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Parkinson's Disease-Induced Zebrafish Models: Focussing on Oxidative Stress Implications and Sleep Processes.
Oxidative Medicine and Cellular Longevity ( IF 7.310 ) Pub Date : 2020-08-18 , DOI: 10.1155/2020/1370837
Madalina-Andreea Robea 1 , Ioana-Miruna Balmus 2, 3 , Alin Ciobica 3 , Stefan Strungaru 3 , Gabriel Plavan 1 , Lucian Dragos Gorgan 1 , Alexandra Savuca 1 , Mircea Nicoara 1
Affiliation  

The complex yet not fully understood pathophysiology of Parkinson’s disease includes an important molecular component consisting of oxidative status changes, thus leading to oxidative stress occurrence. While no particular evidence has been reported that describes the relationship between oxidative stress and the molecular mechanisms behind Parkinson’s disease development, animal model studies has shown that oxidative stress induction could modulate Parkinson’s disease symptomatology. Despite the inability to perfectly replicate human disease in animals and despite that Parkinson’s disease has not been reported in any animal species, animal modeling is one of the most important tools in understanding the complex mechanisms of human disorders. In this way, this study is aimed at detailing this particular relationship and describing the molecular mechanisms underlying Parkinson’s disease in animal models, focusing on the potential advantages and disadvantages of zebrafish in this context. The information relevant to this topic was gathered using major scientific database research (PubMed, Google Scholar, Web of Science, and Scopus) based on related keywords and inclusion criteria. Thus, it was observed that oxidative stress possesses an important role in Parkinson’s disease as shown by numerous animal model studies, many of which are based on rodent experimental models. However, an emerging impact of the zebrafish model was observed in the research of Parkinson’s disease pathological mechanisms with regard to disease development factors and the cause-effect relationship between oxidative stress and comorbidities (such as depression, hyposmia, fatigue, sleep disturbances, and cognitive deficits) and also with regard to the pharmacological potential of antioxidant molecules in Parkinson’s disease treatment.

中文翻译:

帕金森氏病诱发的斑马鱼模型:专注于氧化应激影响和睡眠过程。

帕金森氏病的复杂但尚未完全理解的病理生理学包括由氧化状态变化组成的重要分子成分,因此导致氧化应激的发生。尽管尚无报道描述氧化应激与帕金森氏病发展背后的分子机制之间关系的特殊证据,但动物模型研究表明,氧化应激诱导可以调节帕金森氏症的症状。尽管无法在动物中完美地复制人类疾病,并且尽管尚未在任何动物物种中报道帕金森氏病,但动物模型还是了解人类疾病复杂机制的最重要工具之一。通过这种方式,这项研究旨在详细说明这种特殊的关系,并描述动物模型中帕金森氏病的潜在分子机制,重点是在这种情况下斑马鱼的潜在优势和劣势。与该主题相关的信息是根据相关关键字和纳入标准,使用大型科学数据库研究(PubMed,Google Scholar,Web of Science和Scopus)收集的。因此,观察到氧化应激在帕金森氏病中具有重要作用,如许多动物模型研究所示,其中许多是基于啮齿动物实验模型的。然而,
更新日期:2020-08-19
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