ArticleJournal of Alzheimer's disease : JAD2014
Alzheimer's disease: evidence for the expression of interleukin-33 and its receptor ST2 in the brain.
Article in Journal of Alzheimer's disease : JAD, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers, 2 of them syntheses that pooled it.
What it found
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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
53 citing papers in PubMed, 2 syntheses or guidelines pooled it, 84 citations in OpenAlex.
- Association between Atopic Dermatitis and Dementia: Evidence from Systematic Review, Meta-analysis, and Mendelian Randomization.Acta dermato-venereologica · 2025Pooled it
- Systematic review of human post-mortem immunohistochemical studies and bioinformatics analyses unveil the complexity of astrocyte reaction in Alzheimer's disease.Neuropathology and applied neurobiology · 2022Pooled it
- Dietary Supplementation with Omega-3 Fatty Acids Rescues Neurodevelopmental Deficits in a Combined Exposure Paradigm of Maternal Oxycodone Exposure and Chronic Stress.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Article
- Targeting IL-33 in Precision Neuroimmunology: Cellular Mechanisms and Therapeutic Strategies for CNS Disorders.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2026Review
- Identification of Druggable Targets for Alzheimer's Disease by Analyzing Circulating Inflammatory Proteins With Mendelian Randomization.Brain and behavior · 2025Article
- Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025Review
- Aerobic exercise ameliorates atherosclerosis-induced cognitive impairment via hippocampal IL-33/NF-κB signaling modulation.Frontiers in physiology · 2025Article
- IL-33/ST2 axis in diverse diseases: regulatory mechanisms and therapeutic potential.Frontiers in immunology · 2025Review
- Global Deficiency of Alzheimer's Disease Risk GeneASN neuro · 2025Article
- The role of IL-1 family of cytokines in the pathogenesis and therapy of Alzheimer's disease.Inflammopharmacology · 2024Review
- Roles of Cytokines in Alzheimer's Disease.International journal of molecular sciences · 2024Review
- ST2 levels and neurodegenerative diseases: is this a significant relation?Annals of medicine and surgery (2012) · 2024Review
- Neurovascular unit, neuroinflammation and neurodegeneration markers in brain disorders.Frontiers in cellular neuroscience · 2024Review
- Blocking IL-33 decelerates cartilage degeneration in knee osteoarthritis through mice model.PloS one · 2024Article
- Review
- Increased Risk of Dementia in Patients with Atopic Dermatitis: A Nationwide Population-Based Cohort Study.Acta dermato-venereologica · 2023Article
- Cause or consequence? The role of IL-1 family cytokines and receptors in neuroinflammatory and neurodegenerative diseases.Frontiers in immunology · 2023Article
- The IL-33/ST2 Pathway in Cerebral Malaria.International journal of molecular sciences · 2022Review
- Mast Cell Cytokines in Acute and Chronic Gingival Tissue Inflammation: Role of IL-33 and IL-37.International journal of molecular sciences · 2022Review
- Discovery of small molecular inhibitors for interleukin-33/ST2 protein-protein interaction: a virtual screening, molecular dynamics simulations and binding free energy calculations.Molecular diversity · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Inflammatory responses are increasingly implicated in the pathogenesis of neurodegenerative diseases such as in Alzheimer's disease (AD). Interleukin-33 (IL-33), a member of IL-1 family, is constitutively expressed in the central nervous system and thought to be an important mediator of glial cell response to neuropathological lesions. Proinflammatory molecules are highly expressed at the vicinity of amyloid plaques (APs) and neurofibrillary tangles (NFTs), the hallmarks of AD pathology. We have investigated the expression of IL-33 and ST2 in relation to APs and NFTs in human AD and non-AD control brains by immunohistochemistry. Sections from the entorhinal cortex, where APs and NFTs appear in early stages of AD, were used for immunohistochemistry. Mouse primary astrocytes were cultured and incubated with amyloid-β1-42 (Aβ1-42), component of plaque for 72 h and analyzed for the expression of IL-33 by flow cytometry. We found strong expression of IL-33 and ST2 in the vicinity of Aβ and AT8 labelled APs and NFTs respectively, and in the glial cells in AD brains when compared to non-AD control brains. IL-33 and ST2 positive cells were also significantly increased in AD brains when compared to non-AD brains. Flow cytometric analysis revealed incubation of mouse astrocytes with Aβ1-42 increased astrocytic IL-33 expression in vitro. These results suggest that IL-33, an alamin cytokine, may induce inflammatory molecule release from the glial cells and may play an important role in the pathogenesis of AD.
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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.