神经增生在神经性毒物诱导的帕金森病动物模型中的研究进展

谢明琦 陈治池 王彤彤 周翔 黄厚菊 戚双双 廖敏 孙臣友*

doi:10.16098/j.issn.0529-1356.2017.05.020

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解剖学报 ›› 2017, Vol. 48 ›› Issue (5) : 610-616. DOI: 10.16098/j.issn.0529-1356.2017.05.020

综述

神经增生在神经性毒物诱导的帕金森病动物模型中的研究进展

谢明琦^1,2陈治池^1,2王彤彤^1,2周翔³黄厚菊^2,4 戚双双⁵廖敏^2,4孙臣友^1,2*

作者信息 +

Current status of neurogenesis in neurotoxin-induced animal models for Parkinson’s disease

XIE Ming-qi ^1,2CHEN Zhi-chi ^{1, 2} WANG Tong-tong ^{1, 2} ZHOU Xiang³ HUANG Hou-ju ^2,4 QI Shuang-shuang⁵ LIAO Min ^{2, 4} SUN Chen-you ^{1, 2*}

Author information +

文章历史 +

摘要

帕金森病（PD）动物模型对理解该病病因、发病机制以及检测新的治疗方案具有重要作用。成年哺乳动物脑中内源性神经增生的发现为基于细胞方法治疗神经退行性疾病，如PD，提供了新的探索方向。虽然神经性毒物诱导帕金森病动物模型脑中存在的内源性神经增生引起人们广泛的兴趣，但神经干细胞是否会迁移至受损脑区并促进神经性毒物损伤后成年大脑内减少的多巴胺能神经元数目再增依然存在着争议。我们通过综述关于神经性毒物损伤所致的PD动物模型中神经增生的文献，旨在加深神经增生在神经性毒物诱导的PD动物模型中作用的理解。

Abstract

The animal model of Parkinson’s disease (PD) plays an important role in understanding its etiology, pathogenesis and detection of new treatment regimens. The discovery of endogenous neurogenesis in the adult mammalian brain provides a new direction for the therapy of neurodegenerative diseases, such as PD, based on cellular approaches. Although a lot of attention has been focused on neurotoxininduced endogenous neurogenesis in the brain of animal models for PD, it remains controversial whether neural stem cells migrate to the damaged brain region and promote the repopulation of reduced dopaminergic neurons in adult neurotoxic injured animals. In this paper, we review various literatures on neurogenesis in neurotoxininduced animal models for PD, aiming to deepen the understanding of the role of neurogenesis in neurotoxicity-induced animal models for PD.

导出引用

谢明琦陈治池王彤彤周翔黄厚菊戚双双廖敏孙臣友. 神经增生在神经性毒物诱导的帕金森病动物模型中的研究进展[J]. 解剖学报. 2017, 48(5): 610-616 https://doi.org/10.16098/j.issn.0529-1356.2017.05.020

XIE Ming-qi CHEN Zhi-chi WANG Tong-tong ZHOU Xiang HUANG Hou-ju QI Shuang-shuang LIAO Min SUN Chen-you. Current status of neurogenesis in neurotoxin-induced animal models for Parkinson’s disease[J]. Acta Anatomica Sinica. 2017, 48(5): 610-616 https://doi.org/10.16098/j.issn.0529-1356.2017.05.020

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