ArticleAlzheimer's research & therapy2020
The role of interleukin-33 in patients with mild cognitive impairment and Alzheimer's disease.
Article in Alzheimer's research & therapy, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 41 citations in OpenAlex.
- Neuroinflammation as a Link in Parkinson's and Alzheimer's Diseases: A Systematic Review and Meta-Analysis.Aging and disease · 2024Pooled it
- Article
- The Role of the IL-33/ST2 Axis in Nervous System Development and Diseases.Immunology and cell biology · 2026Review
- Immunomodulatory mediators IL-33, soluble ST2, IL-10, IFN-Frontiers in oral health · 2026Article
- Identification of plasma inflammatory biomarkers for Alzheimer's disease reveals IFN-γ as a regulator of ACSL1-mediated microglia phenotype.Frontiers in immunology · 2026Article
- Perceiving traumatic brain injury from glymphatic system.Molecular psychiatry · 2025Review
- The role of plasma inflammatory markers in late-life depression and conversion to dementia: a 3-year follow-up study.Molecular psychiatry · 2025Article
- Deciphering genetic causality between plasma BDNF and 91 circulating inflammatory proteins through bidirectional mendelian randomization.Scientific reports · 2025Article
- Association of Rapidly Elevated Plasma Tau Protein With Cognitive Decline in Patients With Amnestic Mild Cognitive Impairment and Alzheimer's Disease.Psychiatry investigation · 2025Article
- Exploring peripheral fluid biomarkers for early detection of Alzheimer's disease in Down syndrome: A literature review.Heliyon · 2025Review
- IL-33/ST2 axis in diverse diseases: regulatory mechanisms and therapeutic potential.Frontiers in immunology · 2025Review
- IL-33 prevents age-related bone loss and memory impairment by suppression of Th17 response: evidence in a d-galactose-induced aging mouse model.JBMR plus · 2024Article
- Cellular Components of the Blood-Brain Barrier and Their Involvement in Aging-Associated Cognitive Impairment.Aging and disease · 2024Review
- The neuroinflammatory role of microglia in Alzheimer's disease and their associated therapeutic targets.CNS neuroscience & therapeutics · 2024Review
- The emerging role of brain neuroinflammatory responses in Alzheimer's disease.Frontiers in aging neuroscience · 2024Review
- Longitudinal assessment of plasma biomarkers for early detection of cognitive changes in subjective cognitive decline.Frontiers in aging neuroscience · 2024Article
- Review
- Exogenous interleukin 33 enhances the brain's lymphatic drainage and toxic protein clearance in acute traumatic brain injury mice.Acta neuropathologica communications · 2023Article
- Pin1 and Alzheimer's disease.Translational research : the journal of laboratory and clinical medicine · 2023Review
- Cause or consequence? The role of IL-1 family cytokines and receptors in neuroinflammatory and neurodegenerative diseases.Frontiers in immunology · 2023Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThe neuroprotective role of interleukin (IL)-33 is supported by numerous preclinical studies, but it remains uninvestigated in clinical studies of Alzheimer's disease (AD). We aimed to examine the association between human blood levels of IL-33 and cognitive preservation in amnestic mild cognitive impairment (aMCI) and AD.
methodsA total of 100 participants (26 controls, 35 aMCI patients, and 39 AD patients) completed two Mini-Mental State Examinations (MMSEs) over a 1-year interval. In all 100 participants at the second MMSE, we examined the plasma levels of IL-33, IL-β, IL-1 receptor agonist (IL-1RA), beta amyloid (Aβ), and tau and apolipoprotein E (ApoE) genotyping; we also performed Hopkins Verbal Learning Test, Trail Making Test, forward and backward digit span, and Clinical Dementia Rating.
resultsIL-33 expression showed a positive trend among controls (1/26 = 3.8%), aMCI (9/35 = 25.7%), and AD (17/39 = 43.6%) (trend analysis: P < 0.001). Patients expressing IL-33 preserved their cognitive function compared with IL-33 non-expressing patients (1-year ΔMMSE, 0.16 ± 1.6 vs - 1.5 ± 2.6; P = 0.006). The cognitive preservation was not associated with the lower levels of Aβ, tau, and ApoE ε4, while higher levels of ApoE ε4 and phosphorylated tau were indeed associated with cognitive decline. The aMCI patients with AD conversion during study period had higher proportion of IL-33(-) than non-AD converters (90.9% vs 53.3%, P = 0.04).
conclusionsIL-33 or its associated signaling pathways may represent a new treatment paradigm for aMCI and AD.
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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.