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Genome-Wide Association and Mechanistic Studies Indicate That Immune Response Contributes to Alzheimer's Disease Development
Liu C, Chyr J, Zhao W, Xu Y, Ji Z, Tan H, Soto C, Zhou X et al.. Frontiers in genetics, 2018-09-24
Topic: Amyloid, tau and blood-test diagnosis
Alzheimer's disease (AD) is the most common cause of dementia. Although genome-wide association study (GWAS) have reported hundreds of single-nucleotide polymorphisms (SNPs) and genes linked to AD, the mechanisms about how these SNPs modulate the development of AD remain largely unknown. In this study, we performed GWAS for three traits in cerebrospinal fluid (CSF) and one clinical trait in the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Liu, C., Chyr, J., Zhao, W., Xu, Y., Ji, Z., Tan, H., et al. (2018). Genome-Wide Association and Mechanistic Studies Indicate That Immune Response Contributes to Alzheimer's Disease Development. Frontiers in genetics. https://doi.org/10.3389/fgene.2018.00410
Vancouver
Liu C, Chyr J, Zhao W, Xu Y, Ji Z, Tan H, et al. Genome-Wide Association and Mechanistic Studies Indicate That Immune Response Contributes to Alzheimer's Disease Development. Frontiers in genetics. 2018. doi:10.3389/fgene.2018.00410. PMID: 30319691.
BibTeX
@article{liu2018-30319691,
author = {Liu, C. and Chyr, J. and Zhao, W. and Xu, Y. and Ji, Z. and Tan, H. and Soto, C. and Zhou, X. and others},
title = {{Genome-Wide Association and Mechanistic Studies Indicate That Immune Response Contributes to Alzheimer's Disease Development}},
journal = {Frontiers in genetics},
year = {2018},
doi = {10.3389/fgene.2018.00410},
pmid = {30319691},
url = {https://doi.org/10.3389/fgene.2018.00410}
}
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
- Although genome-wide association study (GWAS) have reported hundreds of single-nucleotide polymorphisms (SNPs) and genes linked to AD, the mechanisms about how these SNPs modulate the development of AD remain largely unknown.
- In this study, we performed GWAS for three traits in cerebrospinal fluid (CSF) and one clinical trait in the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort.
- Our analysis identified five most significant AD related SNPs (FDR 2) of three TFs (PLAG1, RREB1, and ZBTB33) for two motifs containing SNPs rs2075650 and rs157580.
- In addition, our GWAS showed that both rs2075650 and rs157580 were significantly associated with the poliovirus receptor-related 2 (PVRL2) gene (FDR < 0.25), which is involved in spreading of herpes simplex virus (HSV).
Why it matters
This study performed genome-wide association analyses for cerebrospinal fluid and clinical traits in the ADNI cohort. It identified several Alzheimer's disease-related genetic variants and suggested that immune response contributes to Alzheimer's disease development.
Study details
- Evidence strengthModerate
How this study scored 41/100
Published in a peer-reviewed journal. Scored zero for study design, sample size, effect reported, studied in people and randomised / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 39 of the 96 points we could judge it on, which is 41 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Frontiers in genetics) |
| Journal's citation record | 2 / 4 | Frontiers in Genetics: journal h-index 173 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| 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 | 2018 — within 10 year(s) of the newest study here |
| Sample size | 0 / 4 | Participant count not stated — scores zero (not stated in the record — scored 0) |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 0 / 3 | Not stated whether this was studied in people — scores zero (not stated in the record — scored 0) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 4 / 7 | Cited 56 times (OpenAlex, 2026-10-10) |
| Citations per year | 2 / 5 | 5.6 citations a year over 10 year(s) since 2018 |
| Impact for its field and year | 3 / 6 | Cited 4.0× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 1 / 4 | Cited 12 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | 1 / 3 | The University of Texas Health Science Center at Houston: institution h-index 756 (OpenAlex) |
| Multi-centre collaboration | 0 / 3 | OpenAlex lists 1 institution(s) in 1 country — scores zero (affiliation lists can be incomplete) |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 30319691) |
| Free to read | 2 / 2 | Free to read |
| Points | 39 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 39 of the 96 points we could judge it on is 41 out of 100. |
| Total | 41 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.3389/fgene.2018.00410
- PubMed: 30319691
- Original source →
- Free full text: Frontiers in Genetics →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
Studies this one cites
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Also in Long-term cohort studies
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