ReviewBiomedicines2023
NLRP3 Inflammasome's Activation in Acute and Chronic Brain Diseases-An Update on Pathogenetic Mechanisms and Therapeutic Perspectives with Respect to Other Inflammasomes.
Review in Biomedicines, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 citations in OpenAlex.
- A molecular systems architecture of neuromuscular junction in amyotrophic lateral sclerosis.NPJ systems biology and applications · 2025Pooled it
- The IL-1β-STING Signaling Axis Drives Neuromyelitis Optica Pathogenesis in a Murine Model.Annals of neurology · 2026Article
- Metformin's disruption of gluconeogenesis in type 2 diabetes impairments of the cori and alanine cycles as hidden drivers of metabolic waste accumulation, NF-κBHIF-1α-mediated low-grade inflammation, and multisystem dysfunction.Problemy endokrinologii · 2026Review
- Dissecting PANoptosis in the Nervous System: A Unified Cell-Death Mechanism Driving Neuroimmune Activation and Chronic Neuroinflammation.Molecular neurobiology · 2026Review
- Caffeic acid restores neurogenesis and synaptic integrity under glucolipotoxic stress by suppressing inflammation and pyroptosis.Metabolic brain disease · 2026Article
- Review
- Multiomics Profiling Supports Cathepsin B as a Protective Factor in Cerebral Small Vessel Disease.Research square · 2026Article
- The role of NLRP3 neuroinflammation in cognitive frailty diversity during aging and after LPS administration in mice.Scientific reports · 2026Article
- Dual roles of basal NLRP3 expression in cognitive and neurogenic aging.Biogerontology · 2026Article
- Mechanisms and Risk Factors of Cognitive Impairment in COPD.CHEST pulmonary · 2026Article
- Galectin-3 as a Key Driver of Neuroinflammation and α-Synuclein Aggregation in Parkinson's Disease: Unlocking New Paths for Biomarkers and Therapies.Cell biochemistry and biophysics · 2026Review
- Complement, Inflammasome, and Microglial Crosstalk in Glaucoma: From Neurodegeneration to Immune-Based Precision Therapy.Life (Basel, Switzerland) · 2026Review
- The gut-brain axis: role of gut microbiota in neurological disease pathogenesis and pharmacotherapeutics.Naunyn-Schmiedeberg's archives of pharmacology · 2026Review
- The protective effects of selenium against NLRP3-mediated inflammation and pyroptosis: mechanisms and the potential health benefits.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2026Review
- Electroacupuncture attenuates neuroinflammation by regulating the NLRP3 inflammasome pathway: an animal study.American journal of translational research · 2026Article
- Stem cell-mediated recovery in stroke: partnering with the immune system.Nature reviews. Neuroscience · 2026Review
- FNR-like unit interacts with C-terminal related residues trigger nNOS reductase domain conformational flexibility change.Frontiers in neuroscience · 2026Article
- Neuroinflammation and treatment resistance in major depressive disorder.Frontiers in pharmacology · 2026Review
- Exosomes Regulate the NLRP3/Caspase-1/IL-1β Signaling Pathway in Parkinson's Disease: Mechanisms of Neuroinflammation Modulation and α-Synuclein Propagation.Neuropsychiatric disease and treatment · 2026Review
- NLRP3 Inflammasome Activation in Oxidative Stress: A Key Mechanism Driving Neuroinflammation.Neuroimmunomodulation · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
Increasingly prevalent acute and chronic human brain diseases are scourges for the elderly. Besides the lack of therapies, these ailments share a neuroinflammation that is triggered/sustained by different innate immunity-related protein oligomers called inflammasomes. Relevant neuroinflammation players such as microglia/monocytes typically exhibit a strong NLRP3 inflammasome activation. Hence the idea that NLRP3 suppression might solve neurodegenerative ailments. Here we review the recent Literature about this topic. First, we update conditions and mechanisms, including RNAs, extracellular vesicles/exosomes, endogenous compounds, and ethnic/pharmacological agents/extracts regulating NLRP3 function. Second, we pinpoint NLRP3-activating mechanisms and known NLRP3 inhibition effects in acute (ischemia, stroke, hemorrhage), chronic (Alzheimer's disease, Parkinson's disease, Huntington's disease, MS, ALS), and virus-induced (Zika, SARS-CoV-2, and others) human brain diseases. The available data show that (i) disease-specific divergent mechanisms activate the (mainly animal) brains NLRP3; (ii) no evidence proves that NLRP3 inhibition modifies human brain diseases (yet ad hoc trials are ongoing); and (iii) no findings exclude that concurrently activated other-than-NLRP3 inflammasomes might functionally replace the inhibited NLRP3. Finally, we highlight that among the causes of the persistent lack of therapies are the species difference problem in disease models and a preference for symptomatic over etiologic therapeutic approaches. Therefore, we posit that human neural cell-based disease models could drive etiological, pathogenetic, and therapeutic advances, including NLRP3's and other inflammasomes' regulation, while minimizing failure risks in candidate drug trials.
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What Socratic holds
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 Socratic graph.