ArticleNPJ Parkinson's disease2024
Lack of genetic evidence for NLRP3 inflammasome involvement in Parkinson's disease pathogenesis.
Article in NPJ Parkinson's disease, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
6 citing papers in PubMed.
- Neuroimmune Regulation of NLRP3 Signalling in Parkinson's Disease.Molecular neurobiology · 2026Review
- Neuronal inflammasomes: balancing immunity, neuroinflammation, and homeostasis.Trends in immunology · 2026Review
- Investigating the Genetic Relationship Between Vitamin B12 Metabolism and Parkinson Disease.Neurology. Genetics · 2026Article
- Differential Peripheral NLRP3 Inflammasome Expression in Patients With Parkinson's Disease and Patients With Multiple System Atrophy.Journal of movement disorders · 2026Article
- The NLRP3-α-Synuclein Circuit: A Core Driver and Therapeutic Target in Parkinson's Disease.Journal of inflammation research · 2026Review
- Tackling a disease on a global scale, the Global Parkinson's Genetics Program, GP2: A new generation of opportunities.American journal of human genetics · 2025Review
Corrections and comments
- Update of
Authors and funding
7 authors.
Funding
Abstract
Activation of the NLRP3 inflammasome has been implicated in Parkinson's disease (PD) based on in vitro and in vivo studies. Clinical trials targeting the NLRP3 inflammasome in PD are ongoing. However, the evidence supporting NLRP3's involvement in PD from human genetics data is limited. We analyzed common and rare variants in NLRP3 inflammasome-related genes in PD cohorts, performed pathway-specific polygenic risk score (PRS) analyses, and studied causal associations using Mendelian randomization (MR) with the NLRP3 components and the cytokines IL-1β and IL-18. Our findings showed no associations of common or rare variants, nor of the pathway PRS with PD. MR suggests that altering the expression of the NLRP3 inflammasome, IL-1β, or IL-18, does not affect PD risk or progression. Therefore, our results do not support a role for the NLRP3 inflammasome in PD pathogenesis or as a target for drug development.
Identifiers
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.