ArticleArchives of medical science : AMS2025
Causal association of plasminogen activators and their inhibitors with Alzheimer's disease: a Mendelian randomization study.
Article in Archives of medical science : AMS, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Introduction: Alzheimer's disease (AD) is the most common cause of dementia and contributes to a huge burden of disease worldwide. Observational studies have found that tissue plasminogen activator (t-PA) inhibits the development of AD, but little is known about urokinase plasminogen activator (u-PA) or plasminogen activator inhibitor-1 (PAI-1). At present, the causal relationship is not clear. Therefore, this study intended to explore the relationship between plasminogen activators and their inhibitors with Alzheimer's disease through the Mendelian randomization method, so as to provide a reference for the prevention and control of Alzheimer's disease. Material and methods: To investigate causal pathways, we conducted a two-sample Mendelian randomization study using pooled statistics from genome-wide association studies. Inverse-variance weighted (IVW), Mendelian randomization-Egger (MR-Egger), weighted-median, Mendelian randomization pleiotropy residual sum and outlier (MR-PRESSO) and Mendelian randomization-robust adjusted profile score (MR-RAPS) methods were used to evaluate the robustness of the results. Results: In the outcome of AD (more controls excluded), the IVW effect of PAI-1 OR (95% CI) was found as follows: 1.543 (1.010-2.356), whose interval does not include 1 and Conclusions: Our results showed that gene-predicted PAI-1 in Mendelian stochastic analysis was associated with an increased risk of AD.
Indexed as
Identifiers
What OpenQuestion holds
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 OpenQuestion graph.