ArticleFrontiers in molecular neuroscience2022
The Role of Non-canonical and Canonical Inflammasomes in Inflammaging.
Article in Frontiers in molecular neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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Who cites it
28 citing papers in PubMed, 33 citations in OpenAlex.
- Article
- Neuronal inflammasomes: balancing immunity, neuroinflammation, and homeostasis.Trends in immunology · 2026Review
- Inflammasomes in glioblastoma.Journal of neuroinflammation · 2026Review
- Stool-derived extracellular vesicles increase inflammasome signaling and regulate the gut-brain axis after stroke in Alzheimer's disease transgenic mice.Experimental neurology · 2025Article
- Potential Role of Inflammasomes in Aging.International journal of molecular sciences · 2025Review
- IC100 blocks inflammasome activation induced by α-synuclein aggregates and ASC specks.NPJ Parkinson's disease · 2025Article
- Article
- Characterization of gene expression profiles in Alzheimer's disease and osteoarthritis: A bioinformatics study.PloS one · 2025Article
- Increased inflammasome protein expression identified in microglia from postmortem brains with schizophrenia.Journal of neuropathology and experimental neurology · 2024Article
- NLRP1 inflammasome promotes senescence and senescence-associated secretory phenotype.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2024Article
- The Inflammasome Adaptor Protein ASC in Plasma as a Biomarker of Early Cognitive Changes.International journal of molecular sciences · 2024Article
- Pin1-catalyzed conformational regulation after phosphorylation: A distinct checkpoint in cell signaling and drug discovery.Science signaling · 2024Review
- A Perfect Storm: The Convergence of Aging, Human Immunodeficiency Virus Infection, and Inflammasome Dysregulation.Current issues in molecular biology · 2024Review
- Molecular Mechanisms Linking Osteoarthritis and Alzheimer's Disease: Shared Pathways, Mechanisms and Breakthrough Prospects.International journal of molecular sciences · 2024Review
- Roles of the Caspase-11 Non-Canonical Inflammasome in Rheumatic Diseases.International journal of molecular sciences · 2024Review
- Catalpol reduced LPS induced BV2 immunoreactivity through NF-κB/NLRP3 pathways: anFrontiers in pharmacology · 2024Article
- Remote limb ischemic postconditioning inhibits microglia pyroptosis by modulating HGF after acute ischemia stroke.Bioengineering & translational medicine · 2023Article
- Neural-Cardiac Inflammasome Axis after Traumatic Brain Injury.Pharmaceuticals (Basel, Switzerland) · 2023Article
- Dysregulation of inflammasome activation in glioma.Cell communication and signaling : CCS · 2023Review
- Genetic predisposition to Alzheimer's disease alters inflammasome activity after traumatic brain injury.Translational research : the journal of laboratory and clinical medicine · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Neurodegenerative diseases currently affect millions of people worldwide and continues to increase in the expanding elderly population. Neurodegenerative diseases usually involve cognitive decline and are among the top causes of death. Thus, there is a critical need for the development of treatments and preventive strategies for neurodegenerative diseases. One of the risk factors of neurodegeneration is inflammaging, a low level of chronic inflammation due to old age. We have previously shown that the inflammasome contributes to inflammaging in the central nervous system (CNS). The inflammasome is a multiprotein complex of the innate immune response consisting of a sensor protein, apoptosis speck-like protein containing a CARD (ASC), and caspase-1. Our lab has developed a humanized monoclonal antibody against ASC (anti-ASC). Here, we analyzed cortical lysates from young (3 months old), aged (18 months old), and aged anti-ASC treated mice for the expression of canonical and non-canonical inflammasome proteins. We show that the protein levels of NLRP1, ASC, caspase-1, and caspase-8 were elevated in the cortex of aged mice, and that anti-ASC decreased the expression of these proteins, consistent with lower levels of the pro-inflammatory cytokine interleukin (IL)-1β. Additionally, we show that these proteins form a novel NLRP1-caspase-8 non-canonical inflammasome comprised of NLRP1, caspase-8 and ASC. Moreover, these inflammasome proteins were present in neurons in young and aged mice. Together, these results indicate that a novel NLRP1-caspase-8 non-canonical inflammasome is present in the cortex of mice and that anti-ASC is a potential therapeutic to decrease inflammasome-mediated inflammaging in the CNS.
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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.