Transcriptomic and genetic studies identify IL-33 as a candidate gene for Alzheimer's disease
Open accessAbstract
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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Previously, IL-33 was identified as an AD risk gene and its level was decreased in the brains of LOAD patients.
“Previously, IL-33 was identified as an AD risk gene and its level was decreased in the brains of LOAD patients (53).”
From The effect of Abi3 locus deletion on the progression of Alzheimer’s disease-related pathologies (2023) · cites this paper as [53]
The Results (‘In depth analysis of the IL-33 gene’; page unavailable) report lower IL-33 mRNA expression in AD brains than controls, and the paper identifies IL-33 as a candidate AD risk gene. However, the Methods (‘Brain samples’; page unavailable) describe samples from both early- and late-onset AD patients; the reported expression decrease is not shown specifically for LOAD patients. (LLM, conf=0.86)
Experimental — accuracy not yet measuredIL-33 expression is reduced in the brains of patients with AD.
“IL-33 expression is reduced in the brains of patients with AD (15), and sST2 is increased in the serum of patients with MCI, as demonstrated in the present study (Fig. 1A).”
From IL-33 ameliorates Alzheimer's disease-like pathology and cognitive decline (2016) · cites this paper as [15]
Observations in the murine AD model could be extrapolated to humans.
“Indeed, genetic studies have linked IL-33/ST2 single nucleotide polymorphisms to clinical AD (15,51), suggesting that our observations in the murine AD model could be extrapolated to humans.”
From IL-33 ameliorates Alzheimer's disease-like pathology and cognitive decline (2016) · cites this paper as [15]
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Self-citationIL-33 ameliorates Alzheimer's disease-like pathology and cognitive decline
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“Error bars represent mean ± SEM; *p% 0.05; **p% 0.01; ***p% 0.001). disease is correlated with decreased CNS IL-33 expression (Chapuis et al., 2009).”
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- Authors
- Chapuis, J., Hot, D., Hansmannel, F., Kerdraon, O., Ferreira, S., Hubans, C., Maurage, C. A., Huot, L., Bensemain, F., Laumet, G., Ayral, A. M., Fievet, N., Hauw, J. J., DeKosky, S. T., Lemoine, Y., Iwatsubo, T., Wavrant-Devrièze, F., Dartigues, J. F., Tzourio, C., Buée, L., Pasquier, F., Berr, C., Mann, D., Lendon, C., Alpérovitch, A., Kamboh, M. I., Amouyel, P., & Lambert, J. C.
- Affiliations
- Inserm (FR)
- Institut Pasteur de Lille (FR)
- University of Pittsburgh (US)
- The University of Tokyo (JP)
- National Institutes of Health (US)
- Université de Lille (FR)
- University of Manchester (GB)
- QIMR Berghofer Medical Research Institute (AU)
- Corresponding author
- Lambert, J C
- ORCID
- Venue
- Molecular Psychiatry
- Published
- 2009-02-10
- Volume
- 14
- Issue
- 11
- Pages
- 1004-1016
- ISSN
- 1359-4184 (ISSN-L)
- 1476-5578
- PMC
- PMC2860783
- OpenAlex
- W2032679768
- Cited by
- 201
- References
- 45
- Citations by year
- 2026: 5 · 2025: 7 · 2024: 10 · 2023: 12 · 2022: 11 · 2021: 21 · 2020: 8 · 2019: 8 · 2018: 19 · 2017: 10 · 2016: 19 · 2015: 5 · 2014: 15 · 2013: 12 · 2012: 10
- FWCI
- 8.39
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Molecular Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Research Explorer (The University of Manchester) (publishedVersion)
- PubMed Central (acceptedVersion)
- HAL (submittedVersion)
- Funders
- National Institute on Aging (AG 05-133, P50AG005133, AG13672, R01AG013672)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- Alzheimer's disease, IL-33, candidate genes, genetic polymorphism, cerebral amyloid angiopathy, brain transcriptome, differentially expressed genes, haplotypes, amyloid-beta secretion, genetic risk
- MeSH terms
- Interleukin-33, Alzheimer Disease, Animals, Brain, Cell Line, Transformed, Chlorocebus aethiops, Female, Follow-Up Studies, Genotype, Humans, Interleukins, International Cooperation, Male, Neuroblastoma, Peptide Fragments, Retrospective Studies, RNA, Messenger, Transfection, Proportional Hazards Models, Case-Control Studies, Amyloid beta-Peptides, Cerebral Amyloid Angiopathy, COS Cells, Genetic Predisposition to Disease, Oligonucleotide Array Sequence Analysis, Polymorphism, Single Nucleotide, Genetic Load, Apolipoprotein E4, Genome-Wide Association Study
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