Department of Biochemistry and Biophysics, Helen Diller Comprehensive Cancer Center, San Francisco, California.
Toxicology and Experimental Medicine Division, CSIR-Central Drug Research Institute, Lucknow, India.
J Neurosci Res. 2018 Mar;96(3):379-390. doi: 10.1002/jnr.24185. Epub 2017 Oct 26.
Studies in the last decade have suggested the association of both neuroinflammatory processes and immune responses in Parkinson disease (PD) pathology. PD pathology is related to depleted dopamine levels, α-synuclein aggregation, and death of nigrostriatal dopaminergic neurons. Reports have suggested central and peripheral inflammation in the prodromal stage of the disease, which is sustained during disease progression. Alongside the activation of peripheral immune system exacerbates the dissonant central inflammatory responses and could contribute in synergistic neurodegeneration. Activated glial cells contribute significantly in the neuroinflammatory process during the occurrence of the disease and are also acknowledged as a hallmark of disease progression. However, the contribution of glial cells is not well defined in the context of neurodegeneration and neuroprotection. This review provides an overview of the roles of immune and inflammatory responses and their consequences in PD disease pathogenesis and also discusses possible therapeutic strategies for PD based on these findings.
过去十年的研究表明，神经炎症过程和免疫反应都与帕金森病 (PD) 病理学有关。PD 病理学与多巴胺水平降低、α-突触核蛋白聚集以及黑质纹状体多巴胺能神经元死亡有关。有报道称，在疾病的前驱期就存在中枢和外周炎症，并且在疾病进展过程中持续存在。外周免疫系统的激活加剧了不协调的中枢炎症反应，并可能协同导致神经退行性变。在疾病发生时，活化的神经胶质细胞在神经炎症过程中起重要作用，也被认为是疾病进展的标志。然而，在神经退行性变和神经保护的背景下，神经胶质细胞的作用尚未得到很好的定义。本文综述了免疫和炎症反应及其在 PD 发病机制中的后果，并根据这些发现讨论了 PD 的可能治疗策略。
