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Association of IL1RAP-related genetic variation with cerebrospinal fluid concentration of Alzheimer-associated tau protein
Zettergren A, Höglund K, Kern S, Thorvaldsson V, Johan Skoog M, Hansson O, Andreasen N, Bogdanovic N et al.. Scientific reports, 2019-02-21
Topic: Brain proteins, microglia and lab models
A possible involvement of the gene IL1RAP (interleukin-1 receptor-associated protein) in the pathogenesis of Alzheimer's disease (AD) has been suggested in GWASs of cerebrospinal fluid (CSF) tau levels and longitudinal change in brain amyloid burden. The aim of this study was to examine previously implicated genetic markers in and near IL1RAP in relation to AD risk, CSF tau and Aβ biomarkers, as well as cognitive decline, in a case (AD)-control study and an age homogenous population-based cohort. Genotyping of IL1RAP-related single nucleotide polymorphisms (SNPs), selected based on previous GWAS results, was performed. 3446 individuals (1154 AD cases and 2292 controls) were included in the analyses of AD risk, 1400 individuals (cognitively normal = 747, AD = 653) in the CSF biomarker analyses, and 861 individuals in the analyses of cognitive decline.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Zettergren, A., Höglund, K., Kern, S., Thorvaldsson, V., Johan Skoog, M., Hansson, O., et al. (2019). Association of IL1RAP-related genetic variation with cerebrospinal fluid concentration of Alzheimer-associated tau protein. Scientific reports. https://doi.org/10.1038/s41598-018-36650-3
Vancouver
Zettergren A, Höglund K, Kern S, Thorvaldsson V, Johan Skoog M, Hansson O, et al. Association of IL1RAP-related genetic variation with cerebrospinal fluid concentration of Alzheimer-associated tau protein. Scientific reports. 2019. doi:10.1038/s41598-018-36650-3. PMID: 30792413.
BibTeX
@article{zettergren2019-30792413,
author = {Zettergren, A. and Höglund, K. and Kern, S. and Thorvaldsson, V. and Johan Skoog, M. and Hansson, O. and Andreasen, N. and Bogdanovic, N. and others},
title = {{Association of IL1RAP-related genetic variation with cerebrospinal fluid concentration of Alzheimer-associated tau protein}},
journal = {Scientific reports},
year = {2019},
doi = {10.1038/s41598-018-36650-3},
pmid = {30792413},
url = {https://doi.org/10.1038/s41598-018-36650-3}
}
Built from the record alzhub holds for this paper, not looked up. Volume, issue and page numbers are not held in the record. The record's author list ends in “et al.”, so not every author is named. Check the citation against the original before you use it.
Key findings
- The aim of this study was to examine previously implicated genetic markers in and near IL1RAP in relation to AD risk, CSF tau and Aβ biomarkers, as well as cognitive decline, in a case (AD)-control study and an age homogenous population-based cohort.
- Genotyping of IL1RAP-related single nucleotide polymorphisms (SNPs), selected based on previous GWAS results, was performed. 3446 individuals (1154 AD cases and 2292 controls) were included in the analyses of AD risk, 1400 individuals (cognitively normal = 747, AD = 653) in the CSF biomarker analyses, and 861 individuals in the analyses of cognitive decline.
- We found no relation between IL1RAP-related SNPs and AD risk.
- However, CSF total-tau and phospho-tau were associated with the SNP rs9877502 (p = 6 × 10 -3 and p = 5 × 10 -4 ).
Why it matters
This study examined whether genetic variations near the IL1RAP gene are related to Alzheimer's disease risk, spinal fluid tau and amyloid biomarkers, and cognitive decline. It is a genetic association study and does not test any treatment or cure.
New to this subject? Start with our plain-English guide: Blood tests & biomarkers →
Study details
- Study designlongitudinal study
- Participants3,446
- Evidence strengthModerate
How this study scored 56/100
Published in a peer-reviewed journal, and it is a longitudinal study following the same people over time. Scored zero for effect reported and randomized / blinded because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Scientific reports) |
| Journal's citation record | 3 / 4 | Scientific Reports: journal h-index 463 (OpenAlex, 2026-10-29) |
| Study design | 7 / 12 | A longitudinal study following the same people over time |
| Strength of evidence | 3 / 5 | Rated “moderate” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 2 / 5 | 2019 — within 10 year(s) of the newest study here |
| Sample size | 3 / 4 | 3,446 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomized / blinded | 0 / 2 | No randomization or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 2 / 7 | Cited 12 times (OpenAlex, 2026-10-10) |
| Citations per year | 1 / 5 | 1.3 citations a year over 9 year(s) since 2019 |
| Impact for its field and year | 1 / 6 | Cited 0.9× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 1 / 6 | Cited by 2 other studies in this library |
| Still being cited | 1 / 4 | Cited 4 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Henrik Zetterberg: h-index 196 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University College London: institution h-index 2,029 (OpenAlex) |
| Multicenter collaboration | 2 / 3 | OpenAlex lists 9 institution(s) in 2 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30792413) |
| Free to read | 2 / 2 | Free to read |
| Total | 56 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1038/s41598-018-36650-3
- PubMed: 30792413
- Original source →
- Free full text: Scientific Reports →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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