Neuroinflammation in Parkinson's Disease Animal Models: A Cell Stress Response or a Step in Neurodegeneration?
Neuroinflammation in Parkinson's Disease Animal Models: A Cell Stress Response or a Step in Neurodegeneration?
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DOI：
10.1007/7854_2014_356
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发表时间：
2015-01-01
期刊：
影响因子：
--
通讯作者：
Sulzer, David
中科院分区：
文献类型：
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作者：
Cebrian, Carolina;Loike, John D.;Sulzer, David
帕金森病的运动症状是由于黑质多巴胺能神经元的进行性变性造成的。帕金森病中多种神经炎症过程加剧，包括神经胶质介导的反应、促炎物质表达增加和淋巴细胞浸润，特别是在黑质中。神经炎症也与许多帕金森病动物模型的神经变性和随后的行为症状有关，尽管尚不清楚这些特征是否模仿真正疾病中的致病步骤，或者一些炎症特征是否提供保护性应激反应。在这里，我们比较和总结了神经炎症反应和行为的影响，在广泛的毒素为基础的，炎症和遗传性帕金森病动物模型的研究结果。
The motor symptoms of Parkinson's disease are due to the progressive degeneration of dopaminergic neurons in the substantia nigra. Multiple neuroinflammatory processes are exacerbated in Parkinson's disease, including glialmediated reactions, increased expression of proinflammatory substances, and lymphocytic infiltration, particularly in the substantia nigra. Neuroinflammation is also implicated in the neurodegeneration and consequent behavioral symptoms of many Parkinson's disease animal models, although it is not clear whether these features emulate pathogenic steps in the genuine disorder or if some inflammatory features provide protective stress responses. Here, we compare and summarize findings on neuroinflammatory responses and effects on behavior in a wide range of toxin-based, inflammatory and genetic Parkinson's disease animal models.