Journal of Neuroimmune Pharmacology ( IF 5.2 ) Pub Date : 2020-06-11 , DOI: 10.1007/s11481-020-09926-7 Liuna Yang 1 , Kanming Mao 2 , Honglin Yu 2 , Jialong Chen 1
Parkinson’s disease (PD) is the second most common age-related neurodegenerative disorders of the central nervous system, which mainly impairs the motor system. However, the pathogenic mechanisms are still unclear. Gene–environment complex interaction leads to selective dopaminergic neuron death in PD. Growing evidences supports that neuroinflammatory responses are involved in the pathogenesis of PD. This review critically discusses current studies on the inflammatory response of the pathological process of PD. The mechanisms and strategies of modifying inflammatory responses would be potential treatments for neurodegenerative diseases.
Activated microglia canpromote the damage ofdopaminergic neurons, which inturn aggravates the activation ofmicroglia in the process of PD. Atthe same time, microglia canactivate astrocytes throughproliferation and secretion ofinflammatory factors. The role ofastrocytes on the loss ofdopaminergic neurons is stillcontroversial in PD. (Nonsteroidalanti-inflammatory drugs,NSAIDs. adiposed-derived stemcells, ADSCs.nicotinamideadenine dinucleotide phosphate,NADPH. signal transducers andactivators of transcription,STAT.DJ-1,Aliases forPARK7.mesencephalic astrocytederivedneurotrophic factor,MANF.Ciliary neurotrophicfactor,CNTF.glial cell linederivedneurotrophic factor,GDNF.Wnt Family Member1,Wnt1).
Mitochondrial dysfunction causes neuroinflammation throughDAMPs and a series of factors such as oxidative stress andinflammatory bodies in PD. (Damage-associated molecular patterns,DAMPs. reactive oxygen species, ROS).
Various mechanismsparticipate in NLRP3 activation,causing microglia activation inPD. ( -synuclein, -syn.) TolllikeReceptor 2, TLR2. Toll-likeReceptor 4, TLR4. TumorNecrosis Factor, TNF.Apoptosisassociated speck like proteincontaining a CARD, ASC).
中文翻译：
神经炎症反应和帕金森病：致病机制和治疗靶点。
帕金森病 (PD) 是中枢神经系统第二大常见的与年龄相关的神经退行性疾病，主要损害运动系统。然而，其致病机制仍不清楚。基因-环境复杂的相互作用导致 PD 中选择性多巴胺能神经元死亡。越来越多的证据支持神经炎症反应参与 PD 的发病机制。本综述批判性地讨论了当前关于 PD 病理过程的炎症反应的研究。改变炎症反应的机制和策略将是神经退行性疾病的潜在治疗方法。
活化的小胶质细胞可促进多巴胺能神经元的损伤，进而加剧PD过程中小胶质细胞的活化。同时，小胶质细胞可以通过炎症因子的增殖和分泌来激活星形胶质细胞。星形胶质细胞对多巴胺能神经元丢失的作用在 PD 中仍然存在争议。（非甾体抗炎药，NSAIDs。脂肪来源的干细胞，ADSCs。烟酰胺腺嘌呤二核苷酸磷酸，NADPH。信号转导和转录激活剂，STAT.DJ-1，PARK7 的别名。中脑星形胶质细胞衍生的神经营养因子，MANF。睫状神经营养因子，细胞系CNTF。因子,GDNF.Wnt Family Member1,Wnt1)。
线粒体功能障碍通过DAMPs和PD中的氧化应激和炎症小体等一系列因素引起神经炎症。（损伤相关分子模式，DAMPs。活性氧，ROS）。
多种机制参与NLRP3激活，导致PD小胶质细胞激活。(-synuclein, -syn。) TolllikeReceptor 2, TLR2。Toll 样受体 4，TLR4。肿瘤坏死因子，TNF。凋亡相关斑点样蛋白，含有 CARD，ASC)。
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