The effects of ursodeoxycholic acid on Parkinson's disease, a mechanistic review of the recent evidence.

IF 3.5 3区 医学 Q2 ENDOCRINOLOGY & METABOLISM Metabolic brain disease Pub Date : 2025-02-01 DOI:10.1007/s11011-025-01542-9
Seyed Mehrad Razavi, Niusha Esmaealzadeh, Mazyar Ataei, Nadia Afshari, Moloud Saleh, Yasaman Amini, Sadaf Hasrati, Fatemeh Ghazizadeh Hashemi, Abolghasem Mortazavi, Leila Mohaghegh Shalmani, Amir Hossein Abdolghaffari
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Abstract

Introduction: Parkinson`s disease stands as the second-most widespread neurodegenerative disorder. Parkinson`s disease is relentless in progression and irreversible in nature, for which there is no cure. Therapies are only used to attenuate motor symptoms. As Parkinson`s disease is primarily defined by degeneration of dopaminergic neurons in the substantia nigra, and considering that neuroinflammation and mitochondrial dysfunction in these neurons are key factors contributing to disease progression, alternative therapies should aim to preserve healthy mitochondria. Method. Eligible studies on the effect of Ursodeoxycholic acid (UDCA) on Parkinson`s disease were collected from PubMed, Google Scholar, Scopus, Web of Science and Cochrane library for clinical, in-vivo, and in-vitro studies. Result. UDCA and its taurine conjugate (TUDCA), which are endogenous bile acids, have exhibited neuroprotective potential in various neurological conditions, such as Alzheimer's disease, Parkinson's disease and Huntington's disease, in both animal experimental models and clinical investigations. This is attributed to three significant properties, in addition to their capability to cross the blood-brain barrier. First, their anti-inflammatory properties are manifested through the reduction of significant inflammatory factors such as tumor necrosis factor-α, interleukin 1β and other related elements. Second, their antioxidant property is marked by an increase in the expression of superoxide dismuthase, glutathione peroxidase and other antioxidant enzymes. The third property is the antiapoptotic activity, characterized by decreased caspase-3 activity and lower expression of pro-apoptotic Bax in the striatum. Conclusion. Based on this comprehensive review, UDCA and TUDCA have the potential to be considered as a therapeutic agent in the management of the Parkinson's disease.

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熊去氧胆酸对帕金森病的作用,近期证据的机制综述。
简介:帕金森氏病是第二大最广泛的神经退行性疾病。帕金森氏症的发展是无情的,本质上是不可逆转的,目前尚无治愈方法。治疗只用于减轻运动症状。由于帕金森病主要由黑质多巴胺能神经元的退化定义,并且考虑到这些神经元的神经炎症和线粒体功能障碍是促进疾病进展的关键因素,替代疗法应以保持健康的线粒体为目标。方法。从PubMed、谷歌Scholar、Scopus、Web of Science和Cochrane图书馆中收集了熊去氧胆酸(UDCA)治疗帕金森病的符合条件的临床、体内和体外研究。结果。UDCA及其牛磺酸缀合物(TUDCA)是内源性胆汁酸,在动物实验模型和临床研究中显示出对各种神经系统疾病(如阿尔茨海默病、帕金森病和亨廷顿病)的神经保护潜力。除了能够穿过血脑屏障外,这还归因于三个重要的特性。首先,其抗炎特性是通过降低肿瘤坏死因子-α、白细胞介素1β等重要炎症因子等相关元素来体现的。其次,它们的抗氧化性能表现为超氧化物二甲基化酶、谷胱甘肽过氧化物酶和其他抗氧化酶的表达增加。第三个特性是抗凋亡活性,其特征是纹状体中caspase-3活性降低,促凋亡Bax表达降低。结论。基于这一综合综述,UDCA和TUDCA有潜力被认为是治疗帕金森病的一种药物。
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来源期刊
Metabolic brain disease
Metabolic brain disease 医学-内分泌学与代谢
CiteScore
5.90
自引率
5.60%
发文量
248
审稿时长
6-12 weeks
期刊介绍: Metabolic Brain Disease serves as a forum for the publication of outstanding basic and clinical papers on all metabolic brain disease, including both human and animal studies. The journal publishes papers on the fundamental pathogenesis of these disorders and on related experimental and clinical techniques and methodologies. Metabolic Brain Disease is directed to physicians, neuroscientists, internists, psychiatrists, neurologists, pathologists, and others involved in the research and treatment of a broad range of metabolic brain disorders.
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