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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。
The animal model of Parkinson’s disease (PD) plays an important role in understanding the etiology, pathogenesis and detection of new treatment options. The discovery of endogenous neuronal proliferation in the adult mammalian brain provides a new direction of exploration for the treatment of neurodegenerative diseases such as PD based on cellular methods. Although neurotoxic toxicant-induced endogenous neuronal proliferation in the brain of Parkinson’s disease animal models draws widespread interest, whether or not neural stem cells migrate to damaged brain regions and promote decreased dopamine energy in the adult brain following neurotoxic damage There are still controversies over the increase in the number of neurons. We review the literature on neurite outgrowth in PD animal models caused by neurotoxic toxicants in order to deepen the understanding of the role of neural proliferation in neurotoxic toxic-induced PD animal models.