ArticleJournal of Alzheimer's disease : JAD2023
Association of COVID-19 with Risk and Progression of Alzheimer's Disease: Non-Overlapping Two-Sample Mendelian Randomization Analysis of 2.6 Million Subjects.
Article in Journal of Alzheimer's disease : JAD, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 1 synthesis or guideline pooled it, 7 citations in OpenAlex.
- Causal association of COVID-19 with brain structure changes: Findings from a non-overlapping 2-sample Mendelian randomization study.Journal of the neurological sciences · 2023Pooled it
- Neuroimmune pathophysiology of long COVID.Psychiatry and clinical neurosciences · 2025Review
- MINDSETS: Multi-omics Integration with Neuroimaging for Dementia Subtyping and Effective Temporal Study.Scientific reports · 2025Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
backgroundEpidemiological studies showed that COVID-19 increases risk of Alzheimer's disease (AD). However, it remains unknown if there is a potential genetic predispositional effect.
objectiveTo examine potential effects of genetic susceptibility of COVID-19 on the risk and progression of AD, we performed a non-overlapping 2-sample Mendelian randomization (MR) study using summary statistics from genome-wide association studies (GWAS).
methodsTwo-sample Mendelian randomization (MR) analysis of over 2.6 million subjects was used to examine whether genetic susceptibility of COVID-19 is not associated with the risk of AD, cortical amyloid burden, hippocampal volume, or AD progression score. Additionally, a validation analysis was performed on a combined sample size of 536,190 participants.
resultsWe show that the AD risk was not associated with genetic susceptibility of COVID-19 risk (OR = 0.98, 95% CI 0.81-1.19) and COVID-19 severity (COVID-19 hospitalization: OR = 0.98, 95% CI 0.9-1.07, and critical COVID-19: OR = 0.98, 95% CI 0.92-1.03). Genetic predisposition to COVID-19 is not associated with AD progression as measured by hippocampal volume, cortical amyloid beta load, and AD progression score. These findings were replicated in a set of 536,190 participants. Consistent results were obtained across models based on different GWAS summary statistics, MR estimators and COVID-19 definitions.
conclusionsOur findings indicated that the genetic susceptibility of COVID-19 is not associated with the risk and progression of AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.