Journal
NEUROSCIENCE
Volume 446, Issue -, Pages 323-334Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2020.08.004
Keywords
Parkinson's disease; NLRP3 inflammasome; Parkin; alpha-synuclein
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Funding
- National Natural Science Foundation of China [81520108010, 81771216]
- Key Research and Development Program of Zhejiang Province [2020C03020]
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Chronic inflammation might correlate with the formation of alpha-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 (IL1 beta) 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. (c) 2020 IBRO. Published by Elsevier Ltd. All rights reserved.
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