ArticleMolecular psychiatry2009
Transcriptomic and genetic studies identify IL-33 as a candidate gene for Alzheimer's disease.
Article in Molecular psychiatry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 3 of them syntheses that pooled it.
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Who cites it
115 citing papers in PubMed, 3 syntheses or guidelines pooled it, 201 citations in OpenAlex.
- A genome-wide association meta-analysis of plasma Aβ peptides concentrations in the elderly.Molecular psychiatry · 2014Pooled it
- Increased expression of BIN1 mediates Alzheimer genetic risk by modulating tau pathology.Molecular psychiatry · 2013Pooled it
- The CALHM1 P86L polymorphism is a genetic modifier of age at onset in Alzheimer's disease: a meta-analysis study.Journal of Alzheimer's disease : JAD · 2010Pooled it
- Article
- Enhanced chromatin compaction is associated with de novo expression of a nuclear microprotein, global loss of H3 acetylation and local transcriptional changes in retinal rod photoreceptors.Research square · 2026Article
- The Role of the IL-33/ST2 Axis in Nervous System Development and Diseases.Immunology and cell biology · 2026Review
- TNF inhibition differentially impacts regional Abeta immunotherapy efficacy in the humanized hAbAlzheimer's research & therapy · 2026Article
- Central nervous system pericytes express soluble ST2 in inflammation and injury.Molecular brain · 2026Article
- The IL-33/ST2 Axis Protects the Hippocampus from LPS-Induced Inflammation and Damage by Modulating Microglial Phenotype.Biomedicines · 2026Article
- The Role of Astrocytes in Synaptic Dysfunction and Memory Deficits in Alzheimer's Disease.Biomolecules · 2025Review
- Systemic Inflammatory Factors and Neuropsychiatric Disorders: A Bidirectional Mendelian Randomization Study.Brain and behavior · 2025Article
- Brain interleukins and Alzheimer's disease.Metabolic brain disease · 2025Review
- 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
- Is the Relationship Between Cardiovascular Disease and Alzheimer's Disease Genetic? A Scoping Review.Genes · 2024Article
- Article
- 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
- Impact of TNF and IL-33 Cytokines on Mast Cells in Neuroinflammation.International journal of molecular sciences · 2024Review
55 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
28 authors at 13 institutions in 5 countries.
Funding
Abstract
The only recognized genetic determinant of the common forms of Alzheimer's disease (AD) is the epsilon 4 allele of the apolipoprotein E gene (APOE). To identify new candidate genes, we recently performed transcriptomic analysis of 2741 genes in chromosomal regions of interest using brain tissue of AD cases and controls. From 82 differentially expressed genes, 1156 polymorphisms were genotyped in two independent discovery subsamples (n=945). Seventeen genes exhibited at least one polymorphism associated with AD risk, and following correction for multiple testing, we retained the interleukin (IL)-33 gene. We first confirmed that the IL-33 expression was decreased in the brain of AD cases compared with that of controls. Further genetic analysis led us to select three polymorphisms within this gene, which we analyzed in three independent case-control studies. These polymorphisms and a resulting protective haplotype were systematically associated with AD risk in non-APOE epsilon 4 carriers. Using a large prospective study, these associations were also detected when analyzing the prevalent and incident AD cases together or the incident AD cases alone. These polymorphisms were also associated with less cerebral amyloid angiopathy (CAA) in the brain of non-APOE epsilon 4 AD cases. Immunohistochemistry experiments finally indicated that the IL-33 expression was consistently restricted to vascular capillaries in the brain. Moreover, IL-33 overexpression in cellular models led to a specific decrease in secretion of the A beta(40) peptides, the main CAA component. In conclusion, our data suggest that genetic variants in IL-33 gene may be associated with a decrease in AD risk potentially in modulating CAA formation.
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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.