Shared Genetic Architecture Between COVID-19 Severity and Alzheimer's Disease Across European and African Ancestries
Jingchun Chen, Davis Cammann, Tingwei Liu, Yimei Liu, Melika Cummings, Xiangning Chen, Edwin Oh, Jerome Rotter. Research square, 2024-12-24
Topic: Genetics and APOE
The global outbreak of COVID-19, caused by the SARS-CoV-2 virus, has been linked to long-term neurological complications, including an increased risk of Alzheimer's disease (AD) among older adults. However, the precise genetic impact of COVID-19 on long-term AD development remains unclear. This study leveraged genome-wide association study (GWAS) data and genotype data to explore the genetic association between AD and various COVID-19 phenotypes across European ancestry (EA) and African ancestry (AA) cohorts, and the possibility of a causal effect of COVID-19 on AD. We first calculated polygenic risk scores (PRSs) of three COVID-19 phenotypes in AD cases and controls from both EA and AA populations, then determined the genetic associations between COVID-19 PRSs and AD by logistic regression analyses with or without adjusting for age, sex, and APOE genotypes. Significant positive associations were found between AD diagnosis and COVID-19 PRSs in both populations, with the strongest associations identified in the AA population. However, Mendelian randomization (MR) analyses revealed no evidence of a causal effect of COVID-19 phenotypes on AD liability. We explored this finding further through the analysis of shared genomic regions between the COVID-19 phenotypes and AD and found a region of overlap on chromosome 17 that was highly pleiotropic for traits implicating immune function, psychiatric disorders, and lung function phenotypes. These findings suggest that while COVID-19 and AD share overlapping polygenic contributions involving peripheral genes across multiple traits, they lack a direct connection involving core genes that drive the development of their respective pathologies.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Chen, J., Cammann, D., Liu, T., Liu, Y., Cummings, M., Chen, X., et al. (2024). Shared Genetic Architecture Between COVID-19 Severity and Alzheimer's Disease Across European and African Ancestries. Research square. https://doi.org/10.21203/rs.3.rs-5619229/v1
Vancouver
Chen J, Cammann D, Liu T, Liu Y, Cummings M, Chen X, et al. Shared Genetic Architecture Between COVID-19 Severity and Alzheimer's Disease Across European and African Ancestries. Research square. 2024. doi:10.21203/rs.3.rs-5619229/v1. PMID: 39764106.
BibTeX
@article{chen2024-39764106,
author = {Chen, Jingchun and Cammann, Davis and Liu, Tingwei and Liu, Yimei and Cummings, Melika and Chen, Xiangning and Oh, Edwin and Rotter, Jerome},
title = {{Shared Genetic Architecture Between COVID-19 Severity and Alzheimer's Disease Across European and African Ancestries}},
journal = {Research square},
year = {2024},
doi = {10.21203/rs.3.rs-5619229/v1},
pmid = {39764106},
url = {https://doi.org/10.21203/rs.3.rs-5619229/v1}
}
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 names 8 authors; APA and Vancouver show the first six, BibTeX and the downloads carry all of them. Check the citation against the original before you use it.
Key findings
- The global outbreak of COVID-19, caused by the SARS-CoV-2 virus, has been linked to long-term neurological complications, including an increased risk of Alzheimer's disease (AD) among older adults.
- Significant positive associations were found between AD diagnosis and COVID-19 PRSs in both populations, with the strongest associations identified in the AA population.
- However, Mendelian randomization (MR) analyses revealed no evidence of a causal effect of COVID-19 phenotypes on AD liability.
- These findings suggest that while COVID-19 and AD share overlapping polygenic contributions involving peripheral genes across multiple traits, they lack a direct connection involving core genes that drive the development of their respective pathologies.
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Study details
- Evidence strengthLow
How this study scored 16/100
Preprint — not yet peer-reviewed. It scored 22 on the same rubric, but non-peer-reviewed sources are capped at 16, so it shows as 16. 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 times cited, citations per year, impact for its field and year, cited by studies here, still being cited, senior author's track record, institution's track record, multi-centre collaboration and free to read, so those were left out: it earned 13 of the 60 points we could judge it on, which is 22 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 2 / 10 | Tier 4 — not a peer-reviewed journal (Research square) |
| Journal's citation record | 0 / 4 | Not a journal article, so the journal's record does not count |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 4 / 10 | Preprint — not yet peer-reviewed. Hosted on a preprint server. |
| How recent | 4 / 5 | 2024 — within 3 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 | — / 7 | No citation count (not found in OpenAlex) — left out of this score |
| Citations per year | — / 5 | No citation count or no year — left out of this score |
| Impact for its field and year | — / 6 | No field-weighted citation impact (OpenAlex has none yet) — left out of this score |
| Cited by studies here | — / 6 | Not yet checked against this library's citation graph — left out of this score |
| Still being cited | — / 4 | No yearly citation counts — left out of this score |
| Senior author's track record | — / 4 | Senior author's record not available — left out of this score |
| Institution's track record | — / 3 | No institution listed in OpenAlex — left out of this score |
| Multi-centre collaboration | — / 3 | Institutions not listed — left out of this score |
| Indexed in PubMed | 2 / 2 | Indexed in PubMed (PMID 39764106) |
| Free to read | — / 2 | Access not recorded — left out of this score |
| Points | 13 / 60 | Scored on 11 of 20 parts. We have no data for the rest, so they are left out: 13 of the 60 points we could judge it on is 22 out of 100. |
| Total | 22 / 100 | Capped to 16 because this is not a peer-reviewed article. |
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