Athari Seyed Zanyar, Farajdokht Fereshteh, Keyhanmanesh Rana, Mohaddes Gisou
Drug Applied Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Neurosciences Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Adv Pharm Bull. 2024 Mar;14(1):120-131. doi: 10.34172/apb.2024.013. Epub 2023 Oct 14.
Parkinson's disease (PD) is the second most common neurodegenerative disease caused by the loss of dopaminergic neurons. Genetic factors, inflammatory responses, oxidative stress, metabolic disorders, cytotoxic factors, and mitochondrial dysfunction are all involved in neuronal death in neurodegenerative diseases. The risk of PD can be higher in aging individuals due to decreased mitochondrial function, energy metabolism, and AMP-activated protein kinase (AMPK) function. The potential of AMPK to regulate neurodegenerative disorders lies in its ability to enhance antioxidant capacity, reduce oxidative stress, improve mitochondrial function, decrease mitophagy and macroautophagy, and inhibit inflammation. In addition, it has been shown that modulating the catalytic activity of AMPK can protect the nervous system. This article reviews the mechanisms by which AMPK activation can modulate PD.
帕金森病(PD)是由多巴胺能神经元丧失引起的第二常见神经退行性疾病。遗传因素、炎症反应、氧化应激、代谢紊乱、细胞毒性因子和线粒体功能障碍均与神经退行性疾病中的神经元死亡有关。由于线粒体功能、能量代谢和AMP激活蛋白激酶(AMPK)功能下降,老年个体患PD的风险可能更高。AMPK调节神经退行性疾病的潜力在于其增强抗氧化能力、降低氧化应激、改善线粒体功能、减少线粒体自噬和巨自噬以及抑制炎症的能力。此外,已有研究表明,调节AMPK的催化活性可以保护神经系统。本文综述了AMPK激活调节PD的机制。