NLRP3 Inflammasome-Related Proteins Are Upregulated in the Putamen of Patients With Multiple System Atrophy
Abstract
Multiple system atrophy (MSA) is a neurodegenerative disease characterized by parkinsonism, ataxia, and autonomic dysfunction. Microglial infiltration is an important mediator in MSA. The nucleotide-binding domain, leucine-rich repeats-containing family, pyrin domain-containing-3 (NLRP3) inflammasome complex, comprising NLRP3, apoptotic speck protein containing a caspase recruitment domain (ASC), and cysteine aspartic acid protease 1 (Caspase 1), regulates microglial inflammation in several neurodegenerative diseases. However, its role in MSA remains unknown. This study aimed to investigate the role of the NLRP3 inflammasome in MSA. Immunohistochemical staining of postmortem brains from 11 cases of MSA, 5 of Parkinson disease, and 6 age-matched controls were assessed. The relationships among α-synuclein deposition, microglial infiltration, and NLRP3 inflammasome-related proteins (NLRP3, ASC, and Caspase 1) were quantitatively analyzed. Double-labeling immunofluorescence staining confirmed colocalization of NLRP3 inflammasome-related proteins and Cluster of Differentiation 68. We demonstrated that the density of microglia expressing NLRP3 inflammasome-related proteins was increased in the putamina of MSA cases and was significantly related to the deposition of phosphorylated α-synuclein-positive glial cytoplasmic inclusions, tyrosine hydroxylase-positive fiber loss, and gliosis of glial fibrillary acidic protein-positive astrocytes. Our study suggests that the NLRP3 inflammasome is significantly upregulated and correlates with the neurodegenerative process in MSA.
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NLRP3 inflammasome may be related to neurodegeneration in MSA.
“The above evidence suggests that the NLRP3 inflammasome may be related to neurodegeneration in MSA.”
From Microglia in neurodegenerative diseases: mechanism and potential therapeutic targets (2023) · cites this paper as [299]
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Self-citation
- Authors
- Li, F., Ayaki, T., Maki, T., Sawamoto, N., & Takahashi, R.
- Affiliations
- Department of Neurology
- Kyoto University (JP)
- Corresponding author
- Ayaki, Takashi
- Venue
- Journal of Neuropathology & Experimental Neurology
- Publisher
- Oxford University Press (OUP)
- Published
- 2018-10-05
- Volume
- 77
- Issue
- 11
- Pages
- 1055-1065
- ISSN
- 0022-3069 (ISSN-L)
- 1554-6578
- OpenAlex
- W2894767767
- Cited by
- 44
- References
- 36
- Citations by year
- 2026: 8 · 2025: 4 · 2024: 6 · 2023: 5 · 2022: 6 · 2021: 4 · 2020: 7 · 2019: 4
- FWCI
- 1.68
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Journal of Neuropathology & Experimental Neurology (publishedVersion)
- PubMed (publishedVersion)
- Kyoto University Research Information Repository (Kyoto University) (submittedVersion)
- Funders
- MEXT KAKENHI (JP16K18383)
- Topics
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Inflammasome and immune disorders
- Health Sciences › Medicine › Neurology › Parkinson's Disease Mechanisms and Treatments
- Keywords
- multiple system atrophy, NLRP3 inflammasome, microglial infiltration, putamen, glial cytoplasmic inclusions, caspase-1, ASC, neuroinflammation, neurodegeneration, Parkinson's disease, gliosis
- MeSH terms
- NLR Family, Pyrin Domain-Containing 3 Protein, Correlation of Data, Aged, Aged, 80 and over, Cells, Cultured, Female, Glial Fibrillary Acidic Protein, Humans, Male, Neuroglia, Parkinson Disease, Putamen, Tyrosine 3-Monooxygenase, Up-Regulation, Case-Control Studies, Cytokines, Multiple System Atrophy, Caspase 1, alpha-Synuclein, Inflammasomes
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