,对阿尔茨海默病 (AD) 病理生理学作出重大贡献. 用新型药物准氧化应激途径对未来的AD治疗有希望.
科学领域:
- 神经科学是一个神经科学.
- 生物化学 生物化学
- 药理学 药理学是指药理学的学科.
背景情况:
- 阿尔茨海默病 (AD) 的病理生理学仍然不完全理解.
- 越来越多的证据表明氧化应激是AD发展和进展的关键因素.
- 氧化应激通过涉及线粒体功能障碍和反应性氧物种 (ROS) 生成的机制促进神经退行.
研究的目的:
- 详细说明氧化应激在阿尔茨海默病中的作用.
- 阐明参与氧化应激诱导AD的信号通路.
- 审查针对这些途径的当前和正在开发的药物,以了解其治疗潜力.
主要方法:
- 对AD中氧化应激研究的文献综述.
- 分析受氧化应激影响的信号通路,包括ROS,Aβ和tau病理.
- 检查针对氧化应激和相关途径的药物机制.
主要成果:
- 氧化应激通过增加聚合的粉样β (Aβ) 和神经纤维状结来加剧AD.
- 氧化应激调节的关键途径包括Nrf2,GSK-3β,PP2A,以及各种炎症和生存信号级联.
- 一些药物,包括乙太,普拉米醇,美曼丁,卡维迪醇,黑激素,表甲基酸盐,基因斯坦,多尼佩西尔和复星,通过向这些途径来证明其潜力.
结论:
- 氧化应激是AD病变的核心参与者,驱动神经元损伤和亡.
- 调节特定的信号通路 (例如,Nrf2,CREB/ERK,PP2A) 为AD提供了一个可行的治疗策略.
- 用药理学药物向氧化应激途径代表了开发有效AD治疗的有希望的途径.
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