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A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer's disease
Wightman DP, Jansen IE, Savage JE, Shadrin AA, Bahrami S, Holland D, Rongve A, Børte S et al.. Nature genetics, 2021-09-07
Topic: Amyloid, tau and blood-test diagnosis
Late-onset Alzheimer's disease is a prevalent age-related polygenic disease that accounts for 50-70% of dementia cases. Currently, only a fraction of the genetic variants underlying Alzheimer's disease have been identified. Here we show that increased sample sizes allowed identification of seven previously unidentified genetic loci contributing to Alzheimer's disease.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Wightman, D. P., Jansen, I. E., Savage, J. E., Shadrin, A. A., Bahrami, S., Holland, D., et al. (2021). A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer's disease. Nature genetics. https://doi.org/10.1038/s41588-021-00921-z
Vancouver
Wightman DP, Jansen IE, Savage JE, Shadrin AA, Bahrami S, Holland D, et al. A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer's disease. Nature genetics. 2021. doi:10.1038/s41588-021-00921-z. PMID: 34493870.
BibTeX
@article{wightman2021-34493870,
author = {Wightman, D. P. and Jansen, I. E. and Savage, J. E. and Shadrin, A. A. and Bahrami, S. and Holland, D. and Rongve, A. and Børte, S. and others},
title = {{A genome-wide association study with 1,126,563 individuals identifies new risk loci for Alzheimer's disease}},
journal = {Nature genetics},
year = {2021},
doi = {10.1038/s41588-021-00921-z},
pmid = {34493870},
url = {https://doi.org/10.1038/s41588-021-00921-z}
}
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Key findings
- Currently, only a fraction of the genetic variants underlying Alzheimer's disease have been identified.
- Here we show that increased sample sizes allowed identification of seven previously unidentified genetic loci contributing to Alzheimer's disease.
- This study highlights microglia, immune cells and protein catabolism as relevant to late-onset Alzheimer's disease, while identifying and prioritizing previously unidentified genes of potential interest.
- We anticipate that these results can be included in larger meta-analyses of Alzheimer's disease to identify further genetic variants that contribute to Alzheimer's pathology.
Why it matters
By pooling genetic data from 1,126,563 people, this study found seven genetic regions linked to late-onset Alzheimer's disease that had not been identified before, and it points to microglia, immune cells and protein breakdown ("protein catabolism") as relevant. The authors say only "a fraction" of the genetic variants behind Alzheimer's are known and expect larger analyses to find more. These are risk associations to guide research, not a test, treatment or way to prevent the disease.
Study details
- Study designmeta-analysis
- Evidence strengthHigh
How this study scored 80/100
Published in a leading specialty journal, and it is a meta-analysis pooling many studies. Scored zero for sample size, effect reported and studied in people because the record does not state it.
| Component | Points | Why |
|---|---|---|
| Journal tier | 9 / 10 | Tier 2 — leading specialty journal (Nature genetics) |
| Journal's citation record | 4 / 4 | Nature Genetics: journal h-index 776 (OpenAlex, 2026-10-29) |
| Study design | 12 / 12 | A meta-analysis pooling many studies |
| Strength of evidence | 5 / 5 | Rated “high” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 3 / 5 | 2021 — within 6 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 | A review of other studies — randomisation is not credited here |
| Times cited | 7 / 7 | Cited 1,022 times (OpenAlex, 2026-10-10) |
| Citations per year | 5 / 5 | 146.0 citations a year over 7 year(s) since 2021 |
| Impact for its field and year | 6 / 6 | Cited 87.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 4 / 6 | Cited by 34 other studies in this library |
| Still being cited | 4 / 4 | Cited 660 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | 4 / 4 | Last-listed author Kristian Hveem: h-index 107 (OpenAlex, whole career) |
| Institution's track record | 2 / 3 | University of Michigan: institution h-index 2,240 (OpenAlex) |
| Multi-centre collaboration | 3 / 3 | OpenAlex lists 37 institution(s) in 7 countries |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 34493870) |
| Free to read | 0 / 2 | Behind a paywall — scores zero |
| Total | 80 / 100 | — |
What each of these 20 components measures, and what this score is not →
Read the original
- DOI: 10.1038/s41588-021-00921-z
- PubMed: 34493870
- Original source →
- Free full text: Nature Genetics →
Full text: free to read — OpenAlex lists this copy as free to read: the link above (checked 6 Feb 1020).
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