帕金
上睑下垂
炎症体
品脱1
帕金森病
发病机制
吡喃结构域
炎症
α-突触核蛋白
多巴胺能
神经科学
生物
疾病
医学
免疫学
多巴胺
病理
作者
Yiqun Yan,Yi Fang,Ran Zheng,Jiali Pu,Baorong Zhang
出处
期刊:Neuroscience
[Elsevier]
日期:2020-10-01
卷期号:446: 323-334
被引量:49
标识
DOI:10.1016/j.neuroscience.2020.08.004
摘要
Chronic inflammation might correlate with the formation of α-synuclein oligomers, subsequently leading to dopaminergic (DA) neuronal death in Parkinson's disease (PD). As major components of chronic inflammation, NOD-like receptor protein 3 (NLRP3) inflammasomes play a crucial role in PD via caspase 1 activation, primarily induced by mitochondrial damage. NLRP3 binds to apoptosis-associated speck-like protein containing a CARD (PYCARD/ASC), and forms inflammasomes in the brain. Inflammasomes act as a platform for caspase 1 to induce interleukin 1 Beta (IL1β) maturation, leading to neuronal pyroptosis. Furthermore, alpha-synuclein, whose abnormal aggregation is the main pathogenesis of PD, also activates NLRP3 inflammasomes. Mutations to PRKN (encoding Parkin) are the most common cause of autosomal recessive familial and sporadic early-onset PD. Evidence has confirmed a relationship between Parkin and NLRP3 inflammasomes. In this review, we summarize the current understanding of NLRP3 inflammasomes and their role in PD progression, and discuss their regulation by Parkin.
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