帕金森病综述:病理生理学和实验模型

K. Mohamad, S. Wahdan, Reem Elnaga
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引用次数: 0

摘要

帕金森氏病是一种神经退行性疾病,由多巴胺能神经元死亡引起,并伴有僵硬、姿势不稳定以及运动迟缓。这些神经元死亡的原因尚不清楚。由于多巴胺能神经元不能再生,因此帕金森病无法治愈。因此,在过去的几十年里,人们已经做出了巨大的努力来探索帕金森病发展和确定的病因。这篇综述旨在强调在理解帕金森病病理生理方面取得的进展。氧化应激、神经炎症和细胞凋亡在PD发展中的作用已被讨论。人们已经注意到,氧化应激、炎症和细胞凋亡共同作用导致帕金森病的发生,并且这些因素相互影响。此外,还强调了实验模型及其不足。此外,神经毒素诱导帕金森病(即诱导神经炎症和氧化应激)的机制也得到了强调。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Overview on Parkinson’s disease: pathophysiology, and experimental models
Parkinson's disease, a neurodegenerative disease, is caused by dopaminergic neurons death and accompanied by rigidity, and postural instability, as well as bradykinesia. The cause of these neurons’ death is still unclear. Since the dopaminergic neurons couldn’t regenerate, therefore Parkinson's disease couldn’t be cured. Thus, over the past decades, significant effort has been made to explore the etiology of Parkinson's disease development and ascertainment. This review aimed to highlight the progress that has been made in understanding Parkinson’s disease pathophysiology. The role of oxidative stress, neuroinflammation, and apoptosis in the development of PD has been discussed. It has been noticed that oxidative stress, inflammation, and apoptosis are working together to develop Parkinson's disease, and each of these factors affects each other. Additionally, the experimental models and their drawbacks have been emphasized. Additionally, the mechanism of inducing Parkinson’s disease (i.e., inducing neuroinflammation and oxidative stress) by neurotoxin has been highlighted.
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