SynthesisJournal of Alzheimer's disease : JAD2023
Aspirin Use and Risk of Alzheimer's Disease: A 2-Sample Mendelian Randomization Study.
Synthesis 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 9 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
9 citing papers in PubMed, 1 synthesis or guideline pooled it, 13 citations in OpenAlex.
- Association between aspirin use and risk of dementia: a systematic review and meta-analysis.European geriatric medicine · 2024Pooled it
- Aspirin as a neuroprotective scaffold in Alzheimer's disease: inflammation, oxidative stress, and future directions.Molecular biology reports · 2026Review
- Glial Cell Dynamics in Neuroinflammation: Mechanisms, Interactions, and Therapeutic Implications.Biomedicines · 2026Review
- KGiA: Drug repurposing through disease-aware knowledge graph augmentation.Journal of biomedical informatics · 2025Article
- Neuroinflammation: Mechanisms, Dual Roles, and Therapeutic Strategies in Neurological Disorders.Current issues in molecular biology · 2025Review
- Effect of aspirin use on conversion risk from mild cognitive impairment to Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- The causal relationship between cholecystectomy and IBD/IBS and the role of bile acids and gut microbiota: a two-sample Mendelian randomization study.International journal of colorectal disease · 2024Article
- Association of thrombopoietin-related drugs with thromboembolic events: Mendelian randomization and a real-world study.Therapeutic advances in drug safety · 2024Article
- Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
backgroundObservational studies have shown inconsistent findings of the relationships between aspirin use and the risk of Alzheimer's disease (AD).
objectiveSince residual confounding and reverse causality were challenging issues inherent in observational studies, we conducted a 2-sample Mendelian randomization analysis (MR) to investigate whether aspirin use was causally associated with the risk of AD.
methodsWe conducted 2-sample MR analyses utilizing summary genetic association statistics to estimate the potential causal relationship between aspirin use and AD. Single-nucleotide variants associated with aspirin use in a genome-wide association study (GWAS) of UK Biobank were considered as genetic proxies for aspirin use. The GWAS summary-level data of AD were derived from a meta-analysis of GWAS data from the International Genomics of Alzheimer's Project (IGAP) stage I.
resultsUnivariable MR analysis based on these two large GWAS data sources showed that genetically proxied aspirin use was associated with a decreased risk of AD (Odds Ratio (OR): 0.87; 95%CI: 0.77-0.99). In multivariate MR analyses, the causal estimates remained significant after adjusting for chronic pain, inflammation, heart failure (OR = 0.88, 95%CI = 0.78-0.98), or stroke (OR = 0.87, 95%CI = 0.77-0.99), but was attenuated when adjusting for coronary heart disease, blood pressure, and blood lipids.
conclusionFindings from this MR analysis suggest a genetic protective effect of aspirin use on AD, possibly influenced by coronary heart disease, blood pressure, and lipid levels.
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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.